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Article(id=1317885781251834055, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, articleNumber=null, orderNo=null, doi=10.12449/JCH260825, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1773417600000, receivedDateStr=2026-03-14, revisedDate=null, revisedDateStr=null, acceptedDate=1775059200000, acceptedDateStr=2026-04-02, onlineDate=1792138055383, onlineDateStr=2026-10-16, pubDate=1787587200000, pubDateStr=2026-08-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792138055383, onlineIssueDateStr=2026-10-16, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792138055383, creator=13701087609, updateTime=1792138055383, updator=13701087609, issue=Issue{id=1317885672153797495, tenantId=1146029695717560320, journalId=1316781422847033486, year='2026', volume='42', issue='8', pageStart='1745', pageEnd='2000', issueExtLink='null', onlineDate='null', pubDate='1787587200000', pubDateStr='2026-08-25', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1792138029373, creator='13701087609', updateTime=1792138608261, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317888100290900262, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317888100290900263, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1917, endPage=1925, ext={EN=ArticleExt(id=1317885781495103689, articleId=1317885781251834055, tenantId=1146029695717560320, journalId=1316781422847033486, language=EN, title=Expression of splicing factor 3B subunit 6 in pancreatic cancer and its effect on the biological behaviors of pancreatic cancer cells, columnId=1317885781423800520, journalTitle=Journal of Clinical Hepatology, columnName=Pancreatic Disease, runingTitle=null, highlight=null, articleAbstract=
Objective

To systematically clarify the expression profile of splicing factor 3B subunit 6 （SF3B6） in pancreatic cancer，its clinical prognostic value，and its regulatory effect on the malignant phenotype of cancer cells through bioinformatics analysis，clinical sample validation，and in vitro functional experiments，and to assess its potential as a novel tumor biomarker.

Methods

Transcriptomic and clinical data were downloaded from The Cancer Genome Atlas and Xena public databases at The University of California Santa Cruz to investigate the difference in the expression of SF3B6 between pancreatic cancer tissue and normal pancreatic tissue，and the association of SF3B6 with the prognosis and clinical indices of patients with pancreatic cancer was analyzed. Three pancreatic ductal adenocarcinoma cell lines and one normal pancreatic ductal epithelial cell line were cultured，and RT-qPCR was used to measure the expression level of SF3B6 in pancreatic cancer. A total of 43 patients with pancreatic cancer who underwent surgery in Binzhou Medical University Hospitalfrom January 2024 to December 2025 were enrolled as subjects，and Western blot and RT-qPCR were used to measure the expression of SF3B6 in pancreatic cancer tissue. Based on the median expression level of SF3B6 measured by RT-qPCR，the patients were divided into high and low expression groups. The association of SF3B6 expression with clinical features and prognosis was assessed. A pancreatic cancer cell line with stable low SF3B6 expression was constructed，and CCK-8 assay and Transwell migration and invasion assays were used to observe the impact of SF3B6 on the biological behaviors of the pancreatic cancer cell line，including proliferation，migration，and invasion. The independent-samples t test was used for comparison of normally distributed continuous data between two groups，and a one-way analysis of variance was used for comparison between multiple groups，while the least significant difference t-test or the Games-Howell test was used for further comparison between two groups； the Wilcoxon rank-sum test was used for comparison of non-normally distributed continuous data between two groups. The chi-square test was used for comparison of categorical data between two groups. A Logistic regression analysis was used to investigate the influencing factors for the expression of SF3B6，and the univariate and multivariate Cox proportional-hazards regression model analyses were used to investigate the risk factors for prognosis.

Results

The bioinformatics analysis showed that SF3B6 was highly expressed in pancreatic cancer tissue （P<2.2×10-16） and significantly affected the overall survival （P=0.011） and progression-free survival （P=0.002） of patients with pancreatic cancer. Sex，age，clinical stage，and TNM stage were not influencing factors for SF3B6 expression （all P>0.05），and SF3B6 could be used as an independent risk factor for the survival outcome of patients with pancreatic cancer （overall survival：hazard ratio=2.26，95% confidence interval：1.13 — 4.50，P=0.021； progression-free survival：hazard ratio=2.37，95% confidence interval：1.22 — 4.58，P=0.010）. Cellular and tissue experiments confirmed the high expression level of SF3B6 in pancreatic cancer cell lines （P<0.05），and the expression level of SF3B6 increased with the increase in the malignancy of pancreatic cancer，showing the highest relative expression level in PANC-1 cells with the highest degree of malignancy； the expression level of SF3B6 in the solid tissue of pancreatic cancer was significantly higher than that in paracancerous tissue （P<0.01）. The expression level of SF3B6 might affect the overall survival of patients with pancreatic cancer （P<0.05），while it showed no significant association with age，sex，pathological grade，maximum tumor diameter，or clinical stage （all P>0.05）. Knockdown of SF3B6 significantly inhibited the proliferation，migration，and invasion of pancreatic cancer cells （all P<0.01）.

Conclusion

SF3B6 is highly expressed in pancreatic cancer，and the high expression of SF3B6 can promote the proliferation，migration，and invasion of pancreatic cancer cells. Therefore，SF3B6 can be used as a potential biomarker for prognostic evaluation.

, authors=Zhongchen Fan, Kaixuan Zhang, Haoyu Cheng, Xuefeng Cao, Xingyuan Zhang, authorsList=Zhongchen Fan, Kaixuan Zhang, Haoyu Cheng, Xuefeng Cao, Xingyuan Zhang, authorCompany=null, correspAuthors=Xingyuan Zhang, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1317885785991397595, articleId=1317885781251834055, tenantId=1146029695717560320, journalId=1316781422847033486, language=CN, title=剪接因子3B亚基6在胰腺癌中的表达及其对胰腺癌细胞生物学行为的影响, columnId=1317885781620932810, journalTitle=临床肝胆病杂志, columnName=胰腺疾病, runingTitle=null, highlight=null, articleAbstract=
目的

通过生物信息学、临床样本验证及体外功能实验，系统阐明剪接因子3B亚基6（SF3B6）在胰腺癌中的表达特征、临床预后价值及其对癌细胞恶性表型的调控作用，以评估其作为新型肿瘤标志物的价值。

方法

从癌症基因组图谱和加利福尼亚大学圣克鲁兹分校Xena公共数据库中下载转录组和临床信息数据，分析SF3B6在胰腺癌和正常胰腺组织中的表达差异，评估SF3B6表达水平与胰腺癌患者预后、临床指标的关联。培养3种胰腺导管腺癌细胞株和1种正常胰腺导管上皮细胞株，通过实时荧光定量聚合酶链式反应（RT-qPCR）实验初步检测SF3B6在胰腺癌中的表达水平。选取2024年1月—2025年12月在滨州医学院附属医院接受手术的43例胰腺癌患者为研究对象，通过蛋白质印迹实验和RT-qPCR实验进一步探究SF3B6在胰腺癌组织中的表达情况。根据RT-qPCR表达水平的中位数，将胰腺癌患者分为临床样本高、低表达组，评估SF3B6表达与临床特征和预后的关系。构建SF3B6稳定低表达的胰腺癌细胞株，并通过细胞计数试剂盒-8实验、Transwell迁移和侵袭实验，分析SF3B6对胰腺癌细胞株增殖、侵袭和迁移等生物学行为的影响。符合正态分布的计量资料两组间比较采用成组t检验，多组间比较采用单因素方差分析，进一步两两比较采用LSD-t检验或Games-Howell法；不符合正态分布的计量资料两组间比较采用Wilcoxon秩和检验。计数资料两组间比较采用χ2检验。采用Logistic回归分析SF3B6表达的影响因素；采用单因素及多因素Cox比例风险回归模型分析影响预后的危险因素。

结果

生物信息分析结果表明，SF3B6在胰腺癌组织中高表达（P<2.2×10⁻¹⁶），能显著影响胰腺癌患者的总生存期（P=0.011）和无进展生存期（P=0.002）。性别、年龄、临床分期和TNM分期均非SF3B6表达的影响因素（P值均>0.05），SF3B6为影响胰腺癌患者生存的独立危险因素（总生存期：风险比=2.26，95%置信区间：1.13～4.50，P=0.021；无进展生存期：风险比=2.37，95%置信区间：1.22～4.58，P=0.010）。细胞和组织实验证实，SF3B6在胰腺癌细胞株中均高表达（P值均<0.05），且表达水平随胰腺癌恶性程度升高而增高，在恶性程度最高的PANC-1细胞中相对表达量最高；SF3B6在胰腺癌实体组织中的表达水平显著高于癌旁组织（P<0.01）。SF3B6表达水平可影响胰腺癌患者的总生存期（P<0.05），但与年龄、性别、病理分级、肿瘤最大径和临床分期无关（P值均>0.05）。敲低SF3B6表达可显著抑制胰腺癌细胞的增殖、迁移和侵袭能力（P值均<0.01）。

结论

SF3B6在胰腺癌中高表达，并可促进胰腺癌细胞的增殖、迁移和侵袭，其可作为胰腺癌潜在的预后评价指标。

, authors=范钟辰, 张凯旋, 程昊宇, 曹学峰, 张兴元, authorsList=范钟辰, 张凯旋, 程昊宇, 曹学峰, 张兴元, authorCompany=null, correspAuthors=张兴元, authorNote=

作者贡献声明

张兴元、曹学峰负责设计实验思路和论文框架；范钟辰、张凯旋和程昊宇负责实验操作和数据分析；范钟辰负责整理数据和撰写文章；张凯旋、程昊宇负责文章修改；张兴元负责最终定稿。

, correspAuthorsNote=
张兴元， （ORCID：0000-0002-7405-3805）
Zhang Xingyuan， （ORCID：0000-0002-7405-3805）
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DOI: 10.1016/j.bbrc.2021.12.059., articleTitle=SF3B14 is involved in the centrosome regulation through splicing of TUBGCP6 pre-mRNA, refAbstract=null)], funds=null, companyList=[AuthorCompany(id=1317885786226278620, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, xref=null, ext=[AuthorCompanyExt(id=1317885786234667229, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, companyId=1317885786226278620, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=Department of Hepatobiliary Surgery，Binzhou Medical University Hospital，Binzhou，Shandong 256603，China), AuthorCompanyExt(id=1317885786243055838, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, companyId=1317885786226278620, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=滨州医学院附属医院肝胆外科，山东 滨州 256603)])], figs=[ArticleFig(id=1317885790609326336, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 1, caption=Differentially expression analysis of SF3B6 between pancreatic cancer and normal samples, figureFileSmall=y/+0iw76KJG1bSpfxAzRJw==, figureFileBig=v8AmyRufPB7kpUdMvb3i9w==, tableContent=null), ArticleFig(id=1317885790684823809, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图1, caption=SF3B6基因在胰腺癌和正常胰腺样本中的表达差异分析

注：a，火山图；b，热图；c，箱式图。SF3B6，剪接因子3B亚基6。

, figureFileSmall=y/+0iw76KJG1bSpfxAzRJw==, figureFileBig=v8AmyRufPB7kpUdMvb3i9w==, tableContent=null), ArticleFig(id=1317885791049728258, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 2, caption=Survival analysis of pancreatic cancer patients with high and low SF3B6 expression from database, figureFileSmall=2Is1idbQnAeNm53ONqKaRQ==, figureFileBig=KlnyvbPRv0Pjh6slFf3YJQ==, tableContent=null), ArticleFig(id=1317885791108448515, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图2, caption=数据库中不同SF3B6表达组胰腺癌患者的生存分析

注：a，数据库高、低表达组SF3B6表达箱式图；b，SF3B6数据库高、低表达组胰腺癌患者总生存期比较；c，SF3B6数据库高、低表达组胰腺癌患者无进展生存期比较；SF3B6，剪接因子3B亚基6。

, figureFileSmall=2Is1idbQnAeNm53ONqKaRQ==, figureFileBig=KlnyvbPRv0Pjh6slFf3YJQ==, tableContent=null), ArticleFig(id=1317885791188140292, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 3, caption=mRNA expression levels of SF3B6 across different cell lines, figureFileSmall=gFyJBkPxqi1j/GEaEXbKRg==, figureFileBig=pPZyh7M9+PAbY1XIngqF4Q==, tableContent=null), ArticleFig(id=1317885791464964357, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图3, caption=SF3B6 mRNA在不同细胞系中的表达情况

注：SF3B6，剪接因子3B亚基6；mRNA，信使RNA；hTERT-HPNE，人源正常胰腺导管上皮细胞株；BxPC-3，人源胰腺导管原位腺癌细胞株；Capan-1，高分化胰腺导管腺癌细胞株；PANC-1，低分化人源胰腺导管腺癌细胞株。

, figureFileSmall=gFyJBkPxqi1j/GEaEXbKRg==, figureFileBig=pPZyh7M9+PAbY1XIngqF4Q==, tableContent=null), ArticleFig(id=1317885791511101702, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 4, caption=Expression of SF3B6 in pancreatic cancer tissues and adjacent normal tissues, figureFileSmall=AsXE2d5BEXvYdnJiZtl2+Q==, figureFileBig=BRzIaaOFQGhoTarabhnApw==, tableContent=null), ArticleFig(id=1317885791611764999, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图4, caption=SF3B6在胰腺癌实体组织和癌旁组织中的表达

注：SF3B6，剪接因子3B亚基6；GAPDH，甘油醛-3-磷酸脱氢酶。

, figureFileSmall=AsXE2d5BEXvYdnJiZtl2+Q==, figureFileBig=BRzIaaOFQGhoTarabhnApw==, tableContent=null), ArticleFig(id=1317885791683068169, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 5, caption=Effect of SF3B6 expression on overall survival, figureFileSmall=CHSiGZ6SdidiC3M9ibah0A==, figureFileBig=9C937Wrw1O1SMGJTN8tcXw==, tableContent=null), ArticleFig(id=1317885793348206858, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图5, caption=SF3B6表达水平对总生存期的影响

注：SF3B6，剪接因子3B亚基6；HR，风险比；CI，置信区间。

, figureFileSmall=CHSiGZ6SdidiC3M9ibah0A==, figureFileBig=9C937Wrw1O1SMGJTN8tcXw==, tableContent=null), ArticleFig(id=1317885793553727755, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 6, caption=Expression of SF3B6 in pancreatic cell lines with stable SF3B6 knockdown, figureFileSmall=Xt7uBiCkm5TpCGaaciYWGg==, figureFileBig=boI017i4t+QYQEV0bizGew==, tableContent=null), ArticleFig(id=1317885793637613837, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图6, caption=SF3B6在稳定低表达细胞株中的表达情况

注：a，SF3B6 mRNA相对表达量；b，Western Blot实验结果；c，SF3B6蛋白相对表达量。SF3B6，剪接因子3B亚基6；mRNA，信使RNA；NT，未作任何处理的PANC-1细胞株；shNC，空白慢病毒转染的阴性对照PANC-1细胞株；shSF3B6，稳定低表达SF3B6的PANC-1细胞株；β-actin，β-肌动蛋白。

, figureFileSmall=Xt7uBiCkm5TpCGaaciYWGg==, figureFileBig=boI017i4t+QYQEV0bizGew==, tableContent=null), ArticleFig(id=1317885793746665742, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 7, caption=Transwell migration assay of shSF3B6 and shNC groups（×100）, figureFileSmall=83Fib6wBi6fmvRHNirpgzg==, figureFileBig=N9yd3q+XcKnjen5HGji15w==, tableContent=null), ArticleFig(id=1317885793834746127, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图7, caption=shSF3B6组和shNC组的Transwell小室迁移实验（×100）

注：SF3B6，剪接因子3B亚基6；shNC，空白慢病毒转染的阴性对照PANC-1细胞株。

, figureFileSmall=83Fib6wBi6fmvRHNirpgzg==, figureFileBig=N9yd3q+XcKnjen5HGji15w==, tableContent=null), ArticleFig(id=1317885793964769552, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Figure 8, caption=Transwell invasion assay of shSF3B6 and shNC groups（×100）, figureFileSmall=5QcivdVj9cmwLA3JIU9jAg==, figureFileBig=/q2vz8QYyx3ZbYE13cfPWw==, tableContent=null), ArticleFig(id=1317885794061238545, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=图8, caption=shSF3B6组和shNC组的Transwell小室侵袭实验（×100）

注：SF3B6，剪接因子3B亚基6；shNC，空白慢病毒转染的阴性对照PANC-1细胞株。

, figureFileSmall=5QcivdVj9cmwLA3JIU9jAg==, figureFileBig=/q2vz8QYyx3ZbYE13cfPWw==, tableContent=null), ArticleFig(id=1317885794136736018, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Table 1, caption=

Logistic regression analysis of SF3B6 expression

, figureFileSmall=null, figureFileBig=null, tableContent=
指标OR（95%CI）P值
性别（男 vs 女）1.20（0.61～1.98）0.763
年龄（>65岁 vs ≤65岁）0.83（0.46～1.50）0.548
临床分期（Ⅲ～Ⅳ期 vs Ⅰ～Ⅱ期）0.16（0.01～0.96）0.092
T分期（T3～T4 vs T1～T2）1.08（0.50～2.37）0.843
N分期（N1 vs N0）0.98（0.50～7.90）0.944
M分期（M1 vs M0）0.33（0.02～2.73）0.350
), ArticleFig(id=1317885794212233491, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=表1, caption=

SF3B6表达水平的Logistic回归分析

, figureFileSmall=null, figureFileBig=null, tableContent=
指标OR（95%CI）P值
性别（男 vs 女）1.20（0.61～1.98）0.763
年龄（>65岁 vs ≤65岁）0.83（0.46～1.50）0.548
临床分期（Ⅲ～Ⅳ期 vs Ⅰ～Ⅱ期）0.16（0.01～0.96）0.092
T分期（T3～T4 vs T1～T2）1.08（0.50～2.37）0.843
N分期（N1 vs N0）0.98（0.50～7.90）0.944
M分期（M1 vs M0）0.33（0.02～2.73）0.350
), ArticleFig(id=1317885794283536660, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Table 2, caption=

Univariate and multivariate Cox proportional hazards regression analysis with OS as a endpoint

, figureFileSmall=null, figureFileBig=null, tableContent=
指标单因素Cox分析多因素Cox分析
HR95%CIP值HR95%CIP值
性别0.820.55～1.240.350
年龄1.031.01～1.050.0091.021.00～1.040.040
临床分期1.320.90～1.930.150
T分期1.571.01～2.430.0441.050.63～1.730.861
N分期2.111.26～3.550.0051.961.14～3.370.015
M分期1.050.25～4.390.947
SF3B62.711.42～5.160.0022.261.13～4.500.021
), ArticleFig(id=1317885794438725909, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=表2, caption=

OS为生存结局的单因素及多因素Cox分析

, figureFileSmall=null, figureFileBig=null, tableContent=
指标单因素Cox分析多因素Cox分析
HR95%CIP值HR95%CIP值
性别0.820.55～1.240.350
年龄1.031.01～1.050.0091.021.00～1.040.040
临床分期1.320.90～1.930.150
T分期1.571.01～2.430.0441.050.63～1.730.861
N分期2.111.26～3.550.0051.961.14～3.370.015
M分期1.050.25～4.390.947
SF3B62.711.42～5.160.0022.261.13～4.500.021
), ArticleFig(id=1317885794535194903, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Table3, caption=

Univariate and multivariate Cox proportional hazards regression analysis with PFS as a endpoint

, figureFileSmall=null, figureFileBig=null, tableContent=
指标单因素Cox分析多因素Cox分析
HR95%CIP值HR95%CIP值
性别0.950.64～1.400.792
年龄1.021.00～1.040.115
临床分期1.421.03～2.000.0361.030.62～1.710.911
T分期1.751.15～2.670.0101.320.77～2.250.317
N分期1.741.11～2.730.0161.530.97～2.410.069
M分期0.840.26～2.700.768
SF3B63.091.63～5.840.0012.371.22～4.580.010
), ArticleFig(id=1317885794803630360, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=表3, caption=

PFS为生存结局的单因素及多因素Cox分析

, figureFileSmall=null, figureFileBig=null, tableContent=
指标单因素Cox分析多因素Cox分析
HR95%CIP值HR95%CIP值
性别0.950.64～1.400.792
年龄1.021.00～1.040.115
临床分期1.421.03～2.000.0361.030.62～1.710.911
T分期1.751.15～2.670.0101.320.77～2.250.317
N分期1.741.11～2.730.0161.530.97～2.410.069
M分期0.840.26～2.700.768
SF3B63.091.63～5.840.0012.371.22～4.580.010
), ArticleFig(id=1317885794870739225, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=EN, label=Table 4, caption=

Comparison of general clinical data of pancreatic cancer patients in different SF3B6 expression groups

, figureFileSmall=null, figureFileBig=null, tableContent=
指标临床样本高表达组
（n=23）		临床样本低表达组
（n=20）		χ2值P值
年龄［例（%）］2.730.098
≥60岁15（65.22）8（40.00）
<60岁8（34.78）12（60.00）
性别［例（%）］0.610.434
男16（69.57）16（80.00）
女7（30.43）4（20.00）
病理分级［例（%）］0.980.323
高中分化20（86.96）14（70.00）
低分化3（13.04）6（30.00）
肿瘤最大径［例（%）］0.400.526
≤2 cm17（73.91）13（65.00）
>2 cm6（26.09）7（35.00）
临床分期［例（%）］3.310.069
Ⅰ+Ⅱ期11（47.83）15（75.00）
Ⅲ+Ⅳ期12（52.17）5（25.00）
), ArticleFig(id=1317885794958819610, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885781251834055, language=CN, label=表4, caption=

不同SF3B6表达组胰腺癌患者的一般临床资料比较

, figureFileSmall=null, figureFileBig=null, tableContent=
指标临床样本高表达组
（n=23）		临床样本低表达组
（n=20）		χ2值P值
年龄［例（%）］2.730.098
≥60岁15（65.22）8（40.00）
<60岁8（34.78）12（60.00）
性别［例（%）］0.610.434
男16（69.57）16（80.00）
女7（30.43）4（20.00）
病理分级［例（%）］0.980.323
高中分化20（86.96）14（70.00）
低分化3（13.04）6（30.00）
肿瘤最大径［例（%）］0.400.526
≤2 cm17（73.91）13（65.00）
>2 cm6（26.09）7（35.00）
临床分期［例（%）］3.310.069
Ⅰ+Ⅱ期11（47.83）15（75.00）
Ⅲ+Ⅳ期12（52.17）5（25.00）
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剪接因子3B亚基6在胰腺癌中的表达及其对胰腺癌细胞生物学行为的影响
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范钟辰 , 张凯旋 , 程昊宇 , 曹学峰 , 张兴元
临床肝胆病杂志 | 胰腺疾病 2026,42(8): 1917-1925
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临床肝胆病杂志 |胰腺疾病 2026 , 42 (8) : 1917 -1925
剪接因子3B亚基6在胰腺癌中的表达及其对胰腺癌细胞生物学行为的影响
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范钟辰, 张凯旋, 程昊宇, 曹学峰, 张兴元
作者信息
  • 滨州医学院附属医院肝胆外科，山东 滨州 256603
通讯作者:
张兴元， （ORCID：0000-0002-7405-3805）
Zhang Xingyuan， （ORCID：0000-0002-7405-3805）
作者简介:

作者贡献声明

张兴元、曹学峰负责设计实验思路和论文框架；范钟辰、张凯旋和程昊宇负责实验操作和数据分析；范钟辰负责整理数据和撰写文章；张凯旋、程昊宇负责文章修改；张兴元负责最终定稿。

Expression of splicing factor 3B subunit 6 in pancreatic cancer and its effect on the biological behaviors of pancreatic cancer cells
Zhongchen Fan, Kaixuan Zhang, Haoyu Cheng, Xuefeng Cao, Xingyuan Zhang
Affiliations
  • Department of Hepatobiliary Surgery，Binzhou Medical University Hospital，Binzhou，Shandong 256603，China
出版时间: 2026-08-25 doi: 10.12449/JCH260825
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摘要
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目的

通过生物信息学、临床样本验证及体外功能实验，系统阐明剪接因子3B亚基6（SF3B6）在胰腺癌中的表达特征、临床预后价值及其对癌细胞恶性表型的调控作用，以评估其作为新型肿瘤标志物的价值。

方法

从癌症基因组图谱和加利福尼亚大学圣克鲁兹分校Xena公共数据库中下载转录组和临床信息数据，分析SF3B6在胰腺癌和正常胰腺组织中的表达差异，评估SF3B6表达水平与胰腺癌患者预后、临床指标的关联。培养3种胰腺导管腺癌细胞株和1种正常胰腺导管上皮细胞株，通过实时荧光定量聚合酶链式反应（RT-qPCR）实验初步检测SF3B6在胰腺癌中的表达水平。选取2024年1月—2025年12月在滨州医学院附属医院接受手术的43例胰腺癌患者为研究对象，通过蛋白质印迹实验和RT-qPCR实验进一步探究SF3B6在胰腺癌组织中的表达情况。根据RT-qPCR表达水平的中位数，将胰腺癌患者分为临床样本高、低表达组，评估SF3B6表达与临床特征和预后的关系。构建SF3B6稳定低表达的胰腺癌细胞株，并通过细胞计数试剂盒-8实验、Transwell迁移和侵袭实验，分析SF3B6对胰腺癌细胞株增殖、侵袭和迁移等生物学行为的影响。符合正态分布的计量资料两组间比较采用成组t检验，多组间比较采用单因素方差分析，进一步两两比较采用LSD-t检验或Games-Howell法；不符合正态分布的计量资料两组间比较采用Wilcoxon秩和检验。计数资料两组间比较采用χ2检验。采用Logistic回归分析SF3B6表达的影响因素；采用单因素及多因素Cox比例风险回归模型分析影响预后的危险因素。

结果

生物信息分析结果表明，SF3B6在胰腺癌组织中高表达（P<2.2×10⁻¹⁶），能显著影响胰腺癌患者的总生存期（P=0.011）和无进展生存期（P=0.002）。性别、年龄、临床分期和TNM分期均非SF3B6表达的影响因素（P值均>0.05），SF3B6为影响胰腺癌患者生存的独立危险因素（总生存期：风险比=2.26，95%置信区间：1.13～4.50，P=0.021；无进展生存期：风险比=2.37，95%置信区间：1.22～4.58，P=0.010）。细胞和组织实验证实，SF3B6在胰腺癌细胞株中均高表达（P值均<0.05），且表达水平随胰腺癌恶性程度升高而增高，在恶性程度最高的PANC-1细胞中相对表达量最高；SF3B6在胰腺癌实体组织中的表达水平显著高于癌旁组织（P<0.01）。SF3B6表达水平可影响胰腺癌患者的总生存期（P<0.05），但与年龄、性别、病理分级、肿瘤最大径和临床分期无关（P值均>0.05）。敲低SF3B6表达可显著抑制胰腺癌细胞的增殖、迁移和侵袭能力（P值均<0.01）。

结论

SF3B6在胰腺癌中高表达，并可促进胰腺癌细胞的增殖、迁移和侵袭，其可作为胰腺癌潜在的预后评价指标。

胰腺肿瘤  /  剪接因子3B亚基6  /  生物学行为  /  基因表达
Objective

To systematically clarify the expression profile of splicing factor 3B subunit 6 （SF3B6） in pancreatic cancer，its clinical prognostic value，and its regulatory effect on the malignant phenotype of cancer cells through bioinformatics analysis，clinical sample validation，and in vitro functional experiments，and to assess its potential as a novel tumor biomarker.

Methods

Transcriptomic and clinical data were downloaded from The Cancer Genome Atlas and Xena public databases at The University of California Santa Cruz to investigate the difference in the expression of SF3B6 between pancreatic cancer tissue and normal pancreatic tissue，and the association of SF3B6 with the prognosis and clinical indices of patients with pancreatic cancer was analyzed. Three pancreatic ductal adenocarcinoma cell lines and one normal pancreatic ductal epithelial cell line were cultured，and RT-qPCR was used to measure the expression level of SF3B6 in pancreatic cancer. A total of 43 patients with pancreatic cancer who underwent surgery in Binzhou Medical University Hospitalfrom January 2024 to December 2025 were enrolled as subjects，and Western blot and RT-qPCR were used to measure the expression of SF3B6 in pancreatic cancer tissue. Based on the median expression level of SF3B6 measured by RT-qPCR，the patients were divided into high and low expression groups. The association of SF3B6 expression with clinical features and prognosis was assessed. A pancreatic cancer cell line with stable low SF3B6 expression was constructed，and CCK-8 assay and Transwell migration and invasion assays were used to observe the impact of SF3B6 on the biological behaviors of the pancreatic cancer cell line，including proliferation，migration，and invasion. The independent-samples t test was used for comparison of normally distributed continuous data between two groups，and a one-way analysis of variance was used for comparison between multiple groups，while the least significant difference t-test or the Games-Howell test was used for further comparison between two groups； the Wilcoxon rank-sum test was used for comparison of non-normally distributed continuous data between two groups. The chi-square test was used for comparison of categorical data between two groups. A Logistic regression analysis was used to investigate the influencing factors for the expression of SF3B6，and the univariate and multivariate Cox proportional-hazards regression model analyses were used to investigate the risk factors for prognosis.

Results

The bioinformatics analysis showed that SF3B6 was highly expressed in pancreatic cancer tissue （P<2.2×10-16） and significantly affected the overall survival （P=0.011） and progression-free survival （P=0.002） of patients with pancreatic cancer. Sex，age，clinical stage，and TNM stage were not influencing factors for SF3B6 expression （all P>0.05），and SF3B6 could be used as an independent risk factor for the survival outcome of patients with pancreatic cancer （overall survival：hazard ratio=2.26，95% confidence interval：1.13 — 4.50，P=0.021； progression-free survival：hazard ratio=2.37，95% confidence interval：1.22 — 4.58，P=0.010）. Cellular and tissue experiments confirmed the high expression level of SF3B6 in pancreatic cancer cell lines （P<0.05），and the expression level of SF3B6 increased with the increase in the malignancy of pancreatic cancer，showing the highest relative expression level in PANC-1 cells with the highest degree of malignancy； the expression level of SF3B6 in the solid tissue of pancreatic cancer was significantly higher than that in paracancerous tissue （P<0.01）. The expression level of SF3B6 might affect the overall survival of patients with pancreatic cancer （P<0.05），while it showed no significant association with age，sex，pathological grade，maximum tumor diameter，or clinical stage （all P>0.05）. Knockdown of SF3B6 significantly inhibited the proliferation，migration，and invasion of pancreatic cancer cells （all P<0.01）.

Conclusion

SF3B6 is highly expressed in pancreatic cancer，and the high expression of SF3B6 can promote the proliferation，migration，and invasion of pancreatic cancer cells. Therefore，SF3B6 can be used as a potential biomarker for prognostic evaluation.

Pancreatic Neoplasms  /  Splicing Factor 3B Subunit 6  /  Biological Behavior  /  Gene Expression
范钟辰, 张凯旋, 程昊宇, 曹学峰, 张兴元. 剪接因子3B亚基6在胰腺癌中的表达及其对胰腺癌细胞生物学行为的影响. 临床肝胆病杂志, 2026 , 42 (8) : 1917 -1925 . DOI: 10.12449/JCH260825
Zhongchen Fan, Kaixuan Zhang, Haoyu Cheng, Xuefeng Cao, Xingyuan Zhang. Expression of splicing factor 3B subunit 6 in pancreatic cancer and its effect on the biological behaviors of pancreatic cancer cells[J]. Journal of Clinical Hepatology, 2026 , 42 (8) : 1917 -1925 . DOI: 10.12449/JCH260825
正文
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目前，临床上治疗胰腺癌的主要方式包括手术切除、射频消融、放射治疗和化学治疗等。受胰腺癌低免疫原性、高度纤维化、缺氧及免疫抑制的肿瘤微环境等因素的影响，针对胰腺癌的免疫治疗与靶向治疗尚未取得实质性突破［1-2］。在胰腺癌患者中，可检出具有治疗潜力分子变异的患者占所有胰腺癌患者的12%～25%，靶向治疗潜在的受益人群不足25%［3］。前信使RNA的可变剪接可去除未成熟信使RNA（messenger RNA，mRNA）中的内含子或非编码片段，允许在单个基因基础上产生多个成熟的mRNA变体［4］。RNA剪接失调广泛存在于包括胰腺癌在内的多种肿瘤中，被视为“癌症的标志”［5-6］。可变剪接过程主要由剪接体执行，U2核小核糖核蛋白颗粒（U2 small nuclear ribonucleoprotein，U2 snRNP）是癌症中最常发生突变的剪接因子［7］。剪接因子3B复合体是U2 snRNP的重要组成部分，在识别分支点序列和剪接体的组装过程中发挥不可或缺的作用［8］。大量研究表明，剪接因子3B复合体的亚基广泛参与血液系统肿瘤和实体瘤的发生发展。然而，关于剪接因子3B亚基6（splicing factor 3B subunit 6，SF3B6）在胰腺癌中的研究却鲜有报道。本研究通过挖掘癌症基因组图谱（the cancer genome atlas，TCGA）和加利福尼亚大学圣克鲁兹分校（University of California Santa Cruz，UCSC）Xena数据库资料，分析SF3B6在胰腺癌中的表达情况，及其与预后、临床指标的关联，并进一步通过细胞和实体组织实验，验证SF3B6在胰腺癌细胞系中的表达情况，以及对胰腺癌细胞生物学行为的影响，以期为胰腺癌的靶向治疗提供新的理论依据和潜在靶点。
1　材料与方法
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1.1　RNA转录组数据和临床信息数据
胰腺癌癌症样本的普通转录组数据和临床信息来自TCGA数据库，包括原发癌症样本178例。正常胰腺组织样本的转录组数据和临床信息来自UCSC Xena数据库，包括167例正常样本。对合并后的数据进行标准化处理后，开展差异表达分析。根据SF3B6的测序数据和临床信息数据，进行生存分析及其与临床指标的相关性分析。
1.2　细胞及主要试剂
人胰腺导管腺癌细胞株（BxPC-3、Capan-1和PANC-1）和人正常胰腺导管上皮细胞株（hTERT-HPNE）均购自武汉普诺赛生命科技有限公司；各细胞专用培养基均购自武汉普诺赛生命科技有限公司；反转录试剂盒购自湖南艾科瑞生物工程有限公司；人源SF3B6基因干扰慢病毒、细胞计数试剂盒-8（cell counting kit-8，CCK-8）和Transwell染色试剂盒均由山东维真生物科技有限公司提供。
1.3　细胞培养和转染
所有细胞均用含10%胎牛血清的完全培养基培养，置于37 ℃、5% CO2的培养箱中常规培养。当细胞融合至约80%时，加入适量0.25%胰酶消化细胞传代。将人源SF3B6基因干扰慢病毒及阴性对照慢病毒分别转染至PANC-1细胞株，并采用嘌呤霉素筛选。
1.4　胰腺癌人体组织标本
选取2024年1月—2025年12月于本院肝胆外科接受手术并经术后病理证实的43例胰腺导管腺癌标本，包括癌组织和配对癌旁组织。完整收集患者年龄、性别、病理分级、肿瘤最大径、临床分期及术后生存随访资料。
1.5　RNA提取和实时荧光定量聚合酶链式反应（real-time fluorescence quantitative polymerase chain reaction，RT-qPCR）
使用Buffer QLS缓冲裂解液（湖南艾科瑞生物工程有限公司）提取细胞总RNA（组织样本先经液氮研磨），并按照说明书合成互补DNA后进行RT-qPCR检测。引物使用Primer Premier 5软件设计，并由武汉赛维尔生物科技有限公司合成：SF3B6（F：5'-TCACCTATCGG-GATTCAATG-3'，R：5'-GCTTCAACGTTTCCTCCTT-3'），以甘油醛-3-磷酸脱氢酶为内参（F：5'-GGTCGGAGTCAA-CGGATTTG-3'，R：5'-GGAAGATGGTGATGGGATTTC-3'）。采用2-ΔΔCt法分析目的基因的相对表达量。
1.6　蛋白质印迹（Western Blot）实验
加入放射免疫沉淀法裂解缓冲液（上海碧云天生物技术股份有限公司）裂解细胞并提取总蛋白（组织样本先经液氮研磨）。按照说明书经电泳、转膜、5%牛血清白蛋白于25 ℃封闭2 h，随后加入一抗SF3B6（1∶4 000）在4℃条件下孵育16 h，二抗（1∶5 000）于25 ℃孵育1.5 h（一抗、二抗均由武汉赛维尔生物科技有限公司提供）。使用含吐温-20的Tris缓冲盐溶液洗涤聚偏二氟乙烯膜后，置于化学发光仪内成像。采集图像后使用Image J软件对结果进行定量分析，以β-肌动蛋白为内参，计算SF3B6的相对表达量。
1.7　CCK-8实验
取正常生长的空病毒转染阴性对照组细胞株和SF3B6基因干扰混合克隆稳转的PANC-1细胞株，消化后计数分板。将细胞以每孔8×103个接种于96孔板，置于培养箱继续培养。24 h后每孔加入10%的CCK-8检测液，于37 ℃避光反应1 h，在450 nm处读取各孔的光密度（optical density，OD）值。细胞活力率（%）=（ODT－ODB）/（ODC－ODB）×100%。其中ODT、ODC和ODB分别表示shSF3B6组（稳定低表达SF3B6的PANC-1细胞株）、shNC组（空白慢病毒转染的阴性对照PANC-1细胞株）和不含细胞仅含培养基与CCK-8检测液的完全空白组的OD值。
1.8　Transwell迁移和侵袭实验
迁移实验：取正常生长的空病毒转染阴性对照组细胞株和SF3B6基因干扰混合克隆稳转的PANC-1细胞株，消化后计数分板。采用含2%胎牛血清的培养基重悬细胞，以每孔2×105个接种于Transwell小室的上室（8 μm），下室加入2 mL含2% 胎牛血清的培养基。培养24 h后，用4%的多聚甲醛室温下固定15 min。用棉签擦去上室的肿瘤细胞，加入0.1%结晶紫试剂染色15 min。置于室温风干后于显微镜下拍照。侵袭实验：在Transwell上室中预铺基质胶，其余步骤同迁移实验。
1.9　统计学方法
采用SPSS 27.0和R软件4.3.1进行统计分析。符合正态分布的计量资料以x¯±s表示，两组间比较采用成组t检验；多组间比较采用单因素方差分析，方差齐时进一步两两比较采用LSD-t检验，方差不齐时采用Games-Howell法。不符合正态分布的计量资料以M（P25～P75）表示，两组间比较采用Wilcoxon秩和检验。计数资料两组间比较采用χ2检验。采用Logistic回归分析SF3B6表达的影响因素。采用单因素及多因素Cox比例风险回归模型分析影响预后的危险因素。采用Kaplan-Meier法和Log-rank检验进行生存分析。P<0.05为差异有统计学意义。
2　结果
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2.1　数据库中SF3B6在胰腺癌和正常胰腺样本中的表达情况
对合并后的数据进行标准化处理后，利用limma包进行差异表达分析，分析胰腺癌样本和正常胰腺组织样本之间的基因表达差异改变。以|log2FC|>1且错误发现率<0.05为阈值，利用ggVolcano包对结果进行可视化（图1a）。进一步对上调、下调基因按照|log2FC|降序排列，分别选取排名前10位的差异基因和SF3B6基因，利用pheatmap包可视化其表达情况（图1b）。结果显示，在胰腺癌样本（癌症组）和正常胰腺组织样本（正常组）中共筛选得到6 726个差异基因，其中上调基因3 389个，包括TFF1、CEACAM5、TMPRSS4、UGT1A10、CGB5、SF3B6等；下调基因3 337个，包括ATP4A、CELA3B、PNLIPRP1、CLPS、SYCN等。随后，进一步利用箱式图直观分析SF3B6在癌症组和正常组中的表达差异，结果显示，SF3B6属于癌症组和正常组之间的高表达差异基因（P<2.2×10⁻¹⁶）（图1c）。
2.2　SF3B6表达水平和胰腺癌患者生存预后的关系
以SF3B6表达的中位数为截断值，将胰腺癌组织样本划分为SF3B6数据库高表达组和数据库低表达组。为评估分组的有效性，绘制表达量的箱式图进行可视化，结果表明，两组间的SF3B6表达水平存在显著差异（P<2.2×10⁻¹⁶）（图2a）。Kaplan-Meier生存分析表明，数据库高表达组的总生存期（overall survival，OS）和无进展生存期（progression-free survival，PFS）均显著低于数据库低表达组（OS：P=0.011；PFS：P=0.002）（图2b、c）。
2.3　SF3B6表达水平与性别、年龄、临床分期和TNM分期等临床指标的关系
从TCGA数据库中下载178例胰腺癌样本的临床数据，包括性别、年龄、临床分期、T分期、N分期和M分期等。
178例胰腺癌患者的年龄为35～88岁，中位年龄65岁；女性80例，男性98例；临床分期Ⅰ～Ⅳ期分别有21、147、3和4例（3例分期不详）；T分期T1～T4分别有7、24、142和3例（Tx 2例）；淋巴结转移阴性（N0）及阳性（N1）分别有49例和124例（Nx 5例）；远处转移阴性（M0）和阳性（M1）分别有80例和4例（Mx 94例）。以SF3B6基因表达量分组（数据库高、低表达组）作为结局变量，利用Logistic回归分析上述临床指标对SF3B6表达水平的影响。结果表明，性别、年龄、临床分期和TNM分期并非SF3B6表达的影响因素（P值均>0.05）（表1）。
2.4　胰腺癌患者生存预后的单、多因素Cox分析
分别以OS和PFS作为生存结局，对胰腺癌组织样本进行单因素及多因素Cox分析。以OS为生存结局时，单因素Cox分析结果显示，年龄、T分期、N分期及SF3B6表达水平均为胰腺癌患者OS的危险因素（P值均<0.05）。进一步将单因素Cox分析中有统计学意义的变量纳入多因素Cox分析，结果表明，年龄、N分期及SF3B6表达水平是OS的独立危险因素（P值均<0.05）（表2）。以PFS为生存结局时，单因素Cox分析显示，临床分期、T分期、N分期及SF3B6表达水平均为胰腺癌患者PFS的危险因素（P值均<0.05）。将上述变量纳入多因素Cox分析，结果显示，仅SF3B6是影响PFS的独立危险因素（P<0.05）（表3）。
2.5　SF3B6在胰腺癌细胞和临床样本中的表达情况及与胰腺癌患者生存预后的关系
为验证生物信息学分析结果，进一步探究SF3B6在胰腺癌和正常胰腺细胞中的表达情况。本研究选择1种正常人源胰腺导管上皮细胞株hTERT-HPNE和3种常见的胰腺导管腺癌细胞株BxPC-1、Capan-1和PANC-1。RT-qPCR检测结果显示，与正常细胞株比较，SF3B6在胰腺癌细胞株中均高表达（P值均<0.05），且表达水平随胰腺癌恶性程度升高而增高，在恶性程度最高的PANC-1细胞中相对表达量最高（图3）。为进一步验证SF3B6在胰腺癌实体瘤中的表达情况，采用Western Blot实验分析胰腺癌实体组织和癌旁组织中SF3B6蛋白的表达差异。结果表明，SF3B6在胰腺癌实体组织中的表达水平显著高于癌旁组织（P<0.01）（图4）。
43例胰腺癌实体组织样本中SF3B6 mRNA的表达范围为0.022～0.124，中位数为0.067。根据SF3B6表达水平中位数，将胰腺癌实体组织样本划分为临床样本高、低表达组，并分析SF3B6表达水平与胰腺癌患者临床特征及OS的关系。结果显示，两组患者的年龄、性别、病理分级、肿瘤最大径及临床分期比较，差异均无统计学意义（P值均>0.05）（表4），但两组患者的OS差异具有统计学意义（P<0.05）（图5）。
2.6　SF3B6稳定低表达细胞株的建立及验证
为进一步探究SF3B6对胰腺癌细胞株生物学行为的影响，本研究选取SF3B6高表达的PANC-1细胞株作为研究目标，构建稳定低表达SF3B6的PANC-1细胞株（shSF3B6组）以及空白慢病毒转染的阴性对照PANC-1细胞株（shNC组）。经嘌呤霉素筛选培养后，采用RT-qPCR和Western Blot实验验证SF3B6在PANC-1细胞株中的敲低效率。结果显示，shSF3B6组中SF3B6 mRNA的表达水平较shNC组和未做任何处理的PANC-1细胞株（NT组）显著降低（P值均<0.01）（图6a）；SF3B6蛋白的表达水平较shNC组和NT组均降低（P值均<0.05）（图6b、c）。
2.7　SF3B6对胰腺导管腺癌细胞株增殖行为的影响
CCK-8实验显示，shSF3B6组的细胞活力率为54.9%±9.2%，显著低于shNC组的100.0%±8.0%（t=9.804，P<0.01），提示敲低SF3B6可能抑制胰腺导管腺癌细胞的增殖。
2.8　SF3B6对胰腺导管腺癌细胞株迁移行为的影响
Transwell小室迁移实验结果显示，shSF3B6组和shNC组从小室上层迁移至下层的细胞数量分别为（76.00±8.97）个和（216.20±14.57）个，差异有统计学意义（t=18.324，P<0.01）（图7），提示敲低SF3B6可抑制胰腺癌细胞株的迁移能力。
2.9　SF3B6对胰腺导管腺癌细胞株侵袭行为的影响
Transwell小室侵袭实验结果表明，shNC组的穿膜细胞数为（223.42±64.83）个，显著高于shSF3B6组的（66.75±11.51）个（t=8.242，P<0.01）（图8），提示敲低SF3B6可抑制胰腺癌细胞株的侵袭能力。
3　讨论
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胰腺癌中位生存期仅为4～6个月，生存期>5年的患者比例不足13%［9-10］。预计至2030年，胰腺导管腺癌有望成为癌症相关死亡的第二大原因［11］。目前，胰腺癌发生发展过程中的分子机制尚未完全阐明，临床治疗手段存在较大空白。RNA的可变剪接是剪接过程中更为精细复杂的生物学过程，在去除内含子的基础上，可选择性地去除特定外显子群，从而产生更多的成熟mRNA转录本和蛋白质变体。其机制包括外显子跳跃、外显子互斥、使用替代剪接位点和内含子保留［12］。癌细胞在可变剪接过程中普遍存在癌症类型特异性及亚型特异性的改变，这被认为是癌症进展的一个标志性特征［13］。既往研究表明，癌症相关的异常可变剪接可破坏细胞增殖与凋亡之间的平衡、增强肿瘤细胞的侵袭和转移能力、促进肿瘤血管生成并增强需氧糖酵解［14］。剪接体是执行剪接功能的重要载体，而U2 snRNP是剪接体成分中最常发生突变的组分。SF3B复合体是功能性U2 snRNP的内在成分，可直接识别和结合分支点序列，在执行剪接功能中发挥关键作用。SF3B复合体包括SF3B1～SF3B7多个亚基，目前相关研究主要集中在SF3B1。SF3B1在血液系统恶性肿瘤，尤其是骨髓增生异常综合征的研究中已取得突破性进展，世界卫生组织第五版骨髓增生异常综合征分类标准已将SF3B1突变患者列为独立亚型［15］。然而，SF3B其他亚基的研究仍不充分。有研究表明，SF3B6可通过丝裂原活化蛋白激酶信号通路抑制胃癌细胞的增殖和迁移［16］。在乳腺癌细胞系中，敲低SF3B6表达可显著抑制乳腺癌细胞的增殖和迁移能力，并促进凋亡。进一步研究表明，SF3B6可通过与mRNA相互作用，调控蛋白磷酸酶镁/锰离子依赖型1F和脂肪酸合酶等基因的表达，蛋白磷酸酶镁/锰离子依赖型1F的高表达可促进癌细胞迁移和侵袭，并通过转化生长因子β激活激酶1的去磷酸化调控细胞凋亡；脂肪酸合酶的高表达则促进乳腺癌脑转移，并降低35～37岁患者的生存率［17］。在肝癌中，SF3B6也参与恶性生物学进程［18］。敲低SF3B6表达可抑制肝细胞癌细胞的增殖、侵袭和迁移，促进凋亡并导致肝细胞癌细胞株的S期停滞。此外，SF3B6可通过剪接γ微管蛋白复合物组分6的前体mRNA参与中心体调控；敲低SF3B6表达可导致有丝分裂延长，并在中期出现若干有丝分裂缺陷，包括单极纺锤体和染色体错位。然而，SF3B6在胰腺癌中的表达情况及其在胰腺癌恶性进展中的作用尚不明确。因此，本课题组探究SF3B6在胰腺癌中的表达差异及其对胰腺癌细胞表型的影响。
本研究从TCGA和UCSC Xena数据库中获取胰腺癌和正常胰腺组织样本中SF3B6的相关数据，采用生物信息学方法初步分析SF3B6在二者中的表达情况及其与胰腺癌患者生存预后的关系。差异分析发现，在胰腺癌和正常胰腺组织样本中存在6 726个差异基因，包括3 389个上调基因和3 337个下调基因，SF3B6是其中的高表达差异基因。Kaplan-Meier生存曲线表明，SF3B6高表达组的OS和PFS显著低于低表达组（P值均<0.05），提示SF3B6可能与胰腺癌患者的不良预后相关。为进一步探究SF3B6表达与临床特征和生存结局的相关性，采用Logistic回归、单因素及多因素Cox分析，未发现SF3B6与性别、年龄、临床分期和TNM分期之间存在显著关联，但SF3B6可能是影响胰腺癌患者预后的独立危险因素。SF3B6表达与临床指标无关联，但可显著预测生存结局，说明SF3B6可能反映肿瘤的分子生物学特征，可作为潜在的预后评估指标，辅助评估患者的生存风险。上述结果为后续细胞实验提供了理论支撑。RT-qPCR实验证实SF3B6在胰腺癌细胞株中高表达，Western Blot实验进一步证实SF3B6在胰腺癌实体组织中高表达。组间比较结果证实，SF3B6可能影响胰腺癌患者的OS，但与年龄、性别、病理分级、肿瘤最大径和临床分期之间相互独立。鉴于本研究为单中心回顾性分析，收集的胰腺癌样本量仅43例，部分亚组样本量过少，可能存在统计效能不足的问题，因此未进行多因素分析。此外，由于样本量有限和个体的异质性，生存分析结果虽差异显著，但需谨慎解读，并有必要在大样本条件下进一步探究。在建立稳定低表达SF3B6的胰腺癌细胞株后，本研究通过CCK-8、Transwell迁移和侵袭实验揭示，敲低SF3B6基因表达可能抑制胰腺癌细胞株的增殖、迁移和侵袭能力。
尽管本研究阐明了SF3B6在胰腺癌和正常胰腺细胞株中的相对表达情况及其对胰腺癌细胞生物学行为的影响，但尚未揭示引起这些改变的分子机制。推测作为剪接因子SF3B复合体的重要亚基之一，SF3B6表达异常可能导致异常剪接事件的发生，进而导致基因表达失调，这些基因可能在肿瘤发生和进展中发挥重要作用。后续可通过功能富集分析、蛋白质-蛋白质相互作用分析以及与患者生存预后显著相关的差异可变剪接事件分析，筛选出与SF3B6高度相关的关键下游候选靶点，作为后续机制研究的核心对象，并从以下3个方面开展深入研究：（1）SF3B6是否直接结合并调控候选靶点的前体mRNA剪接；（2）该靶点不同的剪接异构体是否具有相反的生物学功能；（3）该靶点能否介导SF3B6对胰腺癌恶性表型的调控作用。此外，还应开展SF3B6与胰腺癌相关的动物实验，以探究SF3B6在完整且复杂机体环境中的作用。
综上所述，本研究虽已取得部分成果，但仍然不充分。后续将深入探讨SF3B6对胰腺癌生物学特征的具体影响及其深层机制，以期为胰腺癌患者，尤其是剪接失调的胰腺癌患者，提供诊断和治疗的理论依据。

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2026年第42卷第8期
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doi: 10.12449/JCH260825
  • 接收时间：2026-03-14
  • 首发时间：2026-10-16
  • 出版时间：2026-08-25
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  • 收稿日期：2026-03-14
  • 录用日期：2026-04-02
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    滨州医学院附属医院肝胆外科，山东 滨州 256603

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张兴元， （ORCID：0000-0002-7405-3805）
Zhang Xingyuan， （ORCID：0000-0002-7405-3805）
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