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Article(id=1208518758021329479, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208518757253779608, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2021.12.10, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1622995200000, receivedDateStr=2021-06-07, revisedDate=1628697600000, revisedDateStr=2021-08-12, acceptedDate=null, acceptedDateStr=null, onlineDate=1766062925104, onlineDateStr=2025-12-18, pubDate=1640620800000, pubDateStr=2021-12-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766062925104, onlineIssueDateStr=2025-12-18, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766062925104, creator=13701087609, updateTime=1766062925104, updator=13701087609, issue=Issue{id=1208518757253779608, tenantId=1146029695717560320, journalId=1189873630562394117, year='2021', volume='46', issue='12', pageStart='1167', pageEnd='1267', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766062924920, creator=13701087609, updateTime=1766062998332, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208519065233125464, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208518757253779608, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208519065233125465, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208518757253779608, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1232, endPage=1238, ext={EN=ArticleExt(id=1208518758453342794, articleId=1208518758021329479, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress of the action mechanism of lncRNA UCA1 and miRNAs in digestive system tumors, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

The incidence and mortality rate of digestive system tumors showed an increasing trend year by year, which seriously threatens human life and health. Recent years, studies have found that urothelial carcinoma embryonic antigen 1 (UCA1)is a long non-coding RNA (lncRNA), its expression significantly increased in a variety of digestive system tumor tissues or cells such as gastric cancer, colorectal cancer and esophageal cancer. In addition, UCA1 can interact with miRNAs to affect the proliferation,migration, invasion, epithelial-to-mesenchymal transition (EMT), apoptosis and drug resistance of tumor cells. The research progress of the action mechanism of lncRNA UCA1 and miRNAs in digestive system tumors (including gastric cancer, colorectal cancer and esophageal cancer) is reviewed, and the application of lncRNA UCA1 as a new biomarker and therapeutic target is prospected in present paper.

, correspAuthors=Yu Wang, authorNote=null, correspAuthorsNote=
*E-mail:
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消化系统肿瘤的发病率和死亡率呈逐年增长趋势，严重威胁着人类的生命健康。近年来研究发现，尿路上皮癌胚抗原1(UCA1)是一种长链非编码RNA(lncRNA)，在胃癌、结直肠癌及食管癌等多种消化系统肿瘤组织或细胞中的表达明显升高，且可通过与miRNAs相互调控而影响肿瘤细胞的增殖、迁移、侵袭、上皮-间质转化、凋亡及耐药等过程。该文综述lncRNA UCA1与miRNAs在胃癌、结直肠癌及食管癌等消化系统肿瘤中的作用机制研究进展，并展望lncRNA UCA1作为新的生物标志物及治疗靶点的应用前景。

, correspAuthors=王宇, authorNote=null, correspAuthorsNote=
王宇，E-mail：
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王思宇，硕士研究生，主要从事肿瘤分子遗传学研究

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王思宇，硕士研究生，主要从事肿瘤分子遗传学研究

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王思宇，硕士研究生，主要从事肿瘤分子遗传学研究

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Mechanisms of lncRNA UCA1 and miRNAs in digestive system tumors

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肿瘤类型肿瘤细胞或组织类型作用机制参考文献
胃癌胃癌组织、SGC-7901细胞、MKN-45细胞UCA1/miR-590-3p/CREB1[18]
胃癌组织、SCG-7901细胞、BGC-823细胞UCA1/miR-203/ZEB2[19]
胃癌组织、MKN-45细胞、BGC-823细胞SATB1/miR-495-3p/UCA1[21]
胃癌组织、AGS细胞、SCG-7901细胞UCA1-miR-26a/b-EZH2/CDK6；UCA1-miR-193a/214-PDL1[22]
MGC-803 Hypo细胞、BGC-823 Hypo细胞UCA1/miR-7-5p/EGFR[23]
SGC-7901细胞UCA1/miR-27b[24]
AGS细胞、NCI-N87细胞、NGC-7901细胞UCA1/miR-513a-3p/CYP1B1[25]
结直肠癌结直肠癌组织、SW480细胞、HT116细胞UCA1/miR-28-5p/HOXB3[28]
结直肠癌组织、HCT116细胞、DLD1细胞UCA1/miR-143/MYO6[29]
结直肠癌组织、HT-29细胞、SW480细胞、HIEC-6细胞UCA1/miR-185-5p/MAPK14/MAPKAPK2/HSP27[30]
HT29细胞、HCT116细胞UCA1-miR-495-SP1/SP3[31]
结直肠癌组织、HEK-293T细胞、HCT8细胞、HCT116细胞、HT29细胞、LoVo细胞、SW480细胞UCA1/miR-204-5p/CREB1[32]
结直肠癌组织、SW480细胞、SW420细胞UCA1/miR-23b-3p/ZNF281[33]
CaCo2细胞、HCT116细胞UCA1-miR-18a/miR-182[34]
食管癌EC9706细胞、KYSE细胞UCA1/miR-204/Sox4[37]
食管癌组织、EC9706细胞UCA1/miR-498/ZEB2[41]
EC109细胞、KYSE150细胞UCA1/miR-203/HK2[44]
), ArticleFig(id=1208518763322929899, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1208518758021329479, language=CN, label=表1, caption=

lncRNA UCA1与miRNAs在消化系统肿瘤中的作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=
肿瘤类型肿瘤细胞或组织类型作用机制参考文献
胃癌胃癌组织、SGC-7901细胞、MKN-45细胞UCA1/miR-590-3p/CREB1[18]
胃癌组织、SCG-7901细胞、BGC-823细胞UCA1/miR-203/ZEB2[19]
胃癌组织、MKN-45细胞、BGC-823细胞SATB1/miR-495-3p/UCA1[21]
胃癌组织、AGS细胞、SCG-7901细胞UCA1-miR-26a/b-EZH2/CDK6；UCA1-miR-193a/214-PDL1[22]
MGC-803 Hypo细胞、BGC-823 Hypo细胞UCA1/miR-7-5p/EGFR[23]
SGC-7901细胞UCA1/miR-27b[24]
AGS细胞、NCI-N87细胞、NGC-7901细胞UCA1/miR-513a-3p/CYP1B1[25]
结直肠癌结直肠癌组织、SW480细胞、HT116细胞UCA1/miR-28-5p/HOXB3[28]
结直肠癌组织、HCT116细胞、DLD1细胞UCA1/miR-143/MYO6[29]
结直肠癌组织、HT-29细胞、SW480细胞、HIEC-6细胞UCA1/miR-185-5p/MAPK14/MAPKAPK2/HSP27[30]
HT29细胞、HCT116细胞UCA1-miR-495-SP1/SP3[31]
结直肠癌组织、HEK-293T细胞、HCT8细胞、HCT116细胞、HT29细胞、LoVo细胞、SW480细胞UCA1/miR-204-5p/CREB1[32]
结直肠癌组织、SW480细胞、SW420细胞UCA1/miR-23b-3p/ZNF281[33]
CaCo2细胞、HCT116细胞UCA1-miR-18a/miR-182[34]
食管癌EC9706细胞、KYSE细胞UCA1/miR-204/Sox4[37]
食管癌组织、EC9706细胞UCA1/miR-498/ZEB2[41]
EC109细胞、KYSE150细胞UCA1/miR-203/HK2[44]
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lncRNA UCA1和miRNAs在消化系统肿瘤中的作用机制研究进展
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王思宇 1 , 王宇 2, *
解放军医学杂志 | 综述 2021,46(12): 1232-1238
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解放军医学杂志 | 综述 2021, 46(12): 1232-1238
lncRNA UCA1和miRNAs在消化系统肿瘤中的作用机制研究进展
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王思宇1, 王宇2, *
作者信息
  • 1陕西中医药大学基础医学院，陕西咸阳 712046
  • 2陕西中医药大学医学科研实验中心，陕西咸阳 712046

    • 王思宇，硕士研究生，主要从事肿瘤分子遗传学研究

通讯作者:

王宇，E-mail：
Research progress of the action mechanism of lncRNA UCA1 and miRNAs in digestive system tumors
Si-Yu Wang1, Yu Wang2, *
Affiliations
  • 1School of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712046, China
  • 2Medical Research Experimental Center, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712046, China
出版时间: 2021-12-28 doi: 10.11855/j.issn.0577-7402.2021.12.10
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摘要
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消化系统肿瘤的发病率和死亡率呈逐年增长趋势，严重威胁着人类的生命健康。近年来研究发现，尿路上皮癌胚抗原1(UCA1)是一种长链非编码RNA(lncRNA)，在胃癌、结直肠癌及食管癌等多种消化系统肿瘤组织或细胞中的表达明显升高，且可通过与miRNAs相互调控而影响肿瘤细胞的增殖、迁移、侵袭、上皮-间质转化、凋亡及耐药等过程。该文综述lncRNA UCA1与miRNAs在胃癌、结直肠癌及食管癌等消化系统肿瘤中的作用机制研究进展，并展望lncRNA UCA1作为新的生物标志物及治疗靶点的应用前景。

长链非编码RNA  /  尿路上皮癌胚抗原1  /  微RNA  /  消化系统肿瘤  /  胃癌  /  结直肠癌  /  食管癌

The incidence and mortality rate of digestive system tumors showed an increasing trend year by year, which seriously threatens human life and health. Recent years, studies have found that urothelial carcinoma embryonic antigen 1 (UCA1)is a long non-coding RNA (lncRNA), its expression significantly increased in a variety of digestive system tumor tissues or cells such as gastric cancer, colorectal cancer and esophageal cancer. In addition, UCA1 can interact with miRNAs to affect the proliferation,migration, invasion, epithelial-to-mesenchymal transition (EMT), apoptosis and drug resistance of tumor cells. The research progress of the action mechanism of lncRNA UCA1 and miRNAs in digestive system tumors (including gastric cancer, colorectal cancer and esophageal cancer) is reviewed, and the application of lncRNA UCA1 as a new biomarker and therapeutic target is prospected in present paper.

long non-coding RNA  /  urothelial carcinoma embryonic antigen 1  /  miRNA  /  digestive system tumors  /  gastric cancer  /  colorectal cancer  /  esophageal cancer
王思宇, 王宇. lncRNA UCA1和miRNAs在消化系统肿瘤中的作用机制研究进展. 解放军医学杂志, 2021 , 46 (12) : 1232 -1238 . DOI: 10.11855/j.issn.0577-7402.2021.12.10
Si-Yu Wang, Yu Wang. Research progress of the action mechanism of lncRNA UCA1 and miRNAs in digestive system tumors[J]. Medical Journal of Chinese People’s Liberation Army, 2021 , 46 (12) : 1232 -1238 . DOI: 10.11855/j.issn.0577-7402.2021.12.10
正文
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消化系统恶性肿瘤已成为全球化的重大公共卫生问题及死亡的重要原因。在中国，消化系统肿瘤导致超过50%的癌症相关死亡。虽然外科手术、化疗、放疗等治疗方法不断发展，但恶性肿瘤的诊断和预后仍不容乐观[1-3]。寻找消化系统肿瘤治疗的分子靶点可能有助于提高患者的生存率，因此越来越多的研究尝试确定新的生物标志物，以用于早期诊断和靶向治疗[4-7]。尿路上皮癌胚抗原1(urothelial carcinoma antigen 1，UCA1)是从膀胱移行细胞癌BLZ-211细胞中获得的一种长链非编码RNA(long non-coding RNA，lncRNA)，有研究发现其在消化系统肿瘤中的表达水平明显升高，且可提示患者预后较差。因此，UCA1可能是与消化系统肿瘤预后相关的新的生物标志物，但其在消化系统肿瘤中的具体作用机制尚未明确[8-9]。大量研究发现，lncRNA UCA1可通过与miRNAs相互作用调控下游靶基因，从而在消化系统肿瘤的发生发展中发挥作用。本文综述lncRNA UCA1与miRNAs在胃癌、结直肠癌及食管癌等消化系统肿瘤中的作用机制研究进展。
1 UCA1
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UCA1基因cDNA全长1442 bp，其5'末端具有TATA盒(TATAAA)，3'末端具有加尾信号(ATTAAA)和polyA尾，定位于人类染色体19p13.12，包含3个外显子和2个内含子[8]。UCA1基因全长启动子区不存在CpG岛，故属于组织特异性基因，其核心启动子区可能与多种转录因子结合，目前已通过染色质免疫沉淀实验确定其可与转录因子Ets-2和c-Myb结合[10-11]。UCA1定位于细胞质中，并在胚胎组织及肿瘤组织中普遍表达，在成体正常组织中不表达(心脏、脾脏除外)，可能参与调控下游分子的蛋白质合成过程[12]。此外，BLZ-211细胞系中包含两个剪接变异体：UCA1a(CUDR)和UCA1b，其cDNA全长分别为2200 bp和2700 bp[13]。大量研究发现，UCA1在不同肿瘤细胞系和肿瘤患者样本中过表达，并在肿瘤的发生发展中发挥致癌作用，参与介导多种肿瘤的耐药[14-15]。因此，UCA1在作为肿瘤生物标志物和治疗靶点方面具有较大的研究价值。
2 lncRNA与miRNA
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lncRNA是一类长度超过200个核苷酸且不被翻译成蛋白质的转录RNA，其异常表达或功能障碍与多种疾病密切相关，可通过多种机制在肿瘤细胞的增殖、凋亡、迁移和侵袭等过程中发挥调控作用，包括与miRNA相互作用[16-17]。miRNA是一种内源性的短单链非编码RNA序列，可通过靶向相应的mRNA在转录后水平调控基因的表达，从而调控肿瘤的发生和发展[18]。lncRNA和miRNA作为非编码RNA，不会被翻译成蛋白质，而是直接在RNA水平发挥作用。有学者对lncRNA与miRNA的相互作用和交叉调控进行研究，发现lncRNA与miRNA可以相互作用并调控肿瘤的发生发展过程，其调控机制主要包括：(1) lncRNA作为miRNA的竞争性内源RNA(competing endogenous RNAs，ceRNA)，阻断miRNA对下游靶mRNA的作用；(2) lncRNA与miRNA相互促进或抑制；(3) miRNA作为lncRNA的负调控因子发挥作用[19]。
3 UCA1和miRNAs在消化系统肿瘤中的作用机制
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3.1 胃癌
胃癌是消化系统最常见的恶性肿瘤之一，在癌症相关死亡原因中居第3位，男性发病率是女性的2倍[20]。目前，手术被认为是胃癌唯一的根治方法，随着手术技术的提高，传统放疗、化疗技术的发展，以及新辅助治疗的实施，早期胃癌5年生存率可达95%。但由于胃癌早期诊断率低，大部分患者在确诊时已处于晚期，错过了最佳的手术时期[21-22]。因此，有必要寻找更有效的胃癌生物标志物用于诊断和治疗。Gu等[23]进行RT-qPCR检测发现，胃癌组织和细胞中UCA1的表达分别高于癌旁正常组织和胃上皮细胞系。UCA1的表达水平与胃癌患者淋巴结转移、TNM分期和总生存期(overall survival，OS)有关。体外研究发现，UCA1可促进胃癌细胞增殖，增强细胞集落形成能力和侵袭能力；体内研究发现，敲低UCA1可抑制肿瘤的生长。进一步研究其机制发现，miR-590-3p是UCA1的靶点，UCA1通过负调控miR-590-3p的表达而促进胃癌细胞的增殖和侵袭。此外，CREB1是miR-590-3p的下游靶点，UCA1通过靶向miR-590-3p激活CREB1的表达。Gong等[24]的研究发现，UCA1可与miR-203竞争性结合，提高靶基因ZEB2的表达水平，促进胃癌细胞的迁移和侵袭。作为ceRNA，UCA1可通过竞争性结合miR-203而诱导胃癌细胞发生上皮-间质转化(epithelial-mesenchymal transition，EMT)，进而调控ZEB2的表达，提示UCA1/miR-203/ZEB2调控网络可能是高侵袭性胃癌的潜在治疗靶点。SATB1是一种组织特异性的核基质蛋白，其高表达与胃癌TNM分期较高及胃癌总生存率和无复发生存率较低有关[25]。Sun等[26]进行PCR检测发现，胃癌组织中SATB1和UCA1的表达高于癌旁正常组织，miR-495-3p的表达低于癌旁正常组织。SATB1的3'-UTR作为miR-495-3p的竞争性内源性RNA，可正向调控UCA1。此外，下调UCA1的表达可降低SATB1在MKN-45细胞中的表达，但对BGC-823细胞中SATB1的表达无影响，表明lncRNA UCA1作为ceRNA介导的miR-495-3p对SATB1的调控作用是细胞依赖性的，且SATB1/miR-495-3p/UCA1网络与胃癌细胞的增殖和侵袭有关。Wang等[27]发现，UCA1可通过靶向多种miRNA促进胃癌细胞的增殖、迁移、免疫逃逸并抑制胃癌细胞凋亡。UCA1可与miR-26a/b相互作用，调控EZH2和CDK6的表达，促进胃癌细胞增殖、迁移和抑制胃癌细胞凋亡；同时，UCA1还可通过miR-214和miR-193a上调PDL1的表达，从而抑制宿主免疫系统。由此可见，UCA1靶向治疗不仅针对肿瘤细胞，还可激活宿主免疫系统。
多种实体肿瘤被缺氧微环境包围，这与其高转移能力和对各种临床治疗的耐药性有关，导致肿瘤患者的生存率较低。研究发现，UCA1在耐缺氧胃癌(hypoxia-resistant gastric cancer，HRGC)细胞中表达上调，可促进HRGC细胞的迁移。生物信息学分析和荧光素酶报告基因分析显示，miR-7-5p可与UCA1的特定位点结合，通过ceRNA的功能调节目标表皮生长因子受体(epidermal growth factor receptor，EGFR)的表达。UCA1直接与miR-7-5p相互作用，可降低miR-7-5p与EGFR 3'-UTR的结合，从而抑制miR-7-5p对EGFR mRNA的降解[28]。由此可见，长期缺氧诱导的UCA1高表达可通过提高EGFR的表达而促进细胞迁移。该研究探索了低氧微环境促进肿瘤转移的新机制，提示UCA1可作为预测胃癌转移的候选生物标志物和潜在的治疗靶点。
此外，多药耐药性(multi-drug resistance，MDR)的出现是导致治疗失败和癌症相关死亡的关键因素，因此，研究导致耐药性的作用机制对胃癌的治疗具有重要意义。Fang等[29]的研究发现，抑制UCA1可明显恢复MDR胃癌细胞中miR-27b的表达。UCA1下调和miR-27b过表达降低了SGC-7901/ADR细胞中阿霉素(adriamycin，ADR)、顺铂(cisplatin，DDP)和氟尿嘧啶(fluorouracil，5-FU)的IC50，增加了ADR诱导的细胞凋亡。UCA1过表达和miR-27b抑制增高了SGC-7901细胞中ADR、DDP和5-FU的IC50，减少了ADR诱导的细胞凋亡。Western blotting检测结果显示，UCA1的下调和miR-27b的过表达降低了抗凋亡蛋白BCL-2的表达，增加了凋亡蛋白cleaved caspase-3的表达，表明UCA1/miR-27b轴参与了胃癌化疗敏感性的调控。Cheng等[30]发现，下调UCA1可通过诱导细胞凋亡增加胃癌细胞对DDP的化疗敏感性。UCA1可通过结合miR-513a-3p促进体外人胃癌细胞中CYP1B1的表达，UCA1和CYP1B1的表达与miR-513a-3p的表达呈负相关，而UCA1的表达与人胃癌组织中CYP1B1的表达呈正相关。此外，在人胃癌细胞中，下调UCA1可增加其对DDP化疗的敏感性，而下调miR-513a-3p或过表达CYP1B1则降低其对DDP化疗的敏感性。由此可见，UCA1/miR-513a-3p/CYP1B1轴可调控人胃癌细胞对DDP的耐药性，UCA1可作为治疗胃癌多种化疗耐药的潜在靶点。
3.2 结直肠癌
目前除手术外，基于肿瘤分期推荐的标准药物治疗也明显提高了结直肠癌的治疗效果，然而，仅根据肿瘤分期决定治疗方案可能导致许多患者的无效治疗及药物不良反应[31]。因此，寻找新的结直肠癌生物标志物和治疗靶点具有重要意义。研究发现，UCA1在结直肠癌组织和细胞中的表达水平明显升高，UCA1高表达与肿瘤大小、组织学分型和肿瘤浸润深度明显相关。此外，与UCA1低表达的患者相比，UCA1高表达患者的预后明显较差，UCA1可调控多个影响肿瘤细胞增殖、细胞周期进展和凋亡的基因的表达，从而促进结直肠癌的发生和进展[32]，但UCA1在结直肠癌中的具体作用机制尚未明确。Cui等[33]研究发现，miR-28-5p过表达可抑制结直肠癌细胞的生长和迁移，而UCA1可通过与miR-28-5p结合而减弱其抑瘤作用。荧光素酶基因报告实验发现，HOXB3为miR-28-5p的靶基因，HOXB3过表达可介导UCA1在结直肠癌细胞增殖和迁移中的功能，表明UCA1/miR-28-5p/HOXB3参与介导结直肠癌细胞的增殖和迁移。此外，UCA1还可通过靶向miR-143而作为ceRNA调节MYO6的表达，进而影响结直肠癌细胞的增殖和凋亡[34]。另有研究发现，沉默UCA1可以抑制结肠癌的侵袭、迁移、EMT和肿瘤形成；UCA1可以负调控肠癌细胞中miR-185-5p的表达，且可通过上调丝裂原激活蛋白激酶14(MAPK14)而激活MAPKAPK2/HSP27通路，提示UCA1可通过靶向miR-185-5p调控MAPK14/MAPKAPK2/HSP27，从而抑制结肠癌细胞的侵袭、迁移和EMT[35]。此外，Liu等[36]发现，miR-495与UCA1的表达呈负相关，UCA1作为miR-495的ceRNA，上调其表达可减弱miR-495对SP1/SP3表达的抑制作用。而SP1/SP3可诱导DNA甲基转移酶的表达，从而增强UCA1介导的促肿瘤作用。UCA1沉默可通过抑制EMT和DNA甲基化关键酶(DNMTs)相关的恶性表型，即迁移和侵袭，从而促进血管生成、化疗耐药和细胞增殖，降低SP1/SP3蛋白水平，发挥抗癌作用，表明UCA1-SP1/SP3在结直肠癌细胞中形成了正反馈闭合环路。以上研究拓展了UCA1在结直肠癌中的作用机制，并提示UCA1可作为结直肠癌潜在的生物标志物和治疗靶点。
5-FU常用于结直肠癌的临床治疗，其耐药性是导致结直肠癌治疗失败的主要原因之一。Bian等[37]研究发现，UCA1可通过抑制细胞凋亡而降低结直肠癌细胞对5-FU的敏感性；UCA1可以靶向miR-204-5p并抑制其功能，调控CREB1、BCL2和RAB22A蛋白的表达，且CREB1的表达与UCA1呈正相关，表明UCA1靶向miR-204-5p可促进癌细胞增殖、抑制癌细胞凋亡、诱导耐药，在结直肠癌的发生发展中发挥重要作用。此外，UCA1可通过促进结直肠癌细胞自噬、抑制结直肠癌细胞凋亡而介导5-FU耐药。研究发现，在结直肠癌细胞中，5-FU耐药与UCA1和细胞自噬水平呈正相关。Western blotting和流式细胞术检测发现，UCA1可通过促进自噬和抑制凋亡增强结直肠癌细胞5-FU耐药。双荧光素酶报告基因实验结果显示，UCA1在结直肠癌细胞中可以直接靶向miR-27b-3p，miR-23b-3p可通过负调控ZNF281(miR-27b-3p的直接靶点)而提高结直肠癌细胞对5-FU的敏感性，体内实验也证实了以上结果。UCA1通过miR-23b-3p/ZNF281促进自噬和抑制凋亡，介导结直肠癌细胞5-FU耐药[38]。另有研究发现，UCA1可抑制miR-18a和miR-182，从而促进CDC42的激活，进而调节溶瘤痘苗病毒(oncolytic vaccinia virus，OVV)在细胞间的扩散，提高结直肠癌细胞对OVV的敏感性[39]。以上研究揭示了UCA1在结直肠癌药物敏感性中的作用机制，为结直肠癌的治疗提供了新思路。
3.3 食管癌
食管癌发病率在所有肿瘤中居第7位，病死率在肿瘤相关死亡原因中居第6位，其中男性患者约占70%[16]。食管鳞状细胞癌(esophageal squamous cell carcinoma，ESCC)是食管癌最常见的类型之一，早期ESCC难以诊断，晚期ESCC常表现为广泛的局部浸润或局部淋巴结转移，全球范围内ESCC患者的5年生存率低于40%[40]。因此，揭示食管癌的潜在机制，寻找新的治疗靶点至关重要。有研究发现，UCA1在ESCC组织中的相对表达水平明显高于癌旁正常组织，UCA1表达较高的ESCC患者临床分期较晚、预后较差；此外，UCA1的下调降低了ESCC细胞的增殖、迁移和侵袭能力[41]，表明UCA1可能是ESCC潜在的预后生物标志物和治疗靶点。
有学者对UCA1在食管癌中的作用机制进行研究。如Jiao等[42]采用CCK-8法检测UCA1对EC9706和KYSE细胞的影响，发现UCA1可以促进食管癌细胞增殖；进一步探寻其作用机制发现，UCA1可直接靶向miR-204并与其相互作用。Sox4是Sox转录因子家族的成员，在肿瘤的发生发展过程中起着双重作用，既可作为肿瘤抑制因子，也可作为癌基因，影响与肿瘤生物学相关的关键过程，包括细胞凋亡、增殖、迁移、EMT和癌症干细胞性[43]。既往有研究发现，Sox4是miR-204的靶基因[44]。而过表达UCA1增加了Sox4的表达，沉默UCA1则抑制了Sox4的表达。过表达miR-204可以抑制UCA1诱导的Sox4上调，而抑制miR-204逆转了UCA1敲低诱导的Sox4下调[42]，表明UCA1在食管癌中以ceRNA的方式促进细胞增殖，miR-204-Sox4作为UCA1的直接靶点，介导了UCA1在食管癌细胞增殖中的作用。
锌指E盒结合的同源盒蛋白2(ZEB2)是一种DNA结合转录调控因子，主要参与EMT，其在EMT诱导的肿瘤细胞增殖、分化、凋亡和血管生成等过程中发挥重要作用[45]。Wang等[46]通过RT-qPCR检测发现，与癌旁正常组织和正常细胞相比，食管癌组织及食管癌细胞系中UCA1和ZEB2表达上调，miR-498表达下调；其中，EC9706细胞中UCA1和ZEB2 mRNA表达水平最高，而miR-498的表达水平最低。下调UCA1可以促进miR-497的表达，同时下调ZEB2的表达，而促进miR-498的表达可以降低ZEB2在食管癌细胞中的表达，表明UCA1可以作为ceRNA降低miR-498的表达，从而提高ZEB2的表达。综上，抑制UCA1可上调miR-498，下调ZEB2，从而抑制食管癌细胞的增殖、侵袭、迁移和EMT。
在肿瘤和其他正在增殖或发育的细胞中，即使在有氧和线粒体功能完全的情况下，也有高效率的乳酸生成和葡萄糖摄取，这一过程被称为Warburg效应。己糖激酶2(HK2)在此过程中发挥着至关重要的作用，可通过促进细胞对葡萄糖的摄取而促进Warburg效应[47-48]。Liu等[49]研究发现，UCA1在恶性表型及预后不佳的食管癌中表达上调，同时体外研究证实，UCA1可介导食管癌细胞的增殖和转移。miR-203是UCA1的直接靶点，在食管癌细胞中，UCA1上调显著抑制了miR-203对HK2的降解。上述结果表明，UCA1通过靶向miR-203，减弱miR-203对HK2的抑制作用来促进糖酵解，从而产生Warburg效应。以上研究从肿瘤代谢的角度分析了UCA1和miRNAs在食管癌发生发展过程中的作用机制，为食管癌的诊断和治疗提供了新的思路。
UCA1与miRNAs在消化系统肿瘤中的作用机制详见表1。
4 总结与展望
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UCA1在胃癌、结直肠癌及食管癌等多种消化系统肿瘤组织和细胞中的表达明显上调，且可与多种miRNA分子相互作用，进而调控miRNA的下游靶基因，以UCA1/miRNAs/mRNA途径的形式影响肿瘤细胞的增殖、迁移、侵袭、EMT、凋亡、耐药等过程，同时UCA1与miRNAs相互作用在肿瘤代谢及免疫过程中发挥重要作用。在UCA1与miRNAs的相互作用中，UCA1可作为ceRNA调控miRNAs的下游靶基因，同时miRNAs可负向调控lncRNA的表达，进而影响肿瘤的病理过程。UCA1可在消化系统肿瘤中作为致癌基因发挥作用，具有作为新的生物标志物和治疗靶点的潜力，利于消化系统肿瘤的早期诊断、靶向治疗及预后评估等。
然而目前的研究尚存在一些不足：虽然UCA1与miRNAs在消化系统肿瘤中的调控作用已被证实，但其具体机制尚未明确，如部分研究仅证实了UCA1可靶向miRNAs而发挥对肿瘤的抑制作用，但miRNAs调控的具体下游靶基因未明确；通过UCA1/miRNAs途径可抑制消化系统肿瘤的耐药性，但其发挥作用后具体的用药剂量范围尚未确定。此外，UCA1被证实在其他消化系统肿瘤中的表达也明显上调，但其作用机制研究尚未开展；部分研究仅在体外验证了UCA1与miRNAs的作用机制，体内的作用机制尚未明确；同时，UCA1的其他剪接变异体在消化系统肿瘤中的作用机制有待研究。由于lncRNA作用机制的多样性和复杂性，目前对lncRNA功能的了解尚处于初级阶段，未来需要对UCA1进行深入研究，以探索其在致癌过程中的作用机制。因此，未来需要大量的研究数据证实UCA1和miRNAs在消化系统肿瘤组织或细胞中的特异性，并阐明UCA1/miRNAs途径调控肿瘤发生发展的具体机制。随着研究的不断深入以及大量研究数据的支撑，UCA1和miRNAs在消化系统肿瘤中的作用机制将会被进一步阐明，可为UCA1从基础研究转向临床应用提供理论依据，并为肿瘤的临床诊断与治疗提供方向。
基金
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  • 国家自然科学基金(81402344)
  • 陕西省青年科技新星项目(2018KJXX-096)
  • 陕西省自然科学基础研究计划项目(2020JM-595)
文献
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2021年第46卷第12期
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doi: 10.11855/j.issn.0577-7402.2021.12.10
  • 接收时间：2021-06-07
  • 首发时间：2025-12-18
  • 出版时间：2021-12-28
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  • 收稿日期：2021-06-07
  • 修回日期：2021-08-12
基金
National Natural Science Foundation of China(81402344)
国家自然科学基金(81402344)
Youth Science and Technology Rising Star Project of Shaanxi Province(2018KJXX-096)
陕西省青年科技新星项目(2018KJXX-096)
Natural Science Research Project of Shaanxi Province(2020JM-595)
陕西省自然科学基础研究计划项目(2020JM-595)
作者信息
    1陕西中医药大学基础医学院，陕西咸阳 712046
    2陕西中医药大学医学科研实验中心，陕西咸阳 712046

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王宇，E-mail：
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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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