Article(id=1292130442510098953, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130366320562708, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.07.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1773590400000, receivedDateStr=2026-03-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997504116, onlineDateStr=2026-08-06, pubDate=1776355200000, pubDateStr=2026-04-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997504116, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997504116, creator=13701087609, updateTime=1785997504116, updator=13701087609, issue=Issue{id=1292130366320562708, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='7', pageStart='901', pageEnd='1050', issueExtLink='null', onlineDate='null', pubDate='1776355200000', pubDateStr='2026-04-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997485952, creator='13701087609', updateTime=1786014433453, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201449350516861, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130366320562708, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201449350516862, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130366320562708, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=962, endPage=967, ext={EN=ArticleExt(id=1292130444389147146, articleId=1292130442510098953, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of the effects of plumbagin in the malignant biological behaviors and glycolysis of tongue squamous cell carcinoma cells through
FNDC3
B, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the mechanism of the inhibitory effects of plumbagin on the malignant biological behaviors and glycolysis of tongue squamous cell carcinoma cells through fibronectin type Ⅲ domain-containing protein 3B (FNDC3B).
Methods Human tongue squamous cell carcinoma cells (TCA8113) in the logarithmic growth phase were obtained. TCA8113 cells were divided into blank group (normal cultured), experimental-L, M, and H group (TCA8113 cells were treated with 1, 2 and 4 μmol·L-1 plumbagin), oe-NC group (TCA8113 cells were transfected with the negative control plasmid oe-NC), oe-FNDC3B group (TCA8113 cells were transfected with oe-FNDC3B), experimental-H+oe-NC group (based on experimental-H group, transfected with the oe-NC plasmid) and experimental-H+oe-FNDC3B group (based on experimental-H group, transfected with the oe-FNDC3B plasmid). Real-time quantitative polymerase chain reaction was used to detect FNDC3B mRNA relative expression levels. Cell viability was assessed using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Cell invasion was evaluated using the Transwell assay. Immunofluorescence staining was performed to detect the protein relative expression levels of FNDC3B, hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA). Cell apoptosis was detected using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay.
Results The numbers of invasive cells in blank group, experimental-H group, experimental-H+oe-NC group and experimental-H+oe-FNDC3B group were (89.71±13.59), (69.67±14.78), (62.33±10.11) and (158.23±20.95), respectively; the apoptosis rates were (10.07±2.41)%, (23.38±4.75)%, (20.65±5.43)% and (8.44±1.18)%, respectively; the relative expression levels of HK2 were 1.00±0.15, 0.58±0.09, 0.55±0.07 and 0.71±0.10, respectively; the relative expression levels of LDHA were 1.00±0.12, 0.63±0.11, 0.61±0.09 and 0.89±0.15, respectively; the relative expression levels of P53 were 1.00±0.15, 1.59±0.31, 1.64±0.28 and 1.25±0.22, respectively; the relative expression levels of P21 were 1.00±0.13, 1.51±0.26, 1.48±0.19 and 1.19±0.17, respectively; the relative expression levels of CDK6 were 1.00±0.13, 0.28±0.04, 0.33±0.06 and 0.79±0.12, respectively. There were statistically significant differences in the above indicators between experimental-H group and blank group, and between experimental-H+oe-FNDC3B group and experimental-H+oe-NC group (all P<0.05).
Conclusion Plumbagin may promote the apoptosis of tongue squamous cell carcinoma cells, and inhibit the invasion and glycolysis of cancer cells by regulating the P53/P21/CDK6 signaling pathway through FNDC3B.
, authors=Qian YAN
1, Yan LI
1, Hong-li CHEN
1, Yu-tao ZHANG
1, Xu-Qin ZHANG
2, authorsList=Qian YAN, Yan LI, Hong-li CHEN, Yu-tao ZHANG, Xu-Qin ZHANG, authorCompany=null, correspAuthors=Qian YAN, 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=1292130444674359819, articleId=1292130442510098953, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=白花丹醌通过
FNDC3
B在舌鳞癌细胞恶性生物学行为与糖酵解中的作用研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨白花丹醌（plumbagin）通过含纤连蛋白Ⅲ型结构域蛋白3B（FNDC3B）对舌鳞癌细胞恶性生物学行为与糖酵解抑制作用的机制。
方法 取对数生长期的人舌鳞癌细胞（TCA8113），将TCA8113细胞分为空白组（正常培养）、低、中、高剂量实验组（分别用1、2、4 μmol·L-1〓白花丹醌处理TCA8113细胞）、oe-NC组（TCA8113细胞转染阴性对照质粒oe-NC）、oe-FNDC3B组（TCA8113细胞转染oe-FNDC3B）、高剂量实验组+oe-NC组（基于高剂量实验组，转染oe-NC质粒）和高剂量实验组+oe-FNDC3B组（基于高剂量实验组，转染oe-FNDC3B质粒）。用实时荧光定量聚合酶链反应检测FNDC3B mRNA相对表达水平；用噻唑蓝法检测细胞存活率；用Transwell实验法检测细胞侵袭水平；用免疫荧光法检测FNDC3B、己糖激酶2（HK2）和乳酸脱氢酶A（LDHA）蛋白相对表达水平；用原位末端转移酶标记技术法检测细胞凋亡水平。
结果 空白组、高剂量实验组、高剂量实验+oe-NC组和高剂量实验+oe-FNDC3B组细胞侵袭个数为（89.71±13.59）、（69.67±14.78）、（62.33±10.11）和（158.23±20.95）个，细胞凋亡率为（10.07±2.41）%、（23.38±4.75）%、（20.65±5.43）%和（8.44±1.18）%，HK2蛋白相对表达水平分别为1.00±0.15、0.58±0.09、0.55±0.07和0.71±0.10，LDHA蛋白相对表达水平水平分别为1.00±0.12、0.63±0.11、0.61±0.09和0.89±0.15，P53蛋白相对表达水平水平分别为1.00±0.15、1.59±0.31、1.64±0.28和1.25±0.22，P21蛋白相对表达水平水平分别为1.00±0.13、1.51±0.26、1.48±0.19和1.19±0.17，CDK6蛋白相对表达水平分别为1.00±0.13、0.28±0.04、0.33±0.06和0.79±0.12，高剂量实验组的上述指标与空白组比较，高剂量实验+oe-FNDC3B组的上述指标与高剂量实验+oe-NC组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 白花丹醌可能通过FNDC3B调控P53/P21/CDK6信号通路来促进舌鳞癌细胞的凋亡，抑制癌细胞的侵袭和糖酵解。
, authors=闫倩
1, 李琰
1, 陈宏丽
1, 张宇涛
1, 张旭琴
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闫倩（1985-），女，实验师，主要从事口腔医学方面的研究
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2.Department of Stomatology, Lüliang People's Hospital, Lüliang 033000, Shanxi Province, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1292130446167532074, tenantId=1146029695717560320, journalId=1246415772164075586, articleId=1292130442510098953, authorId=1292130445978788391, language=CN, stringName=张旭琴, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=
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