Article(id=1291404933723579130, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404875351449891, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.09.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1730217600000, receivedDateStr=2024-10-30, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824529343, onlineDateStr=2026-08-04, pubDate=1747411200000, pubDateStr=2025-05-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824529343, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824529343, creator=13701087609, updateTime=1785824529343, updator=13701087609, issue=Issue{id=1291404875351449891, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='9', pageStart='1201', pageEnd='1350', issueExtLink='null', onlineDate='null', pubDate='1747411200000', pubDateStr='2025-05-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824515426, creator='13701087609', updateTime=1785897088931, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709270765097028, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404875351449891, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709270765097029, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404875351449891, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1242, endPage=1247, ext={EN=ArticleExt(id=1291404934071706363, articleId=1291404933723579130, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of ginsenoside Rh2 affecting the development of colon cancer, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effects of ginsenoside Rh2 on the development of colon cancer through microRNA-128-3p(miR-128-3p)/growth differentiation factor 15(GDF15) mediated wingless-type MMTV integration site family member (Wnt)/β-catenin signaling pathway.
Methods SW620 colorectal cancer cells were randomly divided into the following groups: Control group (standard culture), experimental group (treated with ginsenoside Rh2 at 20 μmol·L-1), NC inhibitor group (transfected with NC inhibitor), miR-128-3p inhibitor group (transfected with miR-128-3p inhibitor), ginsenoside Rh2 + miR-128-3p inhibitor group (treated with ginsenoside Rh2 at 20 μmol·L-1 and transfected with miR-128-3p inhibitor), and ginsenoside Rh2+miR-128-3p inhibitor+si-GDF15 group (treated with ginsenoside Rh2 at 20 μmol·L-1, transfected with miR-128-3p inhibitor and si-GDF15). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of miR-128-3p and GDF15 mRNA. Cell proliferation was assessed using 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay. Western blotting was employed to detect the protein relative levels of myelocytomatosis oncogene (Myc) and β-catenin.
Results The relative expression levels of miR-128-3p in the control group and experimental group were 1.00±0.16 and 1.56±0.25, respectively; the relative expression relative levels of GDF15 mRNA were 1.00±0.12 and 0.43±0.05, respectively; the proliferation rates were (88.76±8.56)% and (35.89±4.05)%, respectively; the v-myc avian myelocytomatosis viral oncogene homolog (Myc) protein levels were 1.00±0.21 and 0.45±0.06, respectively; and the β-catenin protein relative levels were 1.00±0.23 and 0.52±0.07, respectively. Compared with the control group, the above indicators in the experimental group showed statistically significant differences (all P<0.05). In the ginsenoside Rh2+miR-128-3p inhibitor group and ginsenoside Rh2+miR-128-3p inhibitor+si-GDF15 group, the cell proliferation rates were (68.56±7.12)% and (50.56±5.18)%, respectively; the Myc protein relative levels were 0.86±0.12 and 0.61±0.08, respectively; and the β-catenin protein relative levels were 0.71±0.09 and 0.58±0.08, respectively. The above indicators in the ginsenoside Rh2+miR-128-3p inhibitor group compared with the experimental group, and those in the ginsenoside Rh2+miR-128-3p inhibitor+si-GDF15 group compared with the ginsenoside Rh2+miR-128-3p inhibitor group, all showed statistically significant differences (all P<0.05).
Conclusion Ginsenoside Rh2 can inhibit the proliferation and migration of colon cancer SW620 cells, and promote the apoptosis, which may be related to the regulation of ginsenoside Rh2 on the miR-128-3p/GDF15 to inhibit Wnt/β-catenin signaling pathway.
, authors=Jian-zhong YI, Yun-geng LIU, Chuan-yuan LIU, He-fang XIAO, Lei ZHANG, Hong-quan LIU, Chuan-fa FANG, authorsList=Jian-zhong YI, Yun-geng LIU, Chuan-yuan LIU, He-fang XIAO, Lei ZHANG, Hong-quan LIU, Chuan-fa FANG, authorCompany=null, correspAuthors=Jian-zhong YI, 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=1291404934545662716, articleId=1291404933723579130, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=人参皂苷Rh2影响结肠癌发展的研究, 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 探究人参皂苷Rh2通过微小核糖核酸-128-3p（miR-128-3p）/生长分化因子15（GDF15）介导无翅型MMTV整合位点家族成员/β-连环素（Wnt/β-catenin）信号通路影响结肠癌发展的作用机制。
方法 将结肠癌细胞SW620细胞随机分为对照组（常规培养）、实验组（人参皂苷Rh2 20 μmol·L-1）、NC inhibitor组（转染NC inhibitor）、miR-128-3p inhibitor组（转染miR-128-3p inhibitor）、人参皂苷Rh2+miR-128-3p inhibitor组（20 μmol·L-1人参皂苷Rh2、转染miR-128-3p inhibitor）和人参皂苷Rh2+miR-128-3p inhibitor+si-GDF15组（20 μmol·L-1人参皂苷Rh2、转染miR-128-3p inhibitor、si-GDF15）。用实时荧光定量聚合酶链反应检测miR-128-3p和GDF15 mRNA相对表达水平，用5-乙炔基-2′-脱氧尿苷检测细胞增殖情况，用蛋白质印迹法检测骨髓细胞瘤癌基因（Myc）和β-catenin蛋白相对表达水平。
结果 对照组和实验组的miR-128-3p相对表达水平分别为1.00±0.16和1.56±0.25，GDF15 mRNA相对表达水平分别为1.00±0.12和0.43±0.05，增殖率分别为（88.76±8.56）%和（35.89±4.05）%，骨髓细胞瘤癌基因（Myc）蛋白相对表达水平分别为1.00±0.21和0.45±0.06，β-连环素（β-catenin）蛋白相对表达水平分别为1.00±0.23和0.52±0.07，实验组的上述指标与对照组比较，在统计学上差异均有统计学意义（均P<0.05）。人参皂苷Rh2+miR-128-3p inhibitor组和人参皂苷Rh2+miR-128-3p inhibitor+si-GDF15组的细胞增殖率分别为（68.56±7.12）%和（50.56±5.18）%，Myc蛋白相对表达水平分别为0.86±0.12和0.61±0.08，β-catenin蛋白相对表达水平分别为0.71±0.09和0.58±0.08，人参皂苷Rh2+miR-128-3p inhibitor组的上述指标与实验组比较、人参皂苷Rh2+miR-128-3p inhibitor+si-GDF15组的上述指标与人参皂苷Rh2+miR-128-3p inhibitor组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 人参皂苷Rh2可以抑制结肠癌细胞增殖、迁移，促进凋亡，这可能与调控miR-128-3p/GDF15抑制Wnt/β-catenin信号通路有关。
, authors=易建中, 刘云庚, 刘传渊, 肖荷芳, 张磊, 刘红权, 方传发, authorsList=易建中, 刘云庚, 刘传渊, 肖荷芳, 张磊, 刘红权, 方传发, authorCompany=null, correspAuthors=易建中, authorNote=
易建中（1973-），男，副主任医师，主要从事胃肠道恶性肿瘤方向的基础及临床方面的研究
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