Article(id=1292126436094140797, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1764172800000, receivedDateStr=2025-11-27, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996548912, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996548912, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996548912, creator=13701087609, updateTime=1785996548912, updator=13701087609, issue=Issue{id=1292126377440989952, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='1', pageStart='1', pageEnd='147', issueExtLink='null', onlineDate='null', pubDate='1768579200000', pubDateStr='2026-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996534929, creator='13701087609', updateTime=1786014708731, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202603945947673, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202603950141978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=59, endPage=65, ext={EN=ArticleExt(id=1292126437952217470, articleId=1292126436094140797, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the synergistic inhibition of malignant behavior of breast cancer cells by curcumin and chidamide based on IFN-RIG-I-MAVS pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the molecular mechanism by which curcumin (CUR) and chidamide (CHI) synergistically inhibit the malignant behaviors of breast cancer (BC) cells through the interferon (IFN)-retinoic acid-inducible gene Ⅰ (RIG-Ⅰ)-mitochondrial antiviral-signaling protein (MAVS) pathway.
Methods A cellular model was established using MCF-7 breast cancer cells. The cells were divided into five groups: blank group(normol cuttured), CUR group(20 μmol·L-1 CUR), CHI group(10 μmol·L-1 CHI), combination group(20 μmol·L-1 CUR+10 μmol·L-1 CHI) and inhibitor group(sh-IFN+20 μmol·L-1 CUR+10 μmol·L-1 CHI). Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation capacity was evaluated by plate colony formation assay. Cell migration ability was examined using Transwell and wound healing assays. The relative expression levels of apoptosis-related proteins and IFN-RIG-I-MAVS pathway-associated proteins were detected by Western blotting (WB).
Results Under CUR concentrations of 0, 10, 20 and 40 μmol·L-1, the half-maximal inhibitory concentrations (IC50) of CHI were (31.48±2.01), (17.57±0.65), (7.56±0.32) and (0.21±0.02) μmol·L-1, respectively. Statistically significant dose-dependent reductions in IC50 were observed for CHI when combined with 10, 20 and 40 μmol·L-1 CUR compared to 0 μmol·L-1 CUR (all P<0.05). The colony formation numbers were (201.28±23.96) cells for the control group, (113.43±15.59) cells for the CUR group, (109.93±11.64) cells for the CHI group, (59.57±6.91) cells for the combination group, and (87.43±5.04) cells for the inhibitor group, respectively; the numbers of invasive cells were (115.03±13.05), (86.51±9.13), (77.82±6.68), (39.54±5.43) and (68.92±3.95) cells, respectively; the wound closure rates were (51.29±5.17)%, (32.80±2.94)%, (31.23±3.10)%, (16.07±2.11)% and (26.94±1.95)%, respectively; the apoptosis rates were (2.21±0.16)%, (12.03±0.85)%, (12.89±0.99)%, (31.62±2.98)% and (16.85±1.04)%, respectively; the relative expression levels of Caspase-3 were 0.38±0.03, 0.55±0.03, 0.52±0.04, 1.12±0.07 and 0.97±0.05, respectively; the relative expression levels of Caspase-9 levels were 0.33±0.02, 0.53±0.02, 0.55±0.04, 1.05±0.06 and 0.60±0.05, respectively; the relative expression levels of Bax levels were 0.34±0.03, 0.52±0.03, 0.53±0.03, 1.08±0.07 and 0.69±0.06, respectively; the relative expression levels of IFN-β levels were 0.33±0.03, 0.46±0.04, 0.53±0.04, 1.09±0.10 and 0.45±0.03, respectively; the relative expression levels of RIG-Ⅰ levels were 0.32±0.02, 0.57±0.05, 0.65±0.04, 1.02±0.11 and 0.59±0.05, respectively; and the relative expression levels of MAVS levels were 0.34±0.02, 0.41±0.03, 0.49±0.04, 1.04±0.12 and 0.51±0.04, respectively. Statistically significant differences were observed when comparing the CUR and CHI groups to the control group, the combination group to the CUR and CHI groups, and the inhibitor group to the combination group (all P<0.05).
Conclusion CUR enhances the sensitivity of BC cells to CHI and synergistically exerts anti-BC effects with CHI, and its mechanism of action is related to the activation of the IFN-RIG-I-MAVS pathway by CUR.
, authors=Yue PAN
1, Chen-ming ZHANG
2, authorsList=Yue PAN, Chen-ming ZHANG, authorCompany=null, correspAuthors=Chen-ming 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=1292126438220652927, articleId=1292126436094140797, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=姜黄素与西达苯胺基于IFN-RIG-I-MAVS通路协同抑制乳腺癌细胞恶性行为的研究, 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 探索姜黄素(CUR)与西达苯胺(CHI)通过干扰素(IFN)-视黄酸诱导基因Ⅰ(RIG-Ⅰ)-线粒体抗病毒信号蛋白(MAVS)通路协同抑制乳腺癌(BC)细胞恶性行为的分子机制。
方法 用乳腺癌细胞MCF-7建立细胞模型。将细胞分为5组,包括空白组(正常培养)、CUR组(20 μmol·L-1 CUR)、CHI组(10 μmol·L-1 CHI),联合组(20 μmol·L-1 CUR+10 μmol·L-1 CHI)和抑制剂组(sh-IFN+20 μmol·L-1 CUR+10 μmol·L-1 CHI)。用3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐(MTT)法检测细胞活力,用平板克隆形成实验法检测细胞增殖能力,用Transwell和细胞划痕实验法检测细胞迁移能力,用蛋白质印迹法(WB)检测凋亡相关蛋白和IFN-RIG-Ⅰ-MAVS通路相关蛋白的相对表达水平。
结果 在0、10、20和40 μmol·L-1 CUR中,CHI的半数抑制浓度(IC50)分别为(31.48±2.01)、(17.57 ±0.65)、(7.56 ±0.32)和(0.21 ±0.02)μmol·L-1,10、20和40 μmol·L-1 CUR与0 μmol·L-1CUR相比,IC50在统计学上差异均有统计学意义,并呈剂量依赖性(均P<0.05)。空白组、CUR组、CHI组、联合组和抑制剂组的克隆形成数分别为(201.28±23.96)、(113.43±15.59)、(109.93±11.64)、(59.57±6.91)和(87.43±5.04)个;穿膜细胞数分别为(115.03±13.05)、(86.51±9.13)、(77.82±6.68)、(39.54±5.43)和(68.92±3.95)个;划痕修复率分别为(51.29±5.17)%、(32.80±2.94)%、(31.23±3.10)%、(16.07±2.11)%和(26.94±1.95)%;细胞凋亡率分别为(2.21±0.16)%、(12.03±0.85)%、(12.89±0.99)%、(31.62±2.98)%和(16.85±1.04)%;Caspase-3相对表达水平分别为0.38±0.03、0.55±0.03、0.52±0.04、1.12±0.07和0.97±0.05;Caspase-9相对表达水平分别为0.33±0.02、0.53±0.02、0.55±0.04、1.05±0.06和0.60±0.05;Bax相对表达水平分别为0.34±0.03、0.52±0.03、0.53±0.03、1.08±0.07和0.69±0.06;IFN-β相对表达水平分别为0.33±0.03、0.46±0.04、0.53±0.04、1.09±0.10和0.45±0.03;RIG-Ⅰ相对表达水平分别为0.32±0.02、0.57±0.05、0.65±0.04、1.02±0.11和0.59±0.05;MAVS相对表达水平分别为0.34±0.02、0.41±0.03、0.49±0.04、1.04±0.12和0.51±0.04,CUR组和CHI组的上述指标与空白组比较,联合组的上述指标与CUR组和CHI组比较,抑制剂组的上述指标与联合组比较,在统计学上差异均有统计学意义(均P<0.05)。
结论 CUR具有增加BC细胞对CHI敏感性的作用,可以协同CHI发挥抗BC作用,其作用机制与CUR激活IFN-RIG-I-MAVS通路有关。
, authors=潘越
1, 张臣鸣
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