Article(id=1292126453156569585, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126409196064779, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.02.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1746979200000, receivedDateStr=2025-05-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996552980, onlineDateStr=2026-08-06, pubDate=1769529600000, pubDateStr=2026-01-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996552980, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996552980, creator=13701087609, updateTime=1785996552980, updator=13701087609, issue=Issue{id=1292126409196064779, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='2', pageStart='151', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1769529600000', pubDateStr='2026-01-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996542500, creator='13701087609', updateTime=1786014671444, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202447569707674, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126409196064779, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202447569707675, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126409196064779, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=197, endPage=203, ext={EN=ArticleExt(id=1292126453479530994, articleId=1292126453156569585, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of resveratrol on proliferation, migration and glycolysis of breast cancer cells by regulating LKB1/AMPK pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effects and mechanism of resveratrol on the proliferation, migration and glycolysis of breast cancer cells by regulating the liver kinase B1 (LKB1)/AMP activated protein kinase (AMPK) pathway.
Methods Human breast cancer MDA-MB-231 cells were divided into four groups: control group, low-concentration experimental group (25 μmol·L-1 resveratrol), high-concentration experimental group (50 μmol·L-1 resveratrol) and inhibitor group (50 μmol·L-1 resveratrol + 4 μmol·L-1 AMPK inhibitor BML-275). The cell proliferation of each group was detected by thiazolyl blue (MTT) assay and Edu staining; the cell migration was detected by scratch test; the cell apoptosis was detected by flow cytometry; the glucose consumption and lactic acid production of cells in each group were measured by glucose content kit and lactic acid content kit, respectively; the protein expressions of glucose transporter 1 (GLUT1), lactate dehydrogenase A (LDHA), hexokinase 2 (HK2), LKB1 and AMPK in each group were detected by Western blot.
Results The cell proliferation inhibition rates of control group, low-concentration experimental group, high-concentration experimental group and inhibitor group were (0±0)%, (32.27±3.68)%, (56.75±5.82)% and (24.41±3.06)%, respectively; the Edu-positive rates were (52.64±6.95)%, (30.72±4.21)%, (18.86±2.54)% and (41.37±4.88)%, respectively; the scratch healing rates were (34.24±3.82)%, (23.67±2.74)%, (14.85±2.03)% and (29.74±3.42)%, respectively; the cell apoptosis rates were (3.04±0.32)%, (21.81±2.64)%, (34.43±3.86)% and (12.67±1.93)%, respectively; the glucose consumption levels were (31.74±3.52), (23.18±2.64), (14.33±1.67) and (28.27±3.12) μmol·L-1, respectively; the lactic acid production levels were (48.12±4.43), (31.27±3.75), (18.85±2.14) and (42.36±4.19) μmol·L-1, respectively; the relative expression levels of GLUT1 were 1.14±0.12, 0.76±0.08, 0.41±0.04 and 0.94±0.09, respectively; the relative expression levels of LDHA were 1.32±0.14, 0.89±0.09, 0.47±0.05 and 1.13±0.12, respectively; the relative expression levels of HK2 were 0.97±0.09, 0.61±0.06, 0.34±0.04 and 0.86±0.09, respectively; the relative expression levels of LKB1 were 0.93±0.10, 1.38±0.14, 1.75±0.17 and 1.12±0.11, respectively; the relative expression levels of AMPK were 1.02±0.11, 1.56±0.16, 2.04±0.23 and 1.18±0.13, respectively. Compared with control group, the above indicators in the low- and high-concentration experimental groups were statistically significantly different (all P<0.05); compared with the high-concentration experimental group, the above indicators in the inhibitor group were statistically significantly different (all P<0.05).
Conclusion Resveratrol may inhibit the proliferation, migration and glycolysis of breast cancer cells by activating the LKB1/AMPK pathway.
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目的 探索白藜芦醇通过调控肝激酶B1（LKB1）/腺苷酸活化激酶（AMPK）通路对乳腺癌细胞增殖、迁移和糖酵解的影响及其机制。
方法 将人乳腺癌细胞MDA-MB-231分为对照组、低浓度试验组（25 μmol·L-1白藜芦醇）、高浓度实验组（50 μmol·L-1白藜芦醇）和抑制剂组（50 μmol·L-1白藜芦醇和4 μmol·L-1AMPK抑制剂BML-275）。用噻唑蓝（MTT）法和Edu染色法测定各组细胞增殖情况；用划痕实验法测定各组细胞迁移情况；用流式细胞仪测定细胞凋亡情况；用葡萄糖含量试剂盒、乳酸含量试剂盒测定各组细胞葡萄糖消耗量、乳酸产生量；用蛋白质印迹法测定各组细胞葡萄糖转运蛋白1（GLUT1）、乳酸脱氢酶A（LDHA）、己糖激酶2（HK2）以及LKB1、AMPK蛋白表达情况。
结果 对照组、低、高浓度实验组和抑制剂组的细胞增殖抑制率分别为（0±0）%、（32.27±3.68）%、（56.75±5.82）%和（24.41±3.06）%；Edu阳性率分别为（52.64±6.95）%、（30.72±4.21）%、（18.86±2.54）%和（41.37±4.88）%；划痕愈合率分别为（34.24±3.82）%、（23.67±2.74）%、（14.85±2.03）%和（29.74±3.42）%；细胞凋亡率分别为（3.04±0.32）%、（21.81±2.64）%、（34.43±3.86）%和（12.67±1.93）%；葡萄糖消耗量分别为（31.74±3.52）、（23.18±2.64）、（14.33±1.67）和（28.27±3.12）μmol·L-1；和乳酸产生量分别为（48.12±4.43）、（31.27±3.75）、（18.85±2.14）和（42.36±4.19）μmol·L-1；GLUT1相对表达水平分别为1.14±0.12、0.76±0.08、0.41±0.04和0.94±0.09；LDHA相对表达水平分别为1.32±0.14、0.89±0.09、0.47±0.05和1.13±0.12；HK2相对表达水平分别为0.97±0.09、0.61±0.06、0.34±0.04和0.86±0.09；LKB1相对表达水平分别为0.93±0.10、1.38±0.14、1.75±0.17和1.12±0.11；AMPK相对表达水平分别为1.02±0.11、1.56±0.16、2.04±0.23和1.18±0.13。低、高浓度实验组的上述指标与对照组比较，抑制剂组的上述指标与高浓度实验组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 白藜芦醇可能通过激活LKB1/AMPK通路抑制乳腺癌细胞增殖、迁移和糖酵解。
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李雪曼（1982-），女，副主任医师，主要从事乳腺癌研究
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