miR-29通过ITGB1抑制胃癌侵袭、转移的分子机制

何兵; 余松涛; 吕沐瀚; 吴玉云; 胡长江; 杨仕明

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miR-29通过ITGB1抑制胃癌侵袭、转移的分子机制

论著 | 更新时间：2026-01-09

- miR-29通过ITGB1抑制胃癌侵袭、转移的分子机制
- miR-29 functions as an anti-metastatic microRNA in gastric adenocarcinoma by targeting ITGB1
- 陆军军医大学学报 2013年35卷第11期页码：1037-1042
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  中图分类号： R394-33;R394.3;R735.2
- 纸质出版：2013
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何兵,余松涛,吕沐瀚,吴玉云,胡长江,杨仕明.miR-29通过ITGB1抑制胃癌侵袭、转移的分子机制[J].陆军军医大学学报(原第三军医大学学报),2013,35(11):1037-1042.

　He Bing,Yu Songtao,Lyu Muhan,Wu Yuyun,Hu Changjiang,Yang Shiming.miR-29 functions as an anti-metastatic microRNA in gastric adenocarcinoma by targeting ITGB1[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(11):1037-1042.
何兵,余松涛,吕沐瀚,吴玉云,胡长江,杨仕明.miR-29通过ITGB1抑制胃癌侵袭、转移的分子机制[J].陆军军医大学学报(原第三军医大学学报),2013,35(11):1037-1042. DOI：

　He Bing,Yu Songtao,Lyu Muhan,Wu Yuyun,Hu Changjiang,Yang Shiming.miR-29 functions as an anti-metastatic microRNA in gastric adenocarcinoma by targeting ITGB1[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(11):1037-1042. DOI：

摘要

目的观察miR-29对胃癌细胞体外侵袭力的影响，探讨miR-29通过ITGB1调节胃癌侵袭和转移的具体机制。方法通过基因芯片筛选胃癌与癌旁组织中差异性表达的miRNA；采用生物信息学预测ITGB1调控相关miRNA，通过比对上述2个结果，筛选出miR-29；进一步以miR-29 慢病毒及miR-29 mimics过表达miR-29后，用Western blot检测胃癌细胞中ITGB1的表达变化；采用双荧光素酶实验分析miR-29与ITGB1的作用机制；采用 Transwell侵袭实验及划痕实验检测miR-29 慢病毒感染后细胞体外侵袭能力的变化；qRT-PCR 检测60例胃癌患者癌组织和癌旁组织中 miR-29 的表达差异，并分析 miR-29的表达与肝癌患者临床病理之间的关系。结果基因芯片及生物信息学预测发现miR-29在胃癌组织里高表达，同时又可能调控ITGB1；双荧光素酶实验证实miR-29可以结合在ITGB1 3′UTR， miR-29 慢病毒及miR-29 mimics过表达miR-29都能在蛋白水平下调ITGB1；qRT-PCR 结果显示miR-29家族3条miRNA在胃癌组织中的相对含量均低于癌旁组织[miR-29a：癌旁(32.01±10.38)，癌(14.16±6.25)；miR-29b：癌旁(26.95±5.05)，癌(9.82±1.86)；miR-29c：癌旁(53.56±8.05)，癌(16.79±1.97)，

0.01

]

；进一步统计学分析表明，miR-29a与淋巴结转移有关（

0.05），miR-29b在具有远处转移的病例组织中C/P比值较无远处转移的病例组织明显降低（P0.05）。结论 miR-29可以在转录后水平调控ITGB1的表达，从而抑制胃癌细胞的侵袭和转移。

Abstract

Objective To investigate the underlying molecular mechanisms of miR-29 regulating ITGB1 in the invasion and migration of gastric adenocarcinoma. Methods MicroRNA array was used to screen out miRNAs which were expressed with significant differences in gastric cancer a

nd paracancer tissue. Bioinformatics was employed to predict the miRNAs related to ITGB1 regulation. Gastric cancer cells were infected by lentiviral vectors or transfected with miR-29 mimics to over-express miR-29. Western blotting was used to detect the changes of ITGB1 in gastric cancer cells. Dual luciferase assay was adopted to analyze the mechanism of miR-29 regulating ITGB1. Transwell invasion assay was accomplished to analyze cell invasion ability. The quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to detect the expression differences of miR-29 in 60 pairs of gastric cancer tissue and adjacent noncancerous tissues. The relationship between the expression and clinical pathological data was analyzed. Results MicroRNA array and bioinformatics prediction results supported that miR-29 was in a low expression in gastric carcinoma

and regulated ITGB1. Dual luciferase assay confirmed that miR-29 was bond to the 3′UTR of ITGB1. Western blotting suggestedthat ITGB1 was down-regulated as miR-29 over-expression. The results of qRT-PCR suggested that the relative expression of miR-29 in gastric cancer tissues was lower than in the adjacent noncancerous tissues (miR-29a: 14.16±6.25

32.01±10.38; miR-29b: 9.82±1.86

26.95±5.05; miR-29c: 16.79±1.97 vs 53.56±8.05

0.01). Statistical analysis showed that the expression of miR-29a was closely related with lymph node metastasis (

0.05). The expression ratio of miR-29b in gastric cancer tissues to adjacent noncancerous tissues was significantly lower in the tissue with distant metastasis (

0.05). Conclusion miR-29 regulates ITGB1 expression at post-transcriptional level

and then suppresses the invasion and metastasis of gastric adenocarcinoma.

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