Abstract:
:Several microRNAs (miRNA) have been implicated in H. pylori related gastric cancer (GC). However, the molecular mechanism of miRNAs in gastric cancer has not been fully understood. In this study, we reported that miR-101 is significantly down-regulated in H. pylori positive tissues and cells and in tumor tissues with important functional consequences. Ectopic expression of miR-101 dramatically suppressed cell proliferation and colony formation by inducing G1-phase cell-cycle arrest. We found that miR-101 strongly reduced the expression of SOCS2 oncogene in GC cells. Similar to the restoring miR-26 expression, SOCS2 down-regulation inhibited cell growth and cell-cycle progression, whereas SOCS2 over-expression rescued the suppressive effect of miR-101. Mechanistic investigations revealed that miR-101 suppressed the expression of c-myc, CDK2, CDK4, CDK6, CCND2, CCND3, and CCNE2, while promoted tumor suppressor p14, p16, p21 and p27 expression. In clinical specimens, SOCS2 was over-expressed in tumors and H. pylori positive tissues and its mRNA levels were inversely correlated with miR-101 expression. Taken together, our results indicated that miR-101 functions as a growth-suppressive miRNA in H. pylori related GC, and that its suppressive effects are mediated mainly by repressing SOCS2 expression.
journal_name
Cancer Biol Therjournal_title
Cancer biology & therapyauthors
Zhou X,Xia Y,Li L,Zhang Gdoi
10.4161/15384047.2014.987523subject
Has Abstractpub_date
2015-01-01 00:00:00pages
160-9issue
1eissn
1538-4047issn
1555-8576journal_volume
16pub_type
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journal_title:Cancer biology & therapy
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pub_type: 评论,杂志文章
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更新日期:2004-09-01 00:00:00
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journal_title:Cancer biology & therapy
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journal_title:Cancer biology & therapy
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更新日期:2006-09-01 00:00:00