4.3 Article

Chemotherapy-mediated miR-29b expression inhibits the invasion and angiogenesis of cervical cancer

期刊

ONCOTARGET
卷 8, 期 9, 页码 14655-14665

出版社

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.14738

关键词

cervical cancer; miR-29b; STAT3; chemotherapy; EMT

资金

  1. National Natural Science Foundation of China [81502329]
  2. Program of Science and Technology of Chongqing Commission [KJ1600228]
  3. National Natural Science Foundation of Yongchuan District [2014nc5004]
  4. Programs of Yongchuan Hospital of Chongqing Medical University [YJYB20120012, YJZQN 201514, YCZQN 201511]

向作者/读者索取更多资源

Radiotherapy combined with platinum-based chemotherapy is the standard-of-care of locally advanced cervical cancer (CC) patients, while nearly 50% of patients do not respond to standard chemotherapy. Thus, identification of relative molecules participated in chemotherapy might provide new insights in the treatment of CC. In this study, we found a cohort of miRNAs were dysregulated upon treatment with cisplatin, among of which miR-29b was the most upregulated one. We further detected its expression in CC tissues, and found that miR-29b was significantly suppressed in CC and its precancerous lesions, HSIL tissues, and was negatively related with tumor invasion. However, upon treatment with cisplatin, the expression of miR-29b was significantly up-regulated. The biological function assays showed that overexpression of miR-29b suppressed the invasion, EMT procedure and angiogenesis of cervical cancer cells in vitro and inhibited tumor growth and neovascularization in vivo through targeting STAT3 signal pathway. While, inhibition of miR-29b could prevent the cisplatin-induced epithelial features, cell movement and angiogenesis of CC cells, which means miR-29b/STAT3 axis participates in the chemotherapy of cisplatin in CC. Collectively, our data suggest that chemotherapy-mediated miR-29b expression participates in the initiation and progression of cervical cancer through suppressing the proliferation, EMT procedure and angiogenesis of cervical cancer cells by targeting STAT3 signal pathway.

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