Research Papers:

Hsa-miR-875-5p exerts tumor suppressor function through down-regulation of EGFR in colorectal carcinoma (CRC)

Tiening Zhang, Xun Cai _, Qi Li, Peng Xue, Zhixiao Chen, Xiao Dong and Ying Xue

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Oncotarget. 2016; 7:42225-42240. https://doi.org/10.18632/oncotarget.9944

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Tiening Zhang1,*, Xun Cai1,*, Qi Li1, Peng Xue1, Zhixiao Chen1, Xiao Dong1, Ying Xue1

1Oncology Center, Shanghai General Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai 200080, P. R. China

*These authors contributed equally to this work

Correspondence to:

Xun Cai, email: xuncaisjtu@sina.com

Keywords: hsa-miRNA-875-5p (miR-875-5p), EGFR, colorectal carcinoma (CRC), proliferation, apoptosis

Received: March 21, 2016     Accepted: April 09, 2016     Published: June 10, 2016


Hsa-miRNA-875-5p (miR-875-5p) has recently been discovered to have anticancer efficacy in different organs. However, the role of miR-875-5p on colorectal carcinoma (CRC) is still ambiguous. In this study, we investigated the role of miR-875-5p on the development of CRC. The results indicated that miR-875-5p was significantly down-regulated in primary tumor tissues and very low levels were found in CRC cell lines. Ectopic expression of miR-875-5p in CRC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-875-5p induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-875-5p inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene EGFR was revealed to be a putative target of miR-875-5p, which was inversely correlated with miR-875-5p expression in CRC. Taken together, our results demonstrated that miR-875-5p played a pivotal role on CRC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic EGFR.

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