miR-556-3p/Disabled Homolog 2-Interacting Protein (dab2ip) Promotes Cancer Progression by Down-Regulating Bcl-2-Like Protein 11 (BIM) Expression in Colorectal Cancer

Author:

Liu Jiaqi1,Huang Jingping2,Cheng Xueyuan1,Liao Zuowei1,Gao Xueyuan1

Affiliation:

1. Department of General Surgery, Beihai People’s Hospital, Beihai City, Guangxi Zhuang Autonomous Region, 536000, China

2. Department of Nutrition, Beihai People’s Hospital, Beihai City, Guangxi Zhuang Autonomous Region, 536000, China

Abstract

Colorectal cancer (CRC) is a major threat affecting human health. Studies have shown that miR-556-3p can regulate dab2ip and promote tumor deterioration, and up-regulation of BIM inhibits CRC cell progression. However, the interaction between miR-556-3p/dab2ip and BIM in CRC is unknown. We examined miR-556-3p expression in CRC tissues and cells by RT-qPCR. The impact of miR-556-3p/dab2ip and BIM on CRC cell behaviors were assessed by western blot, transwell and MTT assay. miR-556-3p was highly expressed in CRC and its overexpression increased CRC cell proliferation and migration as well as up-regulated dab2ip and Ki-67 expression. Besides, miR-556-3p could target the BIM and overexpressed miR-556-3p decreased BIM expression. However, silencing of BIM abrogated the impact of overexpressed miR-556-3p on CRC cell proliferation and migration. In conclusion, miR-556-3p/dab2ip promotes cell growth by down-regulating the expression of BIM, thereby promoting the progression of CRC.

Publisher

American Scientific Publishers

Subject

Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology

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