microRNA‐92b‐3p augments colon cancer development through inhibiting KLF3

Author:

Liu Xuezhong1ORCID,Zhang Lei2

Affiliation:

1. Department of Gastrointestinal Surgery Liaocheng People's Hospital Liaocheng Shandong China

2. Department of General Surgery Liaocheng Dongchangfu People's Hospital Liaocheng Shandong China

Abstract

AbstractColon cancer (CC) is a tumor of the large intestine. miR‐92b‐3p is often deregulated in the tumorigensis. Here, the role of miR‐92b‐3p in the development of CC was investigated. miR‐92b‐3p and Kruppel‐like factor 3 (KLF3) expression was examined in CC tissues and cells. miR‐92b‐3p inhibitor or KLF3 overexpression vector was transfected into CC cells, respectively to observe its role in CC cell proliferation, invasion, migration, and apoptosis. The targeting relationship between miR‐92b‐3p and KLF3 was validated. Meanwhile, rescue experiments were performed by co‐transfection of miR‐92b‐3p inhibitor and KLF3 siRNA, followed by determining CC cell proliferation, invasion, migration, and apoptosis. Higher miR‐92b‐3p and lower KLF3 expression levels were observed in CC tissues and cells. miR‐92b‐3p inhibition or KLF3 overexpression reduced proliferation, invasion, and migration whereas induced apoptosis of CC cells. KLF3 was validated to be the target gene of miR‐92b‐3p. Depletion of KLF3 could reverse the antitumor role of miR‐92b‐3p inhibition in CC cells. miR‐92b‐3p augments CC development through inhibiting KLF3, which may confers a novel way to develop future treatment target.

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

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