STAT3 induces colorectal carcinoma progression through a novel miR-572-MOAP-1 pathway

OncoTargets and Therapy. 2018;Volume 11:3475-3484

 

Journal Homepage

Journal Title: OncoTargets and Therapy

ISSN: 1178-6930 (Online)

Publisher: Dove Medical Press

LCC Subject Category: Medicine: Internal medicine: Neoplasms. Tumors. Oncology. Including cancer and carcinogens

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS

Wang N
He X
Zhou R
Jia G
Qiao Q

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 16 weeks

 

Abstract | Full Text

Nan Wang,1 Xianli He,1 Ru Zhou,2 Guozhan Jia,1 Qing Qiao1 1Department of General Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, Shanxi, 710038, China; 2Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi’an, Shanxi, 710032, China Purpose: Colorectal carcinoma (CRC) is among the most common causes of death. Recent studies have shown that both STAT3 and miR-572 contribute to CRC progression. STAT3 plays an important role in miRNA expression. Moreover, MOAP-1, which is a pro-apoptotic protein that induces cell death or apoptosis, has a direct correlation with miRNA. Therefore, the current study is designed to explore whether miR-572 and STAT3 are involved in a common pathway and the role of MOAP-1 in this process. Patients and methods: The expressions of STAT3, miR-572, and MOAP-1 in human CRC tissues and multiple cell lines were estimated by qRT-PCR or Western blot. MTT, transwell migration, and invasion assays were used to assess cell growth, migration, and invasion, respectively. Dual-luciferase reporter assay was applied to examine the association between miR-572 and MOAP-1. Results: Elevated STAT3 levels were accompanied by increased miR-572 and decreased MOAP-1 levels in primary CRC specimens and cell lines. STAT3 promoted CRC cell growth, migration, and invasion via the upregulated expression of miR-572. Subsequently, miR-572 inhibited MOAP-1 protein expression through an interaction with its 3'UTR. Conclusion: Our study proposes a novel STAT3-miR-572-MOAP-1 pathway involved in the process of CRC progression, which might be a potential target for the development of new preventive and therapeutic approaches against human colorectal cancer. Keywords: colorectal neoplasm, STAT3, MOAP-1, miR-572, tumor progression