Oncotarget

Research Papers:

MicroRNA-22 suppresses the growth, migration and invasion of colorectal cancer cells through a Sp1 negative feedback loop

Shu-Sen Xia, Guang-Jun Zhang, Zuo-Liang Liu, Hong-Peng Tian, Yi He, Chang-Yuan Meng, Li-Fa Li, Zi-Wei Wang _ and Tong Zhou

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Oncotarget. 2017; 8:36266-36278. https://doi.org/10.18632/oncotarget.16742

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Abstract

Shu-Sen Xia1,*, Guang-Jun Zhang2,3,*, Zuo-Liang Liu2,3, Hong-Peng Tian2,3, Yi He2,3, Chang-Yuan Meng4, Li-Fa Li5, Zi-Wei Wang1, Tong Zhou2,3

1The Department of Gastrointestinal Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China

2The Department of Gastrointestinal Surgery, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China

3Institute of Hepatobiliary, Pancreatic and Intestinal Disease, North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China

4The Department of Pathology, North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China

5The Department of Medical Microbiology and Parasitology, North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China

*These authors contributed equally to this work

Correspondence to:

Zi-Wei Wang, email: wangziwei571@sina.com

Tong Zhou, email: zhoutong0088@163.com

Keywords: colorectal cancer, miR-22, Sp1, PTEN, AKT

Received: October 15, 2016     Accepted: March 21, 2017     Published: March 31, 2017

ABSTRACT

MicroRNAs have recently emerged as regulators of many biological processes including cell proliferation, development and differentiation. This study identified that miR-22 was statistically decreased in colorectal cancer clinical specimens and highly metastatic cell lines. Moreover, low miR-22 expression was associated with tumor metastasis, advanced clinical stage and relapse. Consistent with clinical observations, miR-22 significantly suppressed the ability of colorectal cancer cells to growth and metastasize in vitro and in vivo. Sp1 was validated as a target of miR-22, and ectopic expression of Sp1 compromised the inhibitory effects of miR-22. In addition, Sp1 repressed miR-22 transcription by binding to the miR-22 promoter, hence forming a negative feedback loop. Further study has shown that miR-22 suppresses the activity of PTEN/AKT pathway by Sp1. Our present results implicate the newly indentified miR-22/Sp1/PTEN/AKT axis might represent a potential therapeutic target for colorectal cancer.


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