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Circ_0006174 Accelerates Colorectal Cancer Progression Through Regulating miR-138-5p/MACC1 Axis

Authors Wei J, Lin Y, Wang Z, Liu Y, Guo W

Received 4 December 2020

Accepted for publication 21 January 2021

Published 18 February 2021 Volume 2021:13 Pages 1673—1686

DOI https://doi.org/10.2147/CMAR.S295833

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Chien-Feng Li


Jianjun Wei,* Yuzhe Lin,* Zhiqiang Wang, Yeguang Liu, Wei Guo

Minimally Invasive Surgery, Linhe People’s Hospital of Bayannur City, Bayannur, Inner Mongolia, 015000, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Zhiqiang Wang Tel +86-04788253451
Email zqwang470018979@163.com

Background: Circular RNAs (circRNAs) were reported to be involved in the progression of a variety of cancers, including colorectal cancer (CRC). However, the precise functions and mechanism of circRNAs in CRC have not been elucidated. This study aimed to investigate the effect and mechanism underlying circ_0006174 in CRC.
Methods: The expression of circ_0006174, microRNA (miR-138-5p) and metastasis associated in colon cancer 1 (MACC1) mRNA was detected by quantitative real-time polymerase chain reaction (RT-qPCR) assay. Western blot was employed to measure MACC1 protein expression. The effects of circ_0006174 knockdown, MACC1 overexpression or miR-138-5p inhibition on cell proliferation, migration, invasion, and apoptosis were assessed by cell counting kit 8 (CCK-8) assay, clone formation assay, transwell assay and flow cytometry assay, respectively. The interaction between miR-138-5p and circ_0006174 or MACC1 was confirmed by RNA pull down assay or dual-luciferase reporter assay. Xenograft tumor model in nude mice was used to verify the function of circ_0006174 in vivo.
Results: Circ_0006174 and MACC1 expression was highly expressed, while miR-138-5p expression was downregulated in CRC cells and tissues. Meanwhile, circ_0006174 functioned as a sponge of miR-138-5p to upregulate MACC1 expression. Furthermore, circ_0006174 knock down-mediated suppression on cell proliferation, migration and invasion, and promotion on cell apoptosis could be alleviated by MACC1 overexpression or miR-138-5p inhibition in CRC cells. Besides, circ_0006174 knockdown also inhibited CRC procession in vivo.
Conclusion: Circ_0006174 advanced CRC progression via sponging miR-138-5p to upregulate MACC1 expression, which may provide a promising molecular target for CRC treatment.

Keywords: colorectal cancer, circ_0006174, miR-138-5p, MACC1

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