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LncRNA AGAP2-AS1 Promotes Cancer Cell Proliferation, Migration and Invasion in Colon Cancer by Forming a Negative Feedback Loop with LINC-PINT

Authors Ji L, Chen S, Gu L, Wang J, Zhang X

Received 28 April 2020

Accepted for publication 25 November 2020

Published 2 March 2021 Volume 2021:13 Pages 2153—2161

DOI https://doi.org/10.2147/CMAR.S260371

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly


Liechen Ji,1,* Shuo Chen,1,* Liqiang Gu,1 Juan Wang,2 Xipeng Zhang1

1Department of Colorectal Surgery, Tianjin Union Medical Center, Nankai University, Tianjin, 300121, People’s Republic of China; 2Department of General Surgery, Tianjin Union Medical Center, Nankai University, Tianjin, 300121, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Xipeng Zhang
Department of Colorectal Surgery, Tianjin Union Medical Center, Nankai University, No. 190 Jieyuan Road, Hongqiao District, Tianjin, 300121, People’s Republic of China
Tel +862287729595
Email [email protected]

Introduction: It has been reported that lncRNA AGAP2-AS1 promotes the development of gastric cancer, lung cancer and breast cancer. This study aimed to investigate the role of AGAP2-AS1 in colon cancer.
Methods: A total of 66 patients with colon cancer were enrolled. RT-qPCR was performed to detect the differential expression of AGAP2-AS1 in tumor tissues and adjacent normal tissues. To test the interaction between AGAP2-AS1 and LINC-PINT in colon cancer, overexpression vector or inhibitor of AGAP2-AS1 and LINC-PINT were transfected into RKO and HCT 116 cells. CCK-8 assay was used to detect cell proliferation. Transwell assays were performed to evaluate cell migration and invasion. The expression of p-LATS1, p-YAP and nuclear YAP were detected by Western blot and immunofluorescence.
Results: The expression of AGAP2-AS1 was upregulated in colon cancer tissues compared with that in adjacent normal tissues, and the expression of AGAP2-AS1 in colon cancer tissues was not significantly affected by tumor stages. In addition, we found that the expression of LINC-PINT was downregulated in colon cancer tissues compared with that in adjacent normal tissues and had a reverse correlation with the expression of AGAP2-AS1 in colon cancer tissues. Moreover, overexpression of AGAP2-AS1 downregulated the expression of LINC-PINT, and overexpression of LINC-PINT also altered the expression of AGAP2-AS1 in colon cancer cells. Inhibition of AGAP2-AS1 upregulated the expression of LINC-PINT, and inhibition of LINC-PINT promoted the expression levels of AGAP2-AS1 in colon cancer cells. Furthermore, overexpression of AGAP2-AS1 could increase the proliferation, invasion and migration of colon cancer cells, while overexpression of LINC-PINT could attenuate the effects of overexpression of AGAP2-AS1 on the proliferation, migration and invasion of colon cancer cells. We also found that AGAP2-AS1 promoted colon cancer cell proliferation, migration and invasion through the Hippo signaling.
Conclusion: Upregulated expression of AGAP2-AS1 promoted proliferation, invasion and migration in colon cancer by forming a negative feedback loop with LINC-PINT.

Keywords: colon cancer, lncRNA AGAP2-AS1, lncRNA LINC-PINT, proliferation, migration, invasion

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