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Long Intergenic Non-Coding RNA LINC00885 Promotes Tumorigenesis of Cervical Cancer by Upregulating MACC1 Expression Through Serving as a Competitive Endogenous RNA for microRNA-432-5p

Authors Chen H, Chi Y, Chen M, Zhao L

Received 12 November 2020

Accepted for publication 13 January 2021

Published 12 February 2021 Volume 2021:13 Pages 1435—1447


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly

Hongwei Chen,1 Yugang Chi,2 Mengyue Chen,1 Limei Zhao1

1Department of Gynaecology, The First People’s Hospital of Chongqing Liangjiang New Area, Chongqing, 401120, People’s Republic of China; 2Department of Gynaecology and Obstetrics, Chongqing Health Center for Women and Children, Chongqing, 400021, People’s Republic of China

Correspondence: Limei Zhao
Department of Gynaecology, The First People’s Hospital of Chongqing Liangjiang New Area, 199 Renxing Road, Chongqing, People’s Republic of China

Purpose: Long intergenic non-protein coding RNA 885 (LINC00885) has been well studied in breast cancer; however, its contribution in cervical cancer remains unclear. In this study, we aimed to determine the detailed functions of LINC00885 in cervical cancer and elucidate the underlying molecular regulation mechanism.
Methods: The expression status of LINC00885 in cervical cancer was determined using reverse transcription-quantitative polymerase chain reaction and by searching The Cancer Genome Atlas database. The detailed functions of LINC00885 in cervical cancer cells were confirmed using Cell Counting Kit 8 assay, flow cytometry analysis, Transwell cell migration and invasion assays, and tumor xenograft assay. Mechanistic experiments included bioinformatics prediction, RNA immunoprecipitation, luciferase reporter assay, and rescue experiments.
Results: LINC00885 was clearly overexpressed in cervical cancer, which was linked with unfavorable clinical outcomes. Functionally, LINC00885 deficiency suppressed cervical cancer cell proliferation, migration, and invasion but stimulated cell apoptosis in vitro. Furthermore, loss of LINC00885 restricted the growth of cervical cancer cells in vivo. Mechanistically, LINC00885 functioned as a competitive endogenous RNA for microRNA-432-5p (miR-432-5p) in cervical cancer. Furthermore, metastasis-associated colon cancer 1 (MACC1) was confirmed as the direct target of miR-432-5p, and LINC00885 could enhance MACC1 expression by sequestering miR-432-5p. Rescue experiments revealed that silencing of miR-432-5p or upregulation of MACC1 expression could effectively counteract the restrained aggressive properties of cervical cancer cells induced by LINC00885 deficiency.
Conclusion: LINC00885 upregulated MACC1 expression in cervical cancer cells by sponging miR-432-5p, thereby promoting cancer progression. The LINC00885/miR-432-5p/MACC1 pathway may help in the identification of potential prognostic biomarkers and therapeutic targets in cervical cancer.

Keywords: non-coding RNA, competitive endogenous RNA, LINC00885, microRNA-432-5p, cervical cancer, MACC1

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