Knockdown of Long Noncoding RNA 01124 Inhibits the Malignant Behaviors of Colon Cancer Cells via miR-654-5p/HAX-1

Yu-Jin Wu; Zhi-Quan Cai; Run-Ming He; Xue-Chuan Wang; Long-Ling Cong; Fang-Hua Qiu

doi:10.1155/2022/1092107

Knockdown of Long Noncoding RNA 01124 Inhibits the Malignant Behaviors of Colon Cancer Cells via miR-654-5p/HAX-1

Evid Based Complement Alternat Med. 2022 Sep 20:2022:1092107. doi: 10.1155/2022/1092107. eCollection 2022.

Authors

Yu-Jin Wu¹, Zhi-Quan Cai¹, Run-Ming He¹, Xue-Chuan Wang¹, Long-Ling Cong¹, Fang-Hua Qiu²

Affiliations

¹ Departments of Gastroenterology, The Affiliated TCM Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510130, China.
² Department of Hospital Office, The Affiliated TCM Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510130, China.

Abstract

Background: Previous studies have shown that long noncoding RNAs (lncRNAs) play a key role in cancer, including colon cancer (CC). However, the exact role of long noncoding RNA 01124 (LINC01124) in CC and its mechanisms of action remain unknown. In this study, we investigated the functional effects and the possible mechanism of LINC01124 in CC.

Methods: We first determined the expression of LINC01124 in CC tissues (The Cancer Genome Atlas (TCGA) database) and cell lines (quantitative real-time polymerase chain reaction (qRT-PCR)). Functional analysis via Cell Counting Kit-8 (CCK-8), colony formation, cell cycle, wound healing and Transwell assays were performed, and a mechanistic experiment was performed with the western blotting. The function of LINC01124 was also determined in vivo using nude BALB/c mice.

Results: The results showed that LINC01124 was upregulated in CC tissues and cell lines. Functional studies showed that knockdown of LINC01124 significantly suppressed the proliferation, migration, and invasion of colon cancer cells in vitro and in vivo. Subsequent mechanistic experiments indicated that LINC01124 acted as a sponge to suppress microRNA 654-5p, which targeted HAX-1. Downregulation of LINC01124 decreased the expression of HAX-1, and overexpression of the miR-654-5p inhibitor attenuated the sh-LINC01124-induced inhibition of CC cell proliferation, migration, and invasion.

Conclusion: Collectively, this study revealed that the knockdown of LINC01124 inhibited the malignant behaviors of CC via the miR-654-5p/HAX-1 axis, suggesting that LINC01124 might be a therapeutic target for CC treatment.