miR-574-5p mediates epithelial-mesenchymal transition in small cell lung cancer by targeting vimentin via a competitive endogenous RNA network

Yanqin Sun; Yanmei Yi; Siyuan Gan; Ruifang Ye; Cailing Huang; Man Li; Jian Huang; Ying Guo

doi:10.3892/ol.2021.12720

miR-574-5p mediates epithelial-mesenchymal transition in small cell lung cancer by targeting vimentin via a competitive endogenous RNA network

Oncol Lett. 2021 Jun;21(6):459. doi: 10.3892/ol.2021.12720. Epub 2021 Apr 8.

Authors

Yanqin Sun^{1

2}, Yanmei Yi³, Siyuan Gan^{1

2}, Ruifang Ye^{1

2}, Cailing Huang^{1

2}, Man Li⁴, Jian Huang^{1

2}, Ying Guo⁵

Affiliations

¹ Department of Pathology, Guangdong Medical University, Dongguan, Guangdong 523808, P.R. China.
² Center of Pathology Diagnosis and Research, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524023, P.R. China.
³ Department of Histology and Embryology, Guangdong Medical University, Zhanjiang, Guangdong 524023, P.R. China.
⁴ Department of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
⁵ Department of Organ Transplantation, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.

Abstract

Numerous studies have suggested that non-coding RNAs mediate tumorigenesis via the epithelial-mesenchymal transition (EMT). However, whether the long non-coding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP) plays a role in the EMT of small cell lung cancer (SCLC) remains unclear. The results of the present study suggest that HOTTIP-knockdown may lead to a significant increase in E-cadherin expression and a decrease in vimentin (VIM) expression; these proteins are two key markers of EMT. Furthermore, a notable morphological change in SCLC cells with HOTTIP-knockdown was observed: After upregulation of microRNA (miR)-574-5p, the cells exhibited a long, fusiform morphology. Investigating these phenomena further revealed that HOTTIP may participate in EMT by binding to miR-574-5p. In addition, using bioinformatics technology and a dual luciferase reporter assay, it was found that miR-574-5p inhibited VIM expression via direct binding and interaction. In summary, the present results indicate that HOTTIP may be involved in the EMT of SCLC by binding to miR-574-5p, and that miR-574-5p may act through VIM, which is a key marker of EMT.

Keywords: HOTTIP; epithelial-mesenchymal transition; miR-574-5p; small cell lung cancer; vimentin.

Grants and funding

The present study was partly supported by the National Natural Science Foundation of China (grant no. 81702285), Funds for the Construction of Basic Medical Disciplines in Guangdong Medical University (grant no. 4SG19047G), Innovation experiment project of Guangdong Medical University in 2020 (grant no. ZZDS007) and Key projects of Guangdong Medical University (grant no. GDMUZ201808).