FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma

Gaoming Wang; Xiaokun Li; Yu Yao; Zhisheng Jiang; Hai Zhou; Kai Xie; Jing Luo; Yi Shen

doi:10.3892/ol.2021.12558

FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma

Oncol Lett. 2021 Apr;21(4):297. doi: 10.3892/ol.2021.12558. Epub 2021 Feb 17.

Authors

Gaoming Wang^{1

2}, Xiaokun Li³, Yu Yao⁴, Zhisheng Jiang⁵, Hai Zhou¹, Kai Xie¹, Jing Luo¹, Yi Shen¹

Affiliations

¹ Department of Cardiothoracic Surgery, Jinling Hospital, School of Medicine, Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
² Department of Thoracic Surgery, Xuzhou Central Hospital, Xuzhou, Jiangsu 221000, P.R. China.
³ Department of Cardiothoracic Surgery, Jinling Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 210000, P.R. China.
⁴ Department of Respiratory Medicine, Nanjing Second Hospital, Nanjing, Jiangsu 210000, P.R. China.
⁵ Department of Cardiothoracic Surgery, Jinling Hospital, Bengbu Medical College, Nanjing, Jiangsu 210000, P.R. China.

Abstract

Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD.

Keywords: FAM83A; FAM83A-AS1; lung adenocarcinoma; miR-495-3p.

Grants and funding

The study was funded by The National Natural Science Foundation for Youth of China (grant no. 81902354), The Science and Technology Program of Xu Zhou (grant no. KC18037), The Xuzhou Clinical Technology Key Research Project (grant no. 2019GG021) and The Excellent Talents Fund Project of Xuzhou Medical University (grant no. XYFY2020017).