Open Access

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

  • Authors:
    • Gaoming Wang
    • Xiaokun Li
    • Yu Yao
    • Zhisheng Jiang
    • Hai Zhou
    • Kai Xie
    • Jing Luo
    • Yi Shen
  • View Affiliations

  • Published online on: February 17, 2021     https://doi.org/10.3892/ol.2021.12558
  • Article Number: 297
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.
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April-2021
Volume 21 Issue 4

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Copy and paste a formatted citation
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Spandidos Publications style
Wang G, Li X, Yao Y, Jiang Z, Zhou H, Xie K, Luo J and Shen Y: FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma. Oncol Lett 21: 297, 2021
APA
Wang, G., Li, X., Yao, Y., Jiang, Z., Zhou, H., Xie, K. ... Shen, Y. (2021). FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma. Oncology Letters, 21, 297. https://doi.org/10.3892/ol.2021.12558
MLA
Wang, G., Li, X., Yao, Y., Jiang, Z., Zhou, H., Xie, K., Luo, J., Shen, Y."FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma". Oncology Letters 21.4 (2021): 297.
Chicago
Wang, G., Li, X., Yao, Y., Jiang, Z., Zhou, H., Xie, K., Luo, J., Shen, Y."FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma". Oncology Letters 21, no. 4 (2021): 297. https://doi.org/10.3892/ol.2021.12558