Long noncoding RNA FAM201A involves in radioresistance of non-small-cell lung cancer by enhancing EGFR expression via

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Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
09:45

Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines

Published on: August 21, 2019

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A-M Liu1, Y Zhu, Z-W Huang

  • 1Department of Nuclear Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, China. chenyuebio@126.com.

European Review for Medical and Pharmacological Sciences
|July 13, 2019
PubMed
Abstract

Insights

Long noncoding RNA FAM201A promotes radioresistance in non-small cell lung cancer (NSCLC) by targeting miR-370, upregulating EGFR and HIF-1α. Silencing FAM201A enhances radiosensitivity, suggesting it as a therapeutic target for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Aberrant expression of long noncoding RNAs (lncRNAs) is implicated in non-small cell lung cancer (NSCLC) pathogenesis.
  • Understanding the role of specific lncRNAs, like lnc-FAM201A, is crucial for deciphering NSCLC's molecular regulation.

Purpose of the Study:

  • To investigate the biological interactions of lnc-FAM201A and its downstream targets.
  • To determine the impact of lnc-FAM201A on the radiotherapy response in NSCLC.
  • To explore lnc-FAM201A as a potential therapeutic target for enhancing NSCLC radiosensitivity.

Main Methods:

  • Quantitative Polymerase Chain Reaction (qPCR) and Chi-square tests assessed FAM201A expression and its association with NSCLC characteristics.
  • Univariate and multivariate Cox regression analyses evaluated prognostic factors for overall survival (OS).
  • In vitro and in vivo experiments using cell lines (A549/SK-MES-1) with short hairpin RNA (shRNA) knockdown of FAM201A, alongside apoptosis assays, proliferation assays, and xenograft models, were employed.
  • Bioinformatics, Dual-luciferase reporter assays, qPCR, and Western blotting identified and confirmed downstream targets.

Main Results:

  • FAM201A was significantly upregulated in NSCLC tissues resistant to radiotherapy, correlating with radioresistance and poorer survival.
  • FAM201A knockdown inhibited NSCLC cell proliferation and induced apoptosis under X-ray irradiation, both in vitro and in vivo.
  • FAM201A competitively targeted miR-370, leading to elevated epidermal growth factor receptor (EGFR) and hypoxia-inducible factor 1alpha (HIF-1α) levels, which were repressed upon FAM201A knockdown, enhancing radiosensitivity.

Conclusions:

  • FAM201A interference disrupts its suppression of miR-370, consequently upregulating EGFR and HIF-1α, thereby enhancing NSCLC radiosensitivity.
  • The identified regulatory axis involving FAM201A, miR-370, EGFR, and HIF-1α represents a potential therapeutic target to improve radiotherapy efficacy in NSCLC.

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