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WITHDRAWN: Oncogenic lncRNA MALAT-1 recruits E2F1 to upregulate RAD51 expression and thus promotes cell autophagy and

Rui Xin1, Boqi Hu2, Danhua Qu3

  • 1Jilin University, Changchun, 130000, PR China; Department of Radiology, The Second Hospital of Jilin University, Changchun, 130000, PR China.

Pulmonary Pharmacology & Therapeutics
|January 23, 2023
PubMed
Abstract

Insights

Silencing long non-coding RNA MALAT-1 enhances non-small-cell lung cancer (NSCLC) cell chemosensitivity by promoting autophagy. This suggests MALAT-1 silencing is a potential strategy to overcome chemoresistance in NSCLC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNA MALAT-1 (lncRNA MALAT-1) plays a role in non-small-cell lung cancer (NSCLC) cell activity.
  • The precise mechanisms by which lncRNA MALAT-1 influences NSCLC chemosensitivity, particularly through autophagy, require further elucidation.

Purpose of the Study:

  • To investigate the impact of lncRNA MALAT-1 on the chemosensitivity of NSCLC cells.
  • To explore the regulatory role of lncRNA MALAT-1 in autophagy and its connection to chemoresistance.

Main Methods:

  • Validated lncRNA MALAT-1 expression in NSCLC cell lines and assessed chemosensitivity to doxorubicin (DOX).
  • Utilized LncMAP database, ChIP, RIP, and luciferase assays to examine the interaction between lncRNA MALAT-1, RAD51, and E2F1.
  • Employed immunofluorescence staining to evaluate autophagosome formation and conducted in vitro/in vivo experiments with ectopic expression and knockdown of lncRNA MALAT-1.

Main Results:

  • lncRNA MALAT-1 was overexpressed in NSCLC cells, promoting autophagy and reducing chemosensitivity.
  • lncRNA MALAT-1 facilitates the transcriptional expression of RAD51 by recruiting E2F1 to its promoter.
  • Silencing lncRNA MALAT-1 enhanced NSCLC chemosensitivity and inhibited tumor growth in vivo, with RAD51 knockdown negating the effect.

Conclusions:

  • Silencing lncRNA MALAT-1 enhances NSCLC chemosensitivity through the promotion of autophagy.
  • This study identifies lncRNA MALAT-1 as a potential therapeutic target to improve chemoresistance in NSCLC treatment.
Keywords:
AutophagyChemosensitivityE2F1Long noncoding RNA MALAT-1Non-small-cell lung cancerRAD51

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