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Long noncoding RNA lnc-LOC645166 promotes adriamycin resistance via NF-κB/GATA3 axis in breast cancer

Ruinian Zheng1, Jun Jia1, Ling Guan2

  • 1Department of Oncology, Affiliated Dongguan People's Hospital, Southern Medical University, Dongguan 523000, Guangdong Province, P.R. China.

Aging
|May 29, 2020
PubMed

Insights

This study reveals that the long noncoding RNA LOC645166 promotes adriamycin chemoresistance in breast cancer. Lowering LOC645166 levels enhances treatment effectiveness by targeting GATA3 expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Adriamycin (ADR) resistance is a major challenge in breast cancer treatment.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their role in cancer progression and drug resistance.

Purpose of the Study:

  • To investigate the role of lncRNA LOC645166 in adriamycin chemoresistance in breast cancer.
  • To elucidate the molecular mechanism by which LOC645166 influences chemoresistance.

Main Methods:

  • Microarray analysis to identify differentially expressed lncRNAs.
  • Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blotting, and immunohistochemistry to validate LOC645166 expression.
  • In vitro and in vivo experiments to assess the effect of LOC645166 modulation on adriamycin sensitivity.
  • Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) assays to determine molecular interactions.

Main Results:

  • lncRNA LOC645166 was found to be upregulated in adriamycin-resistant breast cancer cells and patient tissues.
  • Downregulation of LOC645166 sensitized breast cancer cells to adriamycin, while its upregulation conferred tolerance.
  • LOC645166 was shown to bind with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), increasing GATA binding protein 3 (GATA3) expression.
  • This pathway led to the activation of STAT3, ultimately promoting chemoresistance.

Conclusions:

  • lncRNA LOC645166 plays a critical role in mediating adriamycin chemoresistance in breast cancer.
  • The mechanism involves the regulation of GATA3 expression via NF-κB, leading to STAT3 activation.
  • Targeting lncRNA LOC645166 may represent a potential therapeutic strategy to overcome adriamycin resistance in breast cancer.
Keywords:
GATA3NF-κBbreast cancerchemoresistancelncRNA-LOC645166

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