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Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
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The Long Non-Coding RNA SAMMSON Is a Regulator of Chemosensitivity and Metabolic Orientation in MCF-7

Charlotte Orre1, Xavier Dieu1,2, Jordan Guillon3

  • 1Mitolab Team, Inserm U1083, CNRS 6015, Mito Vasc Institute, SFR ICAT, Angers University, F-49000 Angers, France.

Biology
|November 27, 2021
PubMed

Insights

Long non-coding RNA SAMMSON promotes breast cancer chemoresistance by altering cell metabolism. Silencing SAMMSON in resistant cells restored sensitivity and improved oxidative metabolism, suggesting SAMMSON as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Breast cancer treatment faces challenges with tumor relapse and chemoresistance.
  • Cancer cells exhibit metabolic plasticity, aiding adaptation to therapy and microenvironment.
  • Long non-coding RNAs (lncRNAs) are emerging as key regulators of cellular metabolism.

Purpose of the Study:

  • To investigate the role of the lncRNA SAMMSON in metabolic reprogramming.
  • To determine SAMMSON's impact on doxorubicin resistance in breast cancer cells (MCF-7dox).
  • To explore SAMMSON as a potential therapeutic target for overcoming chemoresistance.

Main Methods:

  • Overexpression analysis of SAMMSON in doxorubicin-resistant MCF-7dox cells compared to sensitive MCF-7 cells.
  • Silencing of SAMMSON using small interfering RNA (siRNA) in MCF-7dox cells.
  • Assessment of metabolic changes, including oxidative metabolism and mitochondrial function.
  • Evaluation of chemoresistance levels after SAMMSON manipulation.

Main Results:

  • SAMMSON was significantly overexpressed in doxorubicin-resistant MCF-7dox cells.
  • siRNA-mediated silencing of SAMMSON led to metabolic rewiring in MCF-7dox cells.
  • Key metabolic improvements included enhanced oxidative metabolism, reduced mitochondrial reactive oxygen species (ROS), and increased mitochondrial replication, transcription, and translation.
  • Attenuation of doxorubicin resistance was observed following SAMMSON silencing.

Conclusions:

  • SAMMSON plays a critical role in the metabolic adaptations that drive chemoresistance in breast cancer.
  • Targeting SAMMSON expression offers a promising strategy to overcome doxorubicin resistance.
  • Modulating SAMMSON could be a novel therapeutic approach for breast cancer patients experiencing treatment failure.
Keywords:
SAMMSONbreast cancercomplex Ilong non-coding RNAmetabolismmitochondriareactive oxygen species

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