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Mitochondrial ribosomal protein S23 (MRPS23) drives breast cancer (BC) progression and metastasis. Reducing MRPS23 levels inhibits BC cell proliferation, migration, and invasion, suggesting it as a potential therapeutic target.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Mitochondrial ribosomal protein S23 (MRPS23) is a nuclear-encoded protein involved in mitochondrial translation.
  • MRPS23 is recognized as a proliferation driver in various cancers, but its role in breast cancer (BC) is understudied.
  • Aberrant MRPS23 expression is linked to malignant phenotypes in cancer cells.

Purpose of the Study:

  • To investigate the expression and functional role of MRPS23 in breast cancer (BC).
  • To determine the impact of MRPS23 on BC cell proliferation, viability, migration, and invasion.
  • To explore MRPS23 as a potential therapeutic target for BC.

Main Methods:

  • MRPS23 expression analysis in BC cells versus non-tumoral breast cells.
  • Overexpression and knockdown of MRPS23 in BC cell lines.
  • Validation of transfection efficiency using Western blot and qRT-PCR.
  • In vitro assays to assess the effects of MRPS23 modulation on malignant behaviors.

Main Results:

  • MRPS23 was found to be aberrantly overexpressed at both transcript and protein levels in BC cells.
  • MRPS23 deficiency led to decreased cell proliferation, viability, migration, and invasion in BC cells.
  • Knockdown of MRPS23 reduced the expression of key metastasis-associated genes (cadherin, SNAI 1, TWIST 1) and proliferation markers (Cyclin D1, Axin 2, LEF1, NKD1, Survivin).

Conclusions:

  • MRPS23 plays a significant role in promoting breast cancer progression and metastasis.
  • MRPS23 knockdown inhibits BC cell migration and invasion, thereby suppressing tumor progression.
  • MRPS23 is identified as a key determinant of BC metastasis and a potential therapeutic target for BC treatment.