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Updated: Aug 10, 2025

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
07:03

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples

Published on: October 2, 2020

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The Orphan GPR50 Receptor Regulates the Aggressiveness of Breast Cancer Stem-like Cells via Targeting the NF-kB

Polash Kumar Biswas1,2, Sang Rok Park1, Jongyub An1

  • 1Department of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.

International Journal of Molecular Sciences
|February 11, 2023
PubMed

Insights

G protein-coupled receptor 50 (GPR50) is highly expressed in cancer stem-like cells (CSLC), driving their proliferation and migration. Silencing GPR50 inhibits these cancer properties by downregulating NF-κB and Notch signaling pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cancer stem-like cells (CSLC) are crucial drivers of tumor progression and therapeutic resistance.
  • The role of G protein-coupled receptor 50 (GPR50) in CSLC biology remains largely unexplored.

Purpose of the Study:

  • To investigate the expression and function of GPR50 in CSLC.
  • To elucidate the signaling pathways regulated by GPR50 in CSLC.

Main Methods:

  • RT-PCR, UALCAN, GEPIA, and R2 gene analysis for GPR50 expression.
  • shGPR50 gene knockdown to assess functional roles.
  • Western blotting and Luciferase Assay to examine signaling pathways.

Main Results:

  • GPR50 expression is significantly higher in CSLC compared to other cancer cells.
  • GPR50 knockdown reduced CSLC sphere formation, proliferation, migration, and stemness.
  • GPR50 silencing downregulated NF-κB signaling and modulated ADAM-17 activity via the AKT/SP1-NOTCH axis.

Conclusions:

  • GPR50 plays a critical role in CSLC progression and aggressiveness.
  • A novel GPR50-mediated regulation of the NF-κB-Notch signaling pathway in CSLC was identified.
  • Targeting GPR50 and its downstream pathways offers potential therapeutic strategies for CSLC.
Keywords:
ADAM17GPR50NF-kBNotchbreast cancer stem cell (BCSC)

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