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GPR110 promotes progression and metastasis of triple-negative breast cancer

Hye-Jung Nam1, Yeon-Ju Kim1, Jae-Hyeok Kang1

  • 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.

Cell Death Discovery
|May 25, 2022
PubMed

Insights

Triple-negative breast cancer (TNBC) shows high GPR110 expression, driving cancer progression via the RAS pathway. Inhibiting GPR110 offers a potential new therapeutic strategy for TNBC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer is a leading cause of cancer in women, with endocrine therapy widely used.
  • Triple-negative breast cancer (TNBC) lacks targeted treatments and has poor outcomes.
  • Estrogen receptor modulators and aromatase inhibitors are common endocrine therapies.

Purpose of the Study:

  • To investigate the role of GPR110 in triple-negative breast cancer (TNBC) progression.
  • To explore GPR110 as a potential therapeutic target for TNBC.

Main Methods:

  • Analysis of GPR110 expression in TNBC.
  • Investigating the involvement of GPR110 in the RAS signaling pathway.
  • Assessing the impact of GPR110 on epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) phenotypes.

Main Results:

  • GPR110 was found to be highly expressed in TNBC.
  • GPR110 activates the RAS signaling pathway (via Gαs) and promotes TNBC progression.
  • High GPR110 expression correlated with increased EMT and CSC phenotypes.

Conclusions:

  • GPR110 plays a critical role in TNBC progression.
  • Targeting GPR110 represents a promising therapeutic strategy for TNBC patients.

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