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Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
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Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

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The implication from RAS/RAF/ERK signaling pathway increased activation in epirubicin treated triple negative breast

Jianbo Huang1, Qingqing Luo1, Yun Xiao2

  • 1Department of Endocrine & Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Oncotarget
|January 4, 2018
PubMed
Abstract

Insights

Chemotherapy may activate the ERK pathway in triple negative breast cancer (TNBC), potentially driving resistance. Targeting this pathway could offer new treatment options for refractory TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple negative breast cancer (TNBC) typically lacks sensitivity to ERK pathway inhibitors.
  • Chemotherapy may induce kinase cascade activation in TNBC, altering treatment response.

Purpose of the Study:

  • To investigate the potential of ERK pathway targeting therapy as an adjuvant treatment for TNBC.
  • To determine if chemotherapy activates the ERK pathway in TNBC.

Main Methods:

  • Gene set enrichment analysis (GSEA) of online datasets (GSE43816, GSE54326) from epirubicin-treated TNBC samples and cells.
  • Analysis of ERK pathway components and regulatory gene expression changes.

Main Results:

  • Enrichment of ERK pathway components (e.g., MAPK13, MAP3K1) observed in epirubicin-treated TNBC.
  • Increased expression of positive and decreased expression of negative ERK pathway regulators in resistant cells.
  • Elevated phosphorylated ERK levels in MDA-MB-231 cells post-epirubicin treatment.

Conclusions:

  • The ERK signaling pathway is activated by epirubicin treatment in TNBC, potentially contributing to drug resistance.
  • Targeting the ERK pathway presents a novel therapeutic strategy for refractory and relapsed TNBC.
Keywords:
GSEARAS/RAF/ERK signaling pathwayTNBCepirubicintargeting therapy

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