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FGFR4 Links Glucose Metabolism and Chemotherapy Resistance in Breast Cancer

Min Xu1,2, Shuzheng Chen3, Weibin Yang1,2

  • 1Key Laboratory of Imaging Diagnosis and Minimally Invasive Intervention Research, Lishui, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|May 16, 2018
PubMed
Abstract

Insights

Fibroblast growth factor receptor 4 (FGFR4) promotes chemoresistance and altered glucose metabolism in breast cancer. Targeting FGFR4 may improve treatment outcomes for chemoresistant tumors.

Area of Science:

  • Oncology
  • Cancer Metabolism
  • Molecular Biology

Background:

  • Chemotherapy resistance is a major cause of cancer relapse and metastasis.
  • Reprogrammed glucose metabolism is a hallmark of cancer, promoting survival and chemoresistance.
  • The role of glucose metabolism in therapy response remains unclear.

Purpose of the Study:

  • To investigate the role of glucose metabolism in doxorubicin resistance in breast cancer.
  • To identify key regulators of chemoresistance and altered glucose metabolism.
  • To explore the therapeutic potential of targeting identified pathways.

Main Methods:

  • Assessed glycolytic phenotype (glucose uptake, lactate release, ECAR) in resistant vs. parental cells.
  • Utilized gene expression microarray and short hairpin RNA (shRNA) for gene knockdown.
  • Investigated signaling pathways (FGFR4, FRS2, MAPK/ERK) using Western blotting and pharmacological inhibitors.

Main Results:

  • Doxorubicin-resistant cells exhibited increased glycolytic flux.
  • Fibroblast growth factor receptor 4 (FGFR4) was identified as a key modulator of resistance and glycolysis.
  • FGFR4 knockdown enhanced chemosensitivity and reduced glycolysis; FGFR4 inhibition blocked chemoresistance.

Conclusions:

  • Elevated FGFR4 expression drives increased glucose metabolism and chemoresistance in breast cancer.
  • Targeting the FGFR4-FRS2-ERK pathway presents a therapeutic strategy for chemoresistant breast cancer.
Keywords:
Breast cancerChemoresistanceFgf receptor 4Glycolytic flux

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