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ERK1/2 activity contributes to gemcitabine resistance in pancreatic cancer cells

Chunning Zheng1, Xuelong Jiao, Yingsheng Jiang

  • 1Department of General Surgery, Jinan Central Hospital of Shandong University, Jinan, China.

The Journal of International Medical Research
|April 10, 2013
PubMed
Abstract

Insights

Chemoresistance in pancreatic cancer involves overactive extracellular signal-regulated protein kinase (ERK) 1/2. Inhibiting ERK 1/2 with U0126 alongside gemcitabine enhances treatment efficacy and reduces tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Pancreatic cancer exhibits significant chemoresistance.
  • Extracellular signal-regulated protein kinase (ERK) 1/2 signaling is implicated in cancer cell survival.

Purpose of the Study:

  • To investigate if extracellular signal-regulated protein kinase (ERK) 1/2 overactivity mediates chemoresistance in pancreatic cancer.
  • To evaluate the therapeutic potential of combining gemcitabine with an ERK 1/2 inhibitor.

Main Methods:

  • Human pancreatic cancer cell lines and a gemcitabine-resistant subline were treated with gemcitabine and the ERK 1/2 inhibitor U0126.
  • Western blotting assessed phosphorylated ERK 1/2 (pERK1/2) levels.
  • Cell proliferation, apoptosis, and xenograft tumor growth were quantified.

Main Results:

  • Gemcitabine increased pERK1/2 levels in sensitive cell lines; resistant cells showed constitutive high pERK1/2.
  • U0126 reversed gemcitabine-induced proliferation and apoptosis resistance.
  • Combination therapy inhibited tumor growth and promoted apoptosis in vivo.

Conclusions:

  • ERK 1/2 activity appears to protect pancreatic cancer cells from gemcitabine-induced apoptosis.
  • Combining an ERK 1/2 inhibitor with gemcitabine may offer synergistic therapeutic benefits in pancreatic cancer.
Keywords:
ChemoresistanceERK1/2extracellular signal-regulated protein kinasegemcitabinepancreatic cancer

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