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Interference with ATF5 function enhances the sensitivity of human pancreatic cancer cells to paclitaxel-induced

Ming Hu1, Bin Wang, Dongmeng Qian

  • 1Department of Neural and Behavioral Sciences, Penn State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA.

Anticancer Research
|October 13, 2012
PubMed
Abstract

Insights

Activating transcription factor 5 (ATF5) is highly expressed in pancreatic cancer. Targeting ATF5 enhances paclitaxel-induced apoptosis, suggesting ATF5 is a potential therapeutic target for pancreatic cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Activating transcription factor 5 (ATF5) is expressed in glioblastoma and breast cancer.
  • Loss of ATF5 function induces apoptosis in tested cancer cell lines.
  • ATF5's role in pancreatic cancer remained uninvestigated.

Purpose of the Study:

  • To investigate ATF5 expression and function in pancreatic cancer.
  • To determine if ATF5 can be a therapeutic target in pancreatic cancer.

Main Methods:

  • Gene expression analysis using quantitative real-time/reverse transcription-polymerase chain reaction (QRT/RT-PCR), western blotting (WB), and immunohistochemistry (IHC).
  • Promoter reporter assays were performed.
  • Cell viability and apoptosis monitored via MTT and fluorescence-activated cell sorting (FACS) assays.

Main Results:

  • ATF5 is highly expressed in pancreatic cancer cells compared to non-tumor tissues.
  • Paclitaxel treatment and ATF5 inhibition induced apoptosis in SW1990 pancreatic cancer cells.
  • Interference with ATF5 function altered BCL-2 and BAX expression, enhancing paclitaxel-induced apoptosis.

Conclusions:

  • ATF5 is significantly overexpressed in pancreatic cancer.
  • Targeting ATF5 amplifies paclitaxel-induced apoptosis in pancreatic cancer cells.
  • ATF5 represents a promising therapeutic target for pancreatic cancer treatment.

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