Autonomous inhibition of apoptosis correlates with responsiveness of colon carcinoma cell lines to ciglitazone

David M. Baron, Ulrike Kaindl, Verena J. Haudek-Prinz, Editha Bayer, Clemens Röhrl, Christopher Gerner, Brigitte Marian

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Colorectal cancer is a leading cause of mortality worldwide. Resistance to therapy is common and often results in patients succumbing to the disease. The mechanisms of resistance are poorly understood. Cells basically have two possibilities to survive a treatment with potentially apoptosis-inducing substances. They can make use of their existing proteins to counteract the induced reactions or quickly upregulate protective factors to evade the apoptotic signal. To identify protein patterns involved in resistance to apoptosis, we studied two colorectal adenocarcinoma cell lines with different growth responses to low-molar concentrations of the thiazolidinedione Ciglitazone: HT29 cells underwent apoptosis, whereas SW480 cells increased cell number. Fluorescence detection and autoradiography scans of 2D-PAGE gels were performed in both cell lines to assess protein synthesis and turnover, respectively. To verify the data we performed shotgun analysis using the same treatment procedure as in 2D-experiments. Biological functions of the identified proteins were mainly associated with apoptosis regulation, chaperoning, intrinsic inflammation, and DNA repair. The present study suggests that different growth response of two colorectal carcinoma cell lines after treatment with Ciglitazone results from cell-specific protein synthesis and differences in protein regulation.

Original languageEnglish
Article numbere114158
Pages (from-to)e114158
JournalPLoS ONE
Issue number12
Publication statusPublished - 11 Dec 2014
Externally publishedYes


  • Adenocarcinoma/pathology
  • Antineoplastic Agents/pharmacology
  • Apoptosis/drug effects
  • Cell Cycle/drug effects
  • Cell Line, Tumor
  • Cell Survival/drug effects
  • Colorectal Neoplasms/pathology
  • Humans
  • PPAR gamma/agonists
  • Protein Biosynthesis/drug effects
  • Thiazolidinediones/pharmacology


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