TGFβ1 induces apoptosis in invasive prostate cancer and bladder cancer cells via Akt-independent, p38 MAPK and JNK/SAPK-mediated activation of caspases

Ahmad Al-Azayzih, Fei Gao, Anna Goc, Payaningal R. Somanath

Research output: Contribution to journalArticlepeer-review

45 Citations (Scopus)

Abstract

Recent findings indicate that advanced stage cancers shun the tumor suppressive actions of TGFβ and inexplicably utilize the cytokine as a tumor promoter. We investigated the effect of TGFβ1 on the survival and proliferation of invasive prostate (PC3) and bladder (T24) cancer cells. Our study indicated that TGFβ1 decreased cell viability and induced apoptosis in invasive human PC3 and T24 cells via activation of p38 MAPK-JNK-Caspase9/8/3 pathway. Surprisingly, no change in the phosphorylation of pro-survival Akt kinase was observed. We postulate that TGFβ1 pathway may be utilized for specifically targeting urological cancers without inflicting side effects on normal tissues.

Original languageEnglish
Pages (from-to)165-170
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume427
Issue number1
DOIs
Publication statusPublished - Oct 12 2012
Externally publishedYes

Keywords

  • Akt
  • Apoptosis
  • JNK
  • P38 MAPK
  • Prostate cancer
  • TGFβ

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint

Dive into the research topics of 'TGFβ1 induces apoptosis in invasive prostate cancer and bladder cancer cells via Akt-independent, p38 MAPK and JNK/SAPK-mediated activation of caspases'. Together they form a unique fingerprint.

Cite this