Tumor suppressor WWOX and p53 alterations and drug resistance in glioblastomas

Ming Fu Chiang, Pei Yi Chou, Wan Jen Wang, Chun I. Sze, Nan Shan Chang

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Tumor suppressor p53 are frequently mutated in glioblastomas (GBMs) and appears to contribute, in part, to resistance to temozolomide (TMZ) and therapeutic drugs. WW domain-containing oxidoreductase WWOX (FOR or WOX1) is a proapoptotic protein and is considered as a tumor suppressor. Loss of WWOX gene expression is frequently seen in malignant cancer cells due to promoter hypermethylation, genetic alterations, and translational blockade. Intriguingly, ectopic expression of wild type WWOX preferentially induces apoptosis in human glioblastoma cells harboring mutant p53. WWOX is known to physically bind and stabilize wild type p53. Here, we provide an overview for the updated knowledge in p53 and WWOX, and postulate potential scenarios that wild type and mutant p53, or isoforms, modulate the apoptotic function of WWOX. We propose that triggering WWOX activation by therapeutic drugs under p53 functional deficiency is needed to overcome TMZ resistance and induce GBM cell death.

Original languageEnglish
Article numberArticle 00043
JournalFrontiers in Oncology
Volume3 MAR
DOIs
Publication statusPublished - 2013

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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