Emerging from the shade of p53 mutants: N-terminally truncated variants of the p53 family in EMT signaling and cancer progression.

Sci Signal. 2014 Sep 30;7(345):re9.

Engelmann D, Pützer BM.

The prevailing view has been that N-terminally truncated p53 family isoforms (ΔNp53, ΔNp63, and DNp73) predominantly counteract cell cycle arrest and apoptosis. Recent progress in the field extend these well-known functions and place these isoforms in the center of a comprehensive regulatory network controlling major epithelial-to-mesenchymal transition (EMT)-relevant signaling pathways [such as transforming growth factor-β (TGF-β), wingless-int (WNT), insulin-like growth factor (IGF), and signal transducer and activator of transcription (STAT)], microRNAs, and EMT-associated transcription factors that promote invasion, loss of tumor cell polarity, and metastatic behavior in conjunction with a chemoresistant phenotype.

Pubmed

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Obituary: Axel Rethwilm (1959-2014).

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E2F1 induces miR-224/452 expression to drive EMT through TXNIP downregulation.

Emerging from the shade of p53 mutants: N-terminally truncated variants of the p53 family in EMT signaling and cancer progression.

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