TAp73 transcriptionally represses BNIP3 expression

Varvara Petrova, Mara Mancini, Massimiliano Agostini, Richard A. Knight, Margherita Annicchiarico-Petruzzelli, Nikolai A. Barlev, Gerry Melino, Ivano Amelio

Research output: Contribution to journalArticlepeer-review


TAp73 is a tumor suppressor transcriptional factor, belonging to p53 family. Alteration of TAp73 in tumors might lead to reduced DNA damage response, cell cycle arrest and apoptosis. Carcinogen-induced TAp73−/− tumors display also increased angiogenesis, associated to hyperactivition of hypoxia inducible factor signaling. Here, we show that TAp73 suppresses BNIP3 expression, directly binding its gene promoter. BNIP3 is a hypoxia responsive protein, involved in a variety of cellular processes, such as autophagy, mitophagy, apoptosis and necrotic-like cell death. Therefore, through different cellular process altered expression of BNIP3 may differently contribute to cancer development and progression. We found a significant upregulation of BNIP3 in human lung cancer datasets, and we identified a direct association between BNIP3 expression and survival rate of lung cancer patients. Our data therefore provide a novel transcriptional target of TAp73, associated to its antagonistic role on HIF signaling in cancer, which might play a role in tumor suppression.

Original languageEnglish
Pages (from-to)2484-2493
Number of pages10
JournalCell Cycle
Issue number15
Publication statusPublished - Jan 1 2015


  • Autophagy
  • HIF
  • Lung cancer
  • P53
  • P73

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Developmental Biology


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