Cutting edge: NANOG activates autophagy under hypoxic stress by binding to BNIP3L promoter

Meriem Hasmim, Bassam Janji, Mehdi Khaled, Muhammad Zaeem Noman, Fawzia Louache, Didier Bordereaux, Abdou Abderamane, Veronique Baud, Fathia Mami-Chouaib, Salem Chouaib*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

34 Citations (Scopus)


Hypoxia upregulates the core pluripotency factors NANOG, SOX2, and OCT4, associated with tumor aggressiveness and resistance to conventional anticancer treatments. We have previously reported that hypoxia-induced NANOG contributed in vitro to tumor cell resistance to autologous-specific CTL and in vivo to the in situ recruitment of immune-suppressive cells. In this study, we investigated the mechanisms underlying NANOG-mediated tumor cell resistance to specific lysis under hypoxia. We demonstrated the tumor-promoting effect of hypoxia on tumor initiation into immunodeficient mice using human non-small lung carcinoma cells. We next showed a link between NANOG and autophagy activation under hypoxia because inhibition of NANOG decreased autophagy in tumor cells. Chromatin immunoprecipitation and luciferase reporter assays revealed a direct binding of NANOG to a transcriptionally active site in a BNIP3L enhancer sequence. These data establish a new link between the pluripotency factor NANOG and autophagy involved in resistance to CTL under hypoxia.

Original languageEnglish
Pages (from-to)1423-1428
Number of pages6
JournalJournal of Immunology
Issue number4
Publication statusPublished - 15 Feb 2017


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