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ATAD3A mediates activation of RAS-independent mitochondrial ERK1/2 signaling, favoring head and neck cancer development.

Liwei LangReid LovelessJuan DouTiffany LamAlex ChenFang WangLi SunJakeline JuarezZhaohui Steve QinNabil F SabaChloe ShayYong Teng
Published in: Journal of experimental & clinical cancer research : CR (2022)
These findings highlight the novel function of ATAD3A in regulating mitochondrial ERK1/2 activation that favors HNSCC development. Combined targeting of ATAD3A and RAS signaling may potentiate anticancer activity for HNSCC therapeutics.
Keyphrases
  • signaling pathway
  • oxidative stress
  • cell proliferation
  • pi k akt
  • wild type
  • small molecule