ATMIN function in p53-deficient GBM
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE76296 | GEO | 2015/12/23
SECONDARY ACCESSION(S): PRJNA306838
REPOSITORIES: GEO
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Project description:Despite the docectaxel-cisplatin-5-fluorouracil (TPF) induction chemotherapy has greatly improved the patients' survival and became the standard of care for advanced nasopharyngeal carcinoma (NPC), some patients could not benefit from this therapy. The mechanism underlying the TPF chemoresistance remains unclear. Here, we identified ATMIN as a chemoresistance gene in response to TPF therapy in NPC patients. We found that USP10 deubiquitinates and stabilizes ATMIN protein. Knockdown of ATMIN inhibits the cell proliferation and facilitates the docetaxel-sensitivity of NPC cells in vitro and in vivo. Mechanistically, RNA-seq combined with ChIP-seq analysis suggests that ATMIN is associated with the cell death signaling. ATMIN transcriptionally activates LCK to facilitate cell proliferation and docetaxel-resistance. Our findings broaden the insight into the mechanism of chemoresistance in NPC and the USP10-ATMIN-LCK axis provides potential therapeutic targets for the management of NPC.
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