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Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma

ABSTRACT: Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma

PROVIDER: PRJNA991494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25145130_1.fastq.gz	Fastqsanger.gz
	SRR25145130_2.fastq.gz	Fastqsanger.gz
	SRR25145131_1.fastq.gz	Fastqsanger.gz
	SRR25145131_2.fastq.gz	Fastqsanger.gz
	SRR25146192_1.fastq.gz	Fastqsanger.gz

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Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma [RNA-seq]

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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Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma [RNA-seq]

Project description:Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma [RNA-seq]

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Project description:Autophagic flux is associated with chemoresistance, the leading cause of chemotherapeutic failure. Here, we showed that HAX-1 promotes chemoresistance by effectively blocking the fusion of autophagosomes with lysosomes. Mass spectrometric and functional studies demonstrated that HAX-1 recruited NEDD4 to promote Rab7a degradation and inhibited the binding of Rab7a with SNAREs by competitively binding to it. Furthermore, HAX-1 could bind to IGF2BP1 mRNA, thereby contributing to its stability and translation. Moreover, IGF2BP1 enhanced HAX-1 m6A methylation, thereby enhancing its stability. Via in vivo and in vitro experiments, we confirmed the positive role of the IGF2BP1-HAX-1 feedback loop in chemoresistance. Our data provide evidence that HAX-1, IGF2BP1, and SQSTM1 levels are useful predictors of clinical outcome and chemoresistance risk. In addition, our data provide new insights into the clinical applications of therapies related to autophagic flux and its associated molecular network in targeting cisplatin chemoresistance in nasopharyngeal carcinoma.

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