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

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

PROVIDER: PRJNA991500 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25146192_1.fastq.gz	Fastqsanger.gz
	SRR25146192_2.fastq.gz	Fastqsanger.gz
	SRR25146193_1.fastq.gz	Fastqsanger.gz
	SRR25146193_2.fastq.gz	Fastqsanger.gz
	SRR25146194_1.fastq.gz	Fastqsanger.gz

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Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma [ChIP-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]

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Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma

Project description:Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma

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

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

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CircIPO7 Promotes Nasopharyngeal Carcinoma Metastasis and Cisplatin Chemoresistance by Regulating YBX1 Nuclear Localization

Project description:The development of therapeutic resistance and metastatic dissemination takes place in 20-30% patients with nasopharyngeal carcinoma (NPC), resulting in poor survival. Hence, a better understanding of the underlying molecular mechanisms will help improve clinical outcome. We have identified a novel circRNA, circIPO7, as a promoter of metastasis and cisplatin chemoresistance in NPC cells. Expression profiling and Genome binding/occupancy profiling by high throughput sequencing were performed to explore the underlying molecular mechanisms.

2022-07-26 | GSE189459 | GEO

Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [RNA-Seq]

Project description:Acquired resistance to chemotherapy is one of the major causes of mortality in advanced nasopharyngeal carcinoma (NPC). However, effective strategies are limited and the underlying molecular mechanisms remain elusive. Using an established NPC cellular model, we demonstrated that the acquisition of chemoresistance was accompanied by massive enhancer remodeling, resulting in aberrant hyperactivation of Notch signaling pathway in NPC. Transcriptomic profiling analysis showed that hyperactivity of Notch signaling pathway was associated with chemoresistance in advanced NPC patients. In addition, overexpression of Notch3-slug axis was correlated with relapses and metastasis of NPC. Importantly, we showed that genetic or pharmacological perturbation of Notch3 could overcome the chemoresistance of NPC in both in vitro and in vivo models. Together, our study indicated that genome-wide enhancer reprogramming activates Notch signaling pathway to confer chemoresistance of NPC, suggesting that targeting Notch3 could provide a potential therapeutic strategy to effectively treat advanced chemoresistant NPC.

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Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma.

Project description:Despite that the docectaxel-cisplatin-5-fluorouracil (TPF) induction chemotherapy has greatly improved patients' survival and became the first-line treatment for advanced nasopharyngeal carcinoma (NPC), not all patients could benefit from this therapy. The mechanism underlying the TPF chemoresistance remains unclear. Here, by analyzing gene-expression microarray data and survival of patients who received TPF chemotherapy, we identify transcription factor ATMIN as a chemoresistance gene in response to TPF chemotherapy in NPC. Mass spectrometry and Co-IP assays reveal that USP10 deubiquitinates and stabilizes ATMIN protein, resulting the high-ATMIN expression in NPC. Knockdown of ATMIN suppresses the cell proliferation and facilitates the docetaxel-sensitivity of NPC cells both in vitro and in vivo, while overexpression of ATMIN exerts the opposite effect. Mechanistically, ChIP-seq combined with RNA-seq analysis suggests that ATMIN is associated with the cell death signaling and identifies ten candidate target genes of ATMIN. We further confirm that ATMIN transcriptionally activates the downstream target gene LCK and stabilizes it to facilitate cell proliferation and docetaxel resistance. Taken together, our findings broaden the insight into the molecular mechanism of chemoresistance in NPC, and the USP10-ATMIN-LCK axis provides potential therapeutic targets for the management of NPC.

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Enhancer remodeling activates Notch signaling to confer chemoresistance in advanced nasopharyngeal carcinoma [ChIP-Seq]

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IGF2BP1-HAX-1 positive feedback loop-mediated HAX-1 overexpression blocks autophagic flux and promotes chemoresistance in nasopharyngeal carcinoma

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.

2023-09-30 | GSE244097 | GEO

microRNA profile of human nasopharyngeal tissues: nasopharyngeal carcinoma tissues vs. normal nasopharyngeal tissues

Project description:MicroRNAs are biomarkers of prognosis and survival for many types of cancer. We evaluated whether microRNAs can predict the survival and efficacy of concurrent chemotherapy in nasopharyngeal carcinoma (NPC) patients. We retrospectively analyzed microRNA expression in 312 paraffin-embedded NPC specimens and 18 normal nasopharyngeal tissues using microarray. We found Forty-one microRNAs are differentially expressed between NPC and normal tissues, and a five-microRNA signature can predict survival independent of stage. NPC patients with the low-risk microRNA signature have a favorable response to concurrent chemotherapy. microRNA profiling of nasopharyngeal carcinoma tissues vs. normal nasopharyngeal tissues 312 paraffin-embedded nasopharyngeal carcinoma tissues and 18 paraffin-embedded normal nasopharyngeal tissues

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