Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA214976 | ENA |
REPOSITORIES: ENA
Similar Datasets
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. High-throughput RNA sequencing analysis was performed in the human nasopharyngeal carcinoma cell line S18 after transfection with control siRNA or circIPO7 siRNA.
2022-07-26 | GSE189458 | GEO
Project description:Methylome study in Nasopharyngeal Carcinoma (NPC)
| PRJNA263873 | ENA
Project description:Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied in the treatment of NPC. However, molecular change and functions of DDP chemo-resistance in nasopharyngeal carcinoma are still poorly understood.
2019-08-01 | GSE135083 | GEO
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.
2024-02-14 | GSE236503 | GEO
Project description:<p>Metabolic reprogramming under therapeutic stress may represent a targetable vulnerability for cancer treatment. Elucidation of the metabolic alterations linked to chemotherapy in nasopharyngeal carcinoma (NPC) could uncover potential therapeutic strategies. Using proteomics and transcriptomic profiles, we identified wild-type IDH1 as a crucial metabolic enzyme upregulated in gemcitabine plus cisplatin chemotherapy (GP)-resistant NPC. IDH1 reprogrammed nucleotide metabolism in response to chemotherapy, linking DNA damage repair (DDR) to ferroptosis resistance via DHODH, thereby contributing to chemoresistance in NPC. Mechanistically, α-ketoglutarate (α-KG), a metabolite of IDH1, enhanced chromatin accessibility to promote DHODH transcription via α-KG-dependent dioxygenase ALKBH5-recruited HNRNPC. The DHODH inhibitor BAY2402234 markedly sensitized NPC cells to chemotherapy. Clinically, a prognostic model based on DDR and ferroptosis signatures effectively predicted disease relapse risk post-chemotherapy in NPC. This study links DDR to ferroptosis defense via the IDH1/α-KG/ALKBH5/DHODH axis, suggesting DHODH inhibition as a promising therapeutic strategy to overcome chemoresistance in tumors harboring wild-type IDH1. </p>
2026-01-14 | MTBLS11531 | MetaboLights
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. circIPO7 was found to bind to YBX1. Genome binding/occupancy profiling by high throughput sequencing were performed to explore the underlying molecular mechanisms.
2022-07-26 | GSE189457 | GEO
Project description:Gene expression data of human nasopharyngeal carcinoma (NPC)
| PRJNA548225 | ENA
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.
2024-02-14 | GSE236504 | GEO
Project description:Heterozygous p53-R280T mutations frequently occur in many nasopharyngeal carcinoma cell lines and nasopharyngeal carcinoma patients. However, the role of this mutation in the progression of nasopharyngeal carcinoma remains unclear. In this study, we successfully generated the tp53 knockout nasopharyngeal carcinoma (NPC) cells by CRISPR/Cas9-mediated genome editing and found that knockout of heterozygous tp53-R280T inhibited the proliferation of NPC cells significantly in vivo and in vitro. Mechanistic analyses indicated that heterozygous p53-R280T can activate the PI3K/Akt Signaling pathway in NPC cells. In conclusion, our findings provide a mechanistic insight into the role of heterozygous p53-R280T in NPC progression.
2019-07-21 | GSE130398 | GEO