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Gene expression profiles of nasopharyngeal carcinoma cell line HNE2 following TP53 overexpression

ABSTRACT: Recent studies have revealed that long non-coding RNAs (lncRNAs) participate in all steps of cancer initiation and progression by regulating protein coding genes at the epigenetic, transcriptional and post-transcriptional levels. LncRNAs are in turn regulated by other genes, forming a complex regulatory network. The regulation networks between the p53 tumor suppressor and lncRNAs in nasopharyngeal carcinoma (NPC) remain unclear. The aim of this study was to investigate the regulatory roles of the TP53 gene in regulating lncRNA and mRNA expression profiles in NPC cell line HNE2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE60379 | GEO | 2015/05/14

SECONDARY ACCESSION(S): PRJNA258153

REPOSITORIES: GEO

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Gene expression profiles of nasopharyngeal carcinoma cell line HNE2 following TP53 overexpression

Project description:Recent studies have revealed that long non-coding RNAs (lncRNAs) participate in all steps of cancer initiation and progression by regulating protein coding genes at the epigenetic, transcriptional and post-transcriptional levels. LncRNAs are in turn regulated by other genes, forming a complex regulatory network. The regulation networks between the p53 tumor suppressor and lncRNAs in nasopharyngeal carcinoma (NPC) remain unclear. The aim of this study was to investigate the regulatory roles of the TP53 gene in regulating lncRNA and mRNA expression profiles in NPC cell line HNE2. p53 induced gene expression in human nasopharyngeal carcinoma cell line HNE2 was measured at 0, 12, 24 and 48 hours after transfected by pCMV-p53 plasmid.

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LINC01770 mediates nasopharyngeal cancer radiation resistance and renders tumor cell vulnerable to ferroptosis [RNA-seq]

Project description:Long noncoding RNAs (lncRNAs) participate in regulation of various essential biological processes including cell proliferation, differentiation, apoptosis, migration, and invasion. However, the clinical significances of lncRNAs and their functions and mechanisms in nasopharyngeal carcinoma (NPC) involved in malignant progression need to be further investigated. We find that the LINC01770-TEAD1 signal axis leads to radiotherapy resistance of NPC and causes NPC cells to be in a fragile oxidative stress equilibrium. Meanwhile radioresistant cells are more sensitive to ferroptosis inducers. LINC01770 stabilizes TEAD1 by competitive binding with microRNA 615-5p and microRNA -1293. Radiation resistant cell is in a delicate balance of lipid peroxidation and more vulnerable to ferroptosis. In conclusion, our research suggest that LINC01770 serves as an independent prognostic factor in NPC. During the malignant progression of NPC caused by high expression of LINC01770, ferroptosis can be induced to effectively kill cancer cells and reverse RT resistance of NPC cells, providing evidence for the clinical application of ferroptosis in the treatment of recurrent and refractory NPC.

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