ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2019
[Long non-coding RNA XIST modulates cisplatin resistance by altering PDCD4 and Fas-Lexpressions in human nasopharyngeal carcinoma HNE1 cells
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Role of long non-coding RNA in chemoradiotherapy resistance of nasopharyngeal carcinoma.Frontiers in oncology · 2024Review
- Potential roles of lncRNA-XIST/miRNAs/mRNAs in human cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Biological Function of Long Non-coding RNA (LncRNA) Xist.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the role of long non-coding RNA (lncRNA) X inactive specific transcript (XIST) in modulating cisplatin (DDP) resistance of human nasopharyngeal carcinoma cells and investigate the possible mechanism.
methodsRealtime PCR was performed to detect the expression of XIST in cisplatin-resistant human nasopharyngeal carcinoma cell line HNE1/DDP. The effects of up-regulation and down-regulation of XIST on DDP resistance, proliferation and apoptosis of HNE1/ DDP cells were assessed using MTT assay, EdU assay and flow cytometry. Western blotting was used to detect the changes in the expressions of programmed cell death 4 (PDCD4) and Fas ligand (Fas-L) proteins in the cells in response to up-regulation or down-regulation of XIST.
resultsThe expression of XIST was significantly up-regulated in HNE1/DDP cells in comparison with HNE1 cells (0.57±0.06
conclusionsXIST is up-regulated in HNE1/DDP cells, and down-regulation and up-regulation of XIST expression reduce and increase DDP resistance of the cells, respectively, possibly as a result of changes in the expressions of PDCD4 and Fas-L.
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Registered trials
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