<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cao W</submitter><funding>the Cooperative research promotion plan of basic medicine and clinical medicine of Anhui Medical University</funding><pagination>6567-6578</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8975274</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(3)</volume><pubmed_abstract>This study explored the function and mechanisms of HOX transcript antisense RNA (HOTAIR) in the drug resistance of nasopharyngeal carcinoma (NPC). Quantitative PCR, Western blotting, MTT assay, flow cytometry, Transwell assay, and luciferase assay were performed. HOTAIR expression levels were upregulated in cisplatin (DDP)-resistant NPC tissues and cells. Knockdown of HOTAIR in DDP-resistant NPC cells increased cell sensitivity of DDP, as well as decreased cell viability, expression of chemoresistance-related proteins, migration and invasion, increased cell apoptosis. In addition, downregulation of microRNA 106a-5p (miR-106a-5p) expression and upregulation of SRY-box transcription factor 4 (SOX4) expression were observed in DDP-resistant NPC tissues and cells. MiR-106a-5p targets HOTAIR an</pubmed_abstract><journal>Bioengineered</journal><pubmed_title>HOTAIR mediates cisplatin resistance in nasopharyngeal carcinoma by regulating miR-106a-5p/SOX4 axis.</pubmed_title><pmcid>PMC8975274</pmcid><funding_grant_id>2020XKjT036</funding_grant_id><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Cao W</pubmed_authors><pubmed_authors>Ji J</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>HOTAIR mediates cisplatin resistance in nasopharyngeal carcinoma by regulating miR-106a-5p/SOX4 axis.</name><description>This study explored the function and mechanisms of HOX transcript antisense RNA (HOTAIR) in the drug resistance of nasopharyngeal carcinoma (NPC). Quantitative PCR, Western blotting, MTT assay, flow cytometry, Transwell assay, and luciferase assay were performed. HOTAIR expression levels were upregulated in cisplatin (DDP)-resistant NPC tissues and cells. Knockdown of HOTAIR in DDP-resistant NPC cells increased cell sensitivity of DDP, as well as decreased cell viability, expression of chemoresistance-related proteins, migration and invasion, increased cell apoptosis. In addition, downregulation of microRNA 106a-5p (miR-106a-5p) expression and upregulation of SRY-box transcription factor 4 (SOX4) expression were observed in DDP-resistant NPC tissues and cells. MiR-106a-5p targets HOTAIR an</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-19T07:47:43.099Z</modification><creation>2025-04-19T07:47:43.099Z</creation></dates><accession>S-EPMC8975274</accession><cross_references><pubmed>35227173</pubmed><doi>10.1080/21655979.2022.2038429</doi></cross_references></HashMap>