<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen L</submitter><funding>Natural Science Foundation of Hebei Province</funding><funding>Natural Science Foundation of Hebei Province,China</funding><funding>National Natural Science Foundation of China</funding><pagination>20186</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9684558</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(1)</volume><pubmed_abstract>Kinectin 1 antisense RNA 1 (KTN1-AS1), a long non-coding RNA (lncRNA), has been proved to have tumor-promoting properties and its expression is enhanced in several human tumors. However, the role of KTN1-AS1 in the pathogenesis of esophageal squamous cell carcinoma (ESCC) remains unknown. This study aimed to investigate the expression status, functional roles, and molecular mechanisms of KTN1-AS1 in the development of ESCC. Considerable upregulation of KTN1-AS1 was confirmed in esophageal cancer cells and ESCC tissues and its expression was associated with TNM stage, pathological differentiation, and lymph node metastasis. SOX2 directly activated transcription of KTN1-AS1, and overexpression of KTN1-AS1 facilitated ESCC cells proliferation and invasion in vitro and in vivo. Furthermore, KTN1-AS1 could bind to retinoblastoma binding protein 4 (RBBP4) in the nucleus and enhanced its binding with histone deacetylase 1 (HDAC1), thereby activating the epithelial-mesenchymal transition (EMT) process through downregulating E-cadherin expression at the epigenetic level. In conclusion, KTN1-AS1, induced by SOX2, acts as a tumor-promoting gene and may serve as a potential therapeutic and prognostic biomarker for ESCC.</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>KTN1-AS1, a SOX2-mediated lncRNA, activates epithelial-mesenchymal transition process in esophageal squamous cell carcinoma.</pubmed_title><pmcid>PMC9684558</pmcid><funding_grant_id>81772612</funding_grant_id><funding_grant_id>H2020206368</funding_grant_id><funding_grant_id>H2021206259</funding_grant_id><funding_grant_id>H2020206363</funding_grant_id><pubmed_authors>Yan Z</pubmed_authors><pubmed_authors>Guo Y</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Lu J</pubmed_authors><pubmed_authors>Dong Z</pubmed_authors><pubmed_authors>Guo W</pubmed_authors><pubmed_authors>Xu T</pubmed_authors></additional><is_claimable>false</is_claimable><name>KTN1-AS1, a SOX2-mediated lncRNA, activates epithelial-mesenchymal transition process in esophageal squamous cell carcinoma.</name><description>Kinectin 1 antisense RNA 1 (KTN1-AS1), a long non-coding RNA (lncRNA), has been proved to have tumor-promoting properties and its expression is enhanced in several human tumors. However, the role of KTN1-AS1 in the pathogenesis of esophageal squamous cell carcinoma (ESCC) remains unknown. This study aimed to investigate the expression status, functional roles, and molecular mechanisms of KTN1-AS1 in the development of ESCC. Considerable upregulation of KTN1-AS1 was confirmed in esophageal cancer cells and ESCC tissues and its expression was associated with TNM stage, pathological differentiation, and lymph node metastasis. SOX2 directly activated transcription of KTN1-AS1, and overexpression of KTN1-AS1 facilitated ESCC cells proliferation and invasion in vitro and in vivo. Furthermore, KTN1-AS1 could bind to retinoblastoma binding protein 4 (RBBP4) in the nucleus and enhanced its binding with histone deacetylase 1 (HDAC1), thereby activating the epithelial-mesenchymal transition (EMT) process through downregulating E-cadherin expression at the epigenetic level. In conclusion, KTN1-AS1, induced by SOX2, acts as a tumor-promoting gene and may serve as a potential therapeutic and prognostic biomarker for ESCC.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2026-06-20T03:18:08.058Z</modification><creation>2025-04-07T10:14:56.648Z</creation></dates><accession>S-EPMC9684558</accession><cross_references><pubmed>36418920</pubmed><doi>10.1038/s41598-022-24743-z</doi></cross_references></HashMap>