PMID- 35218517 OWN - NLM STAT- MEDLINE DCOM- 20220708 LR - 20220714 IS - 1559-0305 (Electronic) IS - 1073-6085 (Linking) VI - 64 IP - 8 DP - 2022 Aug TI - LncRNA NCK1-AS1 Promotes Malignant Cellular Phenotypes of Laryngeal Squamous Cell Carcinoma via miR-137/NCK1 Axis. PG - 888-901 LID - 10.1007/s12033-022-00469-1 [doi] AB - Increasing evidence demonstrates that many long noncoding RNAs (lncRNAs) are implicated with the development of laryngeal squamous cell carcinoma (LSCC). As shown by bioinformatics analysis, lncRNA non-catalytic region of tyrosine kinase adaptor protein 1-antisense 1 (NCK1-AS1) is upregulated in tissues of head and neck squamous cell carcinoma. The study aimed to explore the role and mechanism of NCK1-AS1 in LSCC. NCK1-AS1 expression in LSCC cells was evaluated by reverse transcription qPCR. The viability, proliferation, invasion, migration, and apoptosis of LSCC cells with indicated transfection were evaluated by CCK-8 assays, Ethynyl deoxyuridine incorporation assays, Transwell assays, wound healing assays, and TUNEL assays, respectively. Subcellular fractionation assays were performed to evaluate the cellular distribution of NCK1-AS1 and NCK1. NCK1 protein level in LSCC cells with indicated transfection was quantified by western blotting. The binding relation between miR-137 and NCK1-AS1 (or NCK1) were determined using RNA immunoprecipitation assays and luciferase reporter assays. NCK1-AS1 was highly expressed in LSCC cell lines. NCK1-AS1 depletion suppressed LSCC cell viability, proliferation, invasion, and migration while enhancing cell apoptosis. NCK1, an adjacent gene of NCK1-AS1, is also highly expressed in LSCC cells and was positively regulated by NCK1-AS1. Moreover, NCK1-AS1 interact with miR-137 to upregulate NCK1 expression. NCK1 was the downstream target of miR-137 and was negatively correlated to miR-137. In addition, overexpressed NCK1 reversed the suppressive impact of NCK1-AS1 depletion on malignant behaviors of LSCC cells. NCK1-AS1 contributes to LSCC cellular behaviors by upregulating NCK1 via interaction with miR-137. CI - (c) 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. FAU - Wan, Lanlan AU - Wan L AD - Department of Otolaryngology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 6, Beijing West Road, Huaian, 223300, Jiangsu, China. FAU - Gu, Dongsheng AU - Gu D AD - Department of Otolaryngology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 6, Beijing West Road, Huaian, 223300, Jiangsu, China. FAU - Jin, Xin AU - Jin X AUID- ORCID: 0000-0003-0800-6434 AD - Department of Otolaryngology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 6, Beijing West Road, Huaian, 223300, Jiangsu, China. jinxin6996@hotmail.com. LA - eng PT - Journal Article DEP - 20220226 PL - Switzerland TA - Mol Biotechnol JT - Molecular biotechnology JID - 9423533 RN - 0 (MIRN137 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (RNA, Long Noncoding) SB - IM EIN - Mol Biotechnol. 2022 Mar 22;:. PMID: 35316472 MH - Cell Line, Tumor MH - Cell Proliferation MH - Gene Expression Regulation, Neoplastic MH - *Head and Neck Neoplasms/genetics MH - Humans MH - *MicroRNAs/genetics/metabolism MH - Phenotype MH - *RNA, Long Noncoding/genetics/metabolism MH - Squamous Cell Carcinoma of Head and Neck/genetics OTO - NOTNLM OT - Laryngeal squamous cell carcinoma OT - NCK1 OT - NCK1-AS1 OT - ceRNA OT - miR-137 EDAT- 2022/02/27 06:00 MHDA- 2022/07/09 06:00 CRDT- 2022/02/26 12:07 PHST- 2021/11/17 00:00 [received] PHST- 2022/02/12 00:00 [accepted] PHST- 2022/02/27 06:00 [pubmed] PHST- 2022/07/09 06:00 [medline] PHST- 2022/02/26 12:07 [entrez] AID - 10.1007/s12033-022-00469-1 [pii] AID - 10.1007/s12033-022-00469-1 [doi] PST - ppublish SO - Mol Biotechnol. 2022 Aug;64(8):888-901. doi: 10.1007/s12033-022-00469-1. Epub 2022 Feb 26.