PMID- 33215214 OWN - NLM STAT- MEDLINE DCOM- 20210412 LR - 20210630 IS - 1791-3004 (Electronic) IS - 1791-2997 (Print) IS - 1791-2997 (Linking) VI - 23 IP - 1 DP - 2021 Jan TI - Lung cancer‑associated transcript 1 facilitates tumorigenesis in laryngeal squamous cell carcinoma through the targeted inhibition of miR‑493. LID - 59 [pii] LID - 10.3892/mmr.2020.11697 [doi] AB - Long non‑coding RNAs (lncRNAs) serve important roles in the tumorigenesis of a diverse range of cancer types. The lung cancer‑associated transcript 1 (LUCAT1), has been reported to promote the proliferation, migration and invasion of oral squamous cell carcinoma cells. However, the exact role of LUCAT1 in laryngeal squamous cell carcinoma (LSCC) remains to fully understood. The present study aimed to interrogate the role and modulatory mechanism of LUCAT1 in LSCC. Reverse transcription‑quantitative PCR and western blotting were used to investigate the expression of LUCAT1 and miR‑493, as well as the protein expression of cyclin‑dependent kinase 2, cyclin E1, p21, matrix metalloproteinase (MMP)2, MMP9, vascular endothelial growth factor‑C, Bcl‑2, Bax, cleaved caspase‑3 and procaspase‑3. Cell Counting Kit‑8, flow cytometry, wound healing and Transwell assays were performed to analyze the proliferation, cell cycle, apoptosis levels, and the migratory and invasive abilities, respectively, of the LSCC AMC‑HN‑8 cell line. In addition, dual‑luciferase reporter and ribonucleoprotein immunoprecipitation assays were used to investigate the binding between LUCAT1 and microRNA (miR)‑493. The results of the present study revealed that the expression levels of LUCAT1 were upregulated in AMC‑HN‑8 cells. The genetic knockdown of LUCAT1 expression levels significantly suppressed the cell proliferation, alongside downregulating the expression levels of CDK2 and cyclin E1 and upregulating p21 expression levels. In addition, the knockdown of LUCAT1 inhibited cell migration and invasion, as demonstrated using the wound healing and Transwell assays, respectively. Moreover, LUCAT1 knockdown promoted cell apoptosis and upregulated the expression levels of Bax and cleaved caspase‑3, whilst downregulating the expression levels of Bcl‑2. Furthermore, LUCAT1 was discovered to directly bind to and inhibit the well‑known tumor suppressor, miR‑493. Notably, the specific inhibition of miR‑493 partly blocked the anticancer effects of LUCAT1 knockdown in AMC‑HN‑8 cells. In conclusion, these results suggested that LUCAT1 may facilitate tumorigenesis in LSCC through the targeted inhibition of miR‑493, which provides evidence for a novel target for the treatment of LSCC. FAU - Zhao, Zhen AU - Zhao Z AD - Department of Otorhinolaryngology‑Head and Neck Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China. FAU - Xing, Yan AU - Xing Y AD - The Third Department of Rehabilitation, Shijiazhuang No. 1 Hospital, Shijiazhuang, Hebei 050000, P.R. China. FAU - Liu, Yan AU - Liu Y AD - Department of Otorhinolaryngology‑Head and Neck Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China. FAU - Jing, Shanghua AU - Jing S AD - Department of Otorhinolaryngology‑Head and Neck Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China. LA - eng PT - Journal Article DEP - 20201120 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (BAX protein, human) RN - 0 (BCL2 protein, human) RN - 0 (CCNE1 protein, human) RN - 0 (CDKN1A protein, human) RN - 0 (Cyclin E) RN - 0 (Cyclin-Dependent Kinase Inhibitor p21) RN - 0 (MIRN493 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Oncogene Proteins) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (RNA, Long Noncoding) RN - 0 (Vascular Endothelial Growth Factor C) RN - 0 (bcl-2-Associated X Protein) RN - 0 (long non-coding RNA LUCAT1, human) RN - EC 2.7.11.22 (CDK2 protein, human) RN - EC 2.7.11.22 (Cyclin-Dependent Kinase 2) RN - EC 3.4.22.- (CASP3 protein, human) RN - EC 3.4.22.- (Caspase 3) RN - EC 3.4.24.24 (MMP2 protein, human) RN - EC 3.4.24.24 (Matrix Metalloproteinase 2) RN - EC 3.4.24.35 (MMP9 protein, human) RN - EC 3.4.24.35 (Matrix Metalloproteinase 9) SB - IM MH - Apoptosis/genetics MH - Caspase 3/metabolism MH - Cell Cycle/genetics MH - Cell Line, Tumor MH - Cell Movement/genetics MH - Cell Proliferation/genetics MH - Cell Transformation, Neoplastic MH - Cyclin E/metabolism MH - Cyclin-Dependent Kinase 2/metabolism MH - Cyclin-Dependent Kinase Inhibitor p21/metabolism MH - Gene Knockdown Techniques MH - Head and Neck Neoplasms/*genetics/*metabolism MH - Humans MH - Matrix Metalloproteinase 2/metabolism MH - Matrix Metalloproteinase 9/metabolism MH - MicroRNAs/*antagonists & inhibitors/metabolism MH - Oncogene Proteins/metabolism MH - Proto-Oncogene Proteins c-bcl-2/metabolism MH - RNA, Long Noncoding/*genetics/*metabolism/physiology MH - Squamous Cell Carcinoma of Head and Neck/*genetics/*metabolism MH - Up-Regulation MH - Vascular Endothelial Growth Factor C MH - bcl-2-Associated X Protein/metabolism PMC - PMC7705996 OTO - NOTNLM OT - lung cancer‑associated transcript 1 OT - microRNA‑493 OT - squamous cell carcinoma of the larynx OT - tumorigenesis EDAT- 2020/11/21 06:00 MHDA- 2021/04/13 06:00 PMCR- 2020/11/18 CRDT- 2020/11/20 05:51 PHST- 2020/04/15 00:00 [received] PHST- 2020/07/07 00:00 [accepted] PHST- 2020/11/20 05:51 [entrez] PHST- 2020/11/21 06:00 [pubmed] PHST- 2021/04/13 06:00 [medline] PHST- 2020/11/18 00:00 [pmc-release] AID - 59 [pii] AID - MMR-0-0-11697 [pii] AID - 10.3892/mmr.2020.11697 [doi] PST - ppublish SO - Mol Med Rep. 2021 Jan;23(1):59. doi: 10.3892/mmr.2020.11697. Epub 2020 Nov 20.