Anticancer Research · 2020 · 18 citations · 16 references
MedicineMolecular BiologyOncologyApoptosisCarcinogenesisMolecular OncologyMalignant NeoplasmsNoncoding Rna In CancerRadiation CarcinogenesisRadiation TherapySquamous Cell CarcinomaTumor Suppressor GenesCancer Cell RadiosensitivityCell Viability AssaysCrispr-cas9 Genome EditingCrispr-cas9 KnockoutDna Damage InductionGene Silencing In CancerIonizing Radiation CarcinogenesisRadiation-induced Apoptosis
Background/Aim: Two-thirds of head and neck squamous cell carcinoma (HNSCC) patients present with locally advanced (LA) stages and have a poor survival rate. The aim of this study was to investigate the roles of the long non-coding RNAs MALAT1 on radiation and cisplatin sensitivity of HNSCC cells. Materials and Methods: Clonogenic, cell viability, and apoptosis assays were performed in cells following MALAT1 knockdown using CRISPR/Cas9 system. Results: MALAT1 was overexpressed in HNSCC cell lines as compared to a non-tumorigenic cell line. The number of colonies formed after radiation was significantly reduced in MALAT1 knockdown cells. The IC<sub>50</sub> value of cisplatin in MALAT1 knockdown cells was lower than that of the control cells. MALAT1 knockdown resulted in cell cycle arrest at G<sub>2</sub>/M phase, DNA damage and apoptotic cell death. Conclusion: MALAT1 knockdown enhanced the sensitivity of HNSCC cells to radiation and cisplatin partly through the induction of G<sub>2</sub>/M cell cycle arrest resulting in DNA damage and apoptosis.
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Global cancer statistics, 2012
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