MALAT1 Decreases the Sensitivity of Head and Neck Squamous Cell Carcinoma Cells to Radiation and Cisplatin
| Autor: | P Tangboonduangjit, Pimolpun Changkaew, Suphalak Khachonkham, Patompon Wongtrakoongate, Arthit Chairoungdua, Kornkamon Lertsuwan, Nuttapong Ngamphaiboon, Teerada Siripoon, Kitsada Kangboonruang |
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| Rok vydání: | 2020 |
| Předmět: |
Cisplatin
Cancer Research Gene knockdown Chemistry General Medicine medicine.disease Head and neck squamous-cell carcinoma 03 medical and health sciences 0302 clinical medicine Radiation sensitivity Oncology Cell culture Apoptosis 030220 oncology & carcinogenesis medicine Cancer research Viability assay Clonogenic assay medicine.drug |
| Zdroj: | Anticancer Research. 40:2645-2655 |
| ISSN: | 1791-7530 0250-7005 |
| DOI: | 10.21873/anticanres.14235 |
| Popis: | 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 IC50 value of cisplatin in MALAT1 knockdown cells was lower than that of the control cells. MALAT1 knockdown resulted in cell cycle arrest at G2/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 G2/M cell cycle arrest resulting in DNA damage and apoptosis. |
| Databáze: | OpenAIRE |
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