TY - JOUR
T1 - MALAT1 decreases the sensitivity of head and neck squamous cell carcinoma cells to radiation and cisplatin
AU - Kangboonruang, Kitsada
AU - Wongtrakoongate, Patompon
AU - Lertsuwan, Kornkamon
AU - Khachonkham, Suphalak
AU - Changkaew, Pimolpun
AU - Tangboonduangjit, Puangpen
AU - Siripoon, Teerada
AU - Ngamphaiboon, Nuttapong
AU - Chairoungdua, Arthit
N1 - Publisher Copyright:
© 2020 International Institute of Anticancer Research. All rights reserved.
PY - 2020/5
Y1 - 2020/5
N2 - 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.
AB - 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.
KW - Cisplatin sensitivity
KW - HNSCC
KW - LncRNA
KW - MALAT1
KW - Radiation sensitivity
UR - http://www.scopus.com/inward/record.url?scp=85084277511&partnerID=8YFLogxK
U2 - 10.21873/anticanres.14235
DO - 10.21873/anticanres.14235
M3 - Article
C2 - 32366409
AN - SCOPUS:85084277511
SN - 0250-7005
VL - 40
SP - 2645
EP - 2655
JO - Anticancer Research
JF - Anticancer Research
IS - 5
ER -