TY - EJOU
AU - YUE, HAIYING
AU - WANG, CHUNHUI
AU - ZHU, HUIJUN
AU - DU, QINGHUA
AU - LI, JIAN
AU - OU, XUE
AU - LI, XIANGDE
AU - ZHONG, QIULU
AU - XIE, YITING
AU - LUO, DANJING
AU - LI, YIHE
AU - LIANG, CHUNXIAO
AU - XU, EMEI
AU - DU, SONGNAN
AU - LIU, WENQI
TI - SIRT2 interacts with DDX24 to promote nasopharyngeal carcinoma growth
T2 - BIOCELL
PY - 2023
VL - 47
IS - 11
SN - 1667-5746
AB - Background: Nasopharyngeal carcinoma (NPC) is one of the most prevalent cancers in Southeast Asia. Sirtuin 2 (SIRT2) is a member of the NAD+-dependent deacetylase family and has been shown to play important roles in numerous biological processes. However, Its function in NPC remains uncertain. The primary aim of this study is to clarify the role of SIRT2 in NPC. Methods: In this research, we examined the effect of SIRT2 silencing on NPC cell proliferation and colony formation using vitro NPC cell lines. Co-immunoprecipitation and mass spectrometry was applied to identify SIRT2-interacting proteins in NPC cells. Results: In comparison to nasopharyngeal epithelial NP69 cells, SIRT2 was up-regulated in multiple NPC cell lines, particularly in CNE2 cells. SIRT2 knockdown abrogated CNE2 cell proliferation and colony formation, whereas SIRT2 overexpression promoted HNE1 cell proliferation and colony formation. The SIRT2-interacting proteins were gathered in gene expression and regulation processes including RNA processing and translation. Among the SIRT2-interacting proteins, there were multiple DEAD-box (DDX) family members. Of note, silencing of DDX24 phenocopied the effect of SIRT2 knockdown on NPC growth. Overexpression of DDX24 restored SIRT2-depleted CNE2 cells to proliferative and colony formation. Conclusions: Our study indicates that SIRT2 can interact with DDX24 to enhance NPC growth. The clinical relevance of SIRT2 and DDX24 in NPC warrants further investigation.
KW - Nasopharyngeal carcinoma; Sirtuin 2; DDX24; Proliferation
DO - 10.32604/biocell.2023.042512