Knockdown of RFC4 inhibits cell proliferation of oral squamous cell carcinoma in vitro and in vivo
Pengyue You,
Di Wang,
Zheng Liu,
Shuzhen Guan,
Ning Xiao,
Haotian Chen,
Xin Zhang,
Lichuan Wu,
Guizhen Wang,
Haitao Dong
Affiliations
Pengyue You
Department of Stomatology, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Di Wang
Department of Clinical Laboratory, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Zheng Liu
State Key Laboratory of Molecular Oncology, Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Shuzhen Guan
Medical College of Guangxi University Nanning China
Ning Xiao
Department of Stomatology, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Haotian Chen
Department of Stomatology, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Xin Zhang
Department of Stomatology, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Lichuan Wu
Medical College of Guangxi University Nanning China
Guizhen Wang
State Key Laboratory of Molecular Oncology, Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Haitao Dong
Department of Stomatology, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Oral squamous cell carcinoma (OSCC) is the one of the most common types of malignant tumor found in the head and neck area. Replication factor C subunit 4 (RFC4), an oncogene active in various human cancers, has been rarely studied in OSCC. In the present study, bioinformatics analysis identified RFC4 as a potential key target in OSCC progression. Additional experiments showed that RFC4 expression was significantly higher in OSCC tumor tissues than in normal tissues. Knockdown of RFC4 led to G2/M phase cell cycle arrest and inhibited the proliferation of OSCC cells both in vitro and in vivo. High RFC4 expression in OSCC tumors was linked to increased levels of MET, along with reduced levels of CD274 and CD160. Overall, the present study reveals that RFC4 may play a pivotal role in OSCC tumorigenesis and could serve as a potential predictive marker for the efficacy of immunotherapy.
