SNHG16 promotes hepatocellular carcinoma development via activating ECM receptor interaction pathway
SNHG16通过激活ECM受体相互作用通路促进肝细胞癌发展
SNHG16は、ECM受容体相互作用経路を活性化することにより肝細胞癌の発生を促進します
SNHG16은 ECM 수용체 상호작용 경로를 활성화하여 간세포 암종 발달을 촉진합니다
SNHG16 promueve el desarrollo del carcinoma hepatocelular mediante la activación de la vía de interacción del receptor ECM
SNHG16 favorise le développement du carcinome hépatocellulaire via l'activation de la voie d'interaction des récepteurs ECM
SNHG16 способствует развитию гепатоцеллюлярной карциномы посредством активации пути взаимодействия с рецептором ECM
Qi-Jun Zhang ¹, Da-Zhi Li ², Bing-Yi Lin ², Lei Geng 耿磊 ², Zhe Yang 杨哲 ² ³, Shu-Seng Zheng 郑树森 ² ³
¹ Department of Thyroid Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
中国 杭州 浙江大学附属第一医院甲状腺疾病诊治中心
² NHC Key Laboratory of Combined Multi-organ Transplantation, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
中国 杭州 浙江大学医学院附属第一医院 卫生部多器官联合移植研究重点实验室
³ Department of Hepatobiliary and Pancreatic Surgery, Shulan (Hangzhou) Hospital, Zhejiang Shuren University School of Medicine, Hangzhou 310000, China
中国 杭州 浙江树人大学树兰国际医学院 树兰（杭州）医院肝胆胰外科
Hepatobiliary & Pancreatic Diseases International, 17 January 2022
Background
Accumulating data have suggested that long non-coding RNAs (lncRNAs) play important roles in regulating tumor cell growth. This study was designed to investigate the role of SNHG16 in hep- atocellular carcinoma (HCC).
Methods
SNHG16 expression was detected with real-time polymerase chain reaction (PCR). The cut- off value of SNHG16 for tumor-free survival (TFS) was determined with receiver operating characteristic curve analysis. Small interfering RNA was used to inhibit the expression of SNHG16 in HCC cell lines. The biologic behavior of HCC cell was determined with cell viability assay and Transwell assay in vitro. The potential predictive value of SNHG16 on prognosis was analyzed by Kaplan-Meier curves and Cox proportional hazards regression model.
Results
SNHG16 expression was upregulated in tumor tissues and HCC cell lines. High expression of SNHG16 was associated with tumor recurrence and poor prognosis after surgery. Multivariate analysis revealed that SNHG16 was an independent prognostic factor for poor recurrence-free survival. Moreover, inhibition of SNHG16 in HepG2, Hep3B, and BEL-7402 cells significantly reduced cell invasiveness and proliferation. Mechanistic analyses indicated that the ECM-receptor interaction pathway was remarkably activated by SNHG16.
Conclusions
SNHG16 might be a promising biomarker for predicting tumor recurrence in HCC patients after surgery and a potential therapeutic target for HCC.
