Chaoyang Wang1,2, Hao Zi2, Yang Wang1,2, Binghui Li1,2, Zheng Ge1,2, Xuequn Ren1,2. 1. Department of General Surgery, Huaihe Hospital of Henan University, Kaifeng, Henan, China. 2. Institute of Evidence-Based Medicine and knowledge translation, Henan University, Kaifeng, Henan, China.
Abstract
Objective: The present study aimed to investigate the function of lncRNA CASC15 (cancer susceptibility candidate 15) in hepatocellular carcinoma (HCC), as well as its regulatory roles in SOX4 expression and Wnt/β-catenin pathway. Methods: Quantitative real-time polymerase chain reaction (QRT-PCR) method was used to detect the relative expression of CASC15 mRNA in HCC tissues. Protein detection was performed by western blot. Luciferase assay was used to confirm the potential target of CASC15 in HCC. Cell proliferation, migration and invasion, as well as apoptosis were analyzed using MTT, transwell assays and flow cytometry in vitro, respectively. Results: The expression of CASC15 was significantly increased in HCC tissues (p < .001) and showed positive correlation with tumour size (p = .016), TNM stage (p = .018) and metastasis (p = .021). The knockdown of CASC15 could obviously inhibit HCC cell proliferation, migration and invasion and promote cell apoptosis in vitro (p < .05 for all). Furthermore, the protein levels of SOX4, β-catenin, Cyclin D1 and c-Myc also exhibited decreased trends after CASC15 inhibition. Luciferase assay confirmed that SOX4 might be a targeted gene of CASC15 in HCC. Conclusion: In HCC, CASC15 may activate the Wnt/β-catenin pathway via enhancing the expression of SOX4, thus promote tumour progression.
Objective: The present study aimed to investigate the function of lncRNA CASC15 (cancer susceptibility candidate 15) in hepatocellular carcinoma (HCC), as well as its regulatory roles in SOX4 expression and Wnt/β-catenin pathway. Methods: Quantitative real-time polymerase chain reaction (QRT-PCR) method was used to detect the relative expression of CASC15 mRNA in HCC tissues. Protein detection was performed by western blot. Luciferase assay was used to confirm the potential target of CASC15 in HCC. Cell proliferation, migration and invasion, as well as apoptosis were analyzed using MTT, transwell assays and flow cytometry in vitro, respectively. Results: The expression of CASC15 was significantly increased in HCC tissues (p < .001) and showed positive correlation with tumour size (p = .016), TNM stage (p = .018) and metastasis (p = .021). The knockdown of CASC15 could obviously inhibit HCC cell proliferation, migration and invasion and promote cell apoptosis in vitro (p < .05 for all). Furthermore, the protein levels of SOX4, β-catenin, Cyclin D1 and c-Myc also exhibited decreased trends after CASC15 inhibition. Luciferase assay confirmed that SOX4 might be a targeted gene of CASC15 in HCC. Conclusion: In HCC, CASC15 may activate the Wnt/β-catenin pathway via enhancing the expression of SOX4, thus promote tumour progression.
Entities:
Keywords:
CASC15; Hepatocellular carcinoma; Wnt/β-catenin; long non-coding RNA