Meng Jia1, Li Jiang2, Ya-Dong Wang1, Jin-Zhao Huang1, Miao Yu1, Huan-Zhou Xue3. 1. Department of Hepatobiliary and Pancreas Surgery, People's Hospital of Zhengzhou University, Henan Province People's Hospital, Zhengzhou, China. 2. Department of Hematology, People's Hospital of Zhengzhou University, Henan Province People's Hospital, Zhengzhou, China. 3. Department of Hepatobiliary and Pancreas Surgery, People's Hospital of Zhengzhou University, Henan Province People's Hospital, Zhengzhou, China. huanzhoux@163.com.
Abstract
AIM: Emerging evidence has showed that long non-coding RNA (lncRNA) play an important role in the occurrence and development of various cancers. In the present study, the expression level of lincRNA-p21 was investigated in hepatocellular carcinoma (HCC), and its role in invasion of HCC was also explored. METHODS: The lincRNA-p21 levels in human HCC tumor tissue and cell lines HepG2 and SMMC-7721 were determined by real-time polymerase chain reaction. Transfected HCC cells with pcDNA-lincRNA-p21 or si-lincRNA-p21 for overexpression or downregulation of lincRNA-p21, the Notch signaling and epithelial-mesenchymal transition (EMT)-related proteins and cell invasion were measured by western blot and Transwell assay, respectively. A tumor xenotransplant mouse model was also established to investigate the role of lincRNA-p21 in tumor metastasis in vivo. RESULTS: The lincRNA-p21 expression was downregulated in HCC tissue and cells. Overexpression of lincRNA-p21 inhibited Notch singling and EMT, while its downregulation led to the reverse result. The invasion of HCC cell was also inhibited by pcDNA-lincRNA-p21, and activation of Notch signaling reversed this effect. In vivo, overexpression of lincRNA-p21 decreased the tumor metastasis, as well. CONCLUSION: lincRNA-p21 was downregulated in HCC and lincRNA-p21 overexpression contributed to the inhibition of tumor invasion through mediating Notch signaling induced EMT.
AIM: Emerging evidence has showed that long non-coding RNA (lncRNA) play an important role in the occurrence and development of various cancers. In the present study, the expression level of lincRNA-p21 was investigated in hepatocellular carcinoma (HCC), and its role in invasion of HCC was also explored. METHODS: The lincRNA-p21 levels in humanHCC tumor tissue and cell lines HepG2 and SMMC-7721 were determined by real-time polymerase chain reaction. Transfected HCC cells with pcDNA-lincRNA-p21 or si-lincRNA-p21 for overexpression or downregulation of lincRNA-p21, the Notch signaling and epithelial-mesenchymal transition (EMT)-related proteins and cell invasion were measured by western blot and Transwell assay, respectively. A tumor xenotransplant mouse model was also established to investigate the role of lincRNA-p21 in tumor metastasis in vivo. RESULTS: The lincRNA-p21 expression was downregulated in HCC tissue and cells. Overexpression of lincRNA-p21 inhibited Notch singling and EMT, while its downregulation led to the reverse result. The invasion of HCC cell was also inhibited by pcDNA-lincRNA-p21, and activation of Notch signaling reversed this effect. In vivo, overexpression of lincRNA-p21 decreased the tumor metastasis, as well. CONCLUSION:lincRNA-p21 was downregulated in HCC and lincRNA-p21 overexpression contributed to the inhibition of tumor invasion through mediating Notch signaling induced EMT.