Z-C Wang1, S Yang, M-Q Chen, S-S Wu, H-H Lv, W-X Jin. 1. Department of Spleen, Stomach and Liver Diseases, Guangxi International Zhuang Medical Hospital, Nanning, China. jinwangxun@163.com.
Abstract
OBJECTIVE: The aim of this study was to investigate the role of LINC01296 in the progression of liver cancer (LCa) and to explore its possible molecular mechanisms. PATIENTS AND METHODS: TCGA database was used for information mining to verify the expression of LINC01296 in liver tumor tissues and normal tissues. The levels of LINC01296 in 40 pairs of LCa and adjacent tissues, as well as normal liver cell lines and liver cancer cell lines, were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The Chi-square test was performed to analyze the clinical characteristics of tumor samples and LINC01296 expression. Meanwhile, the Chi-square test was used to explore the relationship between different clinical indicators and the expression of LINC01296. The liver cancer cell lines were screened and transfected with siRNA-LINC01296 and microRNA-760 inhibitor, as well as corresponding negative controls, respectively. Cell counting kit-8 (CCK-8) and Transwell assays were used to determine the effects of LINC01296 on the proliferative and invasive capacities of cells. Furthermore, the regulatory association between LINC01296 and microRNA-760 was verified by the Dual-Luciferase reporter assay. RESULTS: LINC01296 expression was remarkably higher in LCa tissues than that of normal liver tissues. Meanwhile, LINC01296 expression was associated with poor prognosis of LCa. Patients with high LINC01296 expression were more likely to have lymph node metastasis. In vitro experiments showed that the knockdown of LINC01296 significantly inhibited the proliferation and migration of HCC cells. Meanwhile, microRNA-760 was remarkably lowly expressed in LCa tissues and cells. Subsequent experiments indicated that LINC01296 was regulated by miR760 in LCa tissues, and high expression of linc0129 could limit microRNA-760 expression. Furthermore, the inhibition of microRNA-760 in HCC cells reversed the effect of LINC01296 knockdown on cell proliferation and invasion. CONCLUSIONS: LINC01296 could promote the proliferative ability and invasiveness of hepatoma cells by inhibiting the expression of microRNA-760. Moreover, its expression was closely related to lymph node metastasis and poor prognosis of LCa.
OBJECTIVE: The aim of this study was to investigate the role of LINC01296 in the progression of liver cancer (LCa) and to explore its possible molecular mechanisms. PATIENTS AND METHODS: TCGA database was used for information mining to verify the expression of LINC01296 in liver tumor tissues and normal tissues. The levels of LINC01296 in 40 pairs of LCa and adjacent tissues, as well as normal liver cell lines and liver cancer cell lines, were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The Chi-square test was performed to analyze the clinical characteristics of tumor samples and LINC01296 expression. Meanwhile, the Chi-square test was used to explore the relationship between different clinical indicators and the expression of LINC01296. The liver cancer cell lines were screened and transfected with siRNA-LINC01296 and microRNA-760 inhibitor, as well as corresponding negative controls, respectively. Cell counting kit-8 (CCK-8) and Transwell assays were used to determine the effects of LINC01296 on the proliferative and invasive capacities of cells. Furthermore, the regulatory association between LINC01296 and microRNA-760 was verified by the Dual-Luciferase reporter assay. RESULTS:LINC01296 expression was remarkably higher in LCa tissues than that of normal liver tissues. Meanwhile, LINC01296 expression was associated with poor prognosis of LCa. Patients with high LINC01296 expression were more likely to have lymph node metastasis. In vitro experiments showed that the knockdown of LINC01296 significantly inhibited the proliferation and migration of HCC cells. Meanwhile, microRNA-760 was remarkably lowly expressed in LCa tissues and cells. Subsequent experiments indicated that LINC01296 was regulated by miR760 in LCa tissues, and high expression of linc0129 could limit microRNA-760 expression. Furthermore, the inhibition of microRNA-760 in HCC cells reversed the effect of LINC01296 knockdown on cell proliferation and invasion. CONCLUSIONS:LINC01296 could promote the proliferative ability and invasiveness of hepatoma cells by inhibiting the expression of microRNA-760. Moreover, its expression was closely related to lymph node metastasis and poor prognosis of LCa.
Authors: Larissa Nitschke; Ambika Tewari; Stephanie L Coffin; Eder Xhako; Kaifang Pang; Vincenzo A Gennarino; Jennifer L Johnson; Francisco A Blanco; Zhandong Liu; Huda Y Zoghbi Journal: Genes Dev Date: 2020-08-06 Impact factor: 11.361