Wen-Yu Hu1, Hai-Yan Wei2, Ke-Ming Li3, Ren-Ben Wang4, Xiao-Qing Xu4, Rui Feng5. 1. Department of chemotherapy, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academic of Medical Science, Jinan, 250117, China. 2. Department of Physical and Chemical Laboratory, Shandong Academy of Occupational Health and Occupational Medicine, Jinan, 250062, China. 3. Department of Pharmacology, Shandong Academy of Traditional Chinese Medicine, Jinan, 250014, China. 4. Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academic of Medical Science, Jinan, 250117, China. 5. Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academic of Medical Science, Jinan, 250117, China. Electronic address: fengrui20080315@163.com.
Abstract
BACKGROUND: Recently, a growing number of reports indicated that long non-coding RNAs (lncRNAs) were involved in the development of various cancers. However, the performance of LINC00511 is still limited in hepatocellular carcinoma (HCC). Thus, we attempted to assess the effect of LINC00511 and underlying mechanism in HCC progression. METHODS: TCGA and GEO database acted as supporters to provide us clinical samples data. Overall survival (OS) analyses were plotted using Kaplan-Meier method. Five cell lines were utilized to detect LINC00511 expression level and Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were conducted to examine the effects on cell behaviors. The correlations between LINC00511 and miR-195 or eyes absent homolog 1 (EYA1) were confirmed by luciferase reporter assay. Quantitative real-time PCR and western blotting were fulfilled to ascertain the mRNA and protein expression levels. RESULTS: In this study, we found that LINC00511 was high-regulated in HCC tissue samples and cell lines, which might be linked with unfavorable prognosis of HCC patients and clinical parameters. Loss-of-function experiments determined that LINC00511 deficiency inhibited cell proliferation, colony formation and invasive activity in HepG2 cells, while gain-of-function experiments showed the counter impacts in Huh7 cells. Bioinformatics tools and luciferase reporter assays revealed that LINC00511 may act as a competing endogenous RNA (ceRNA) for miR-195 and positively correlate with EYA1, which was reinforced by rescue experiments. CONCLUSION: Taken together, these findings indicated that LINC00511 interacted with EYA1 promoted HCC development via mediating miR-195, proposing a promising therapeutic biomarker for HCC diagnosis and prognosis.
BACKGROUND: Recently, a growing number of reports indicated that long non-coding RNAs (lncRNAs) were involved in the development of various cancers. However, the performance of LINC00511 is still limited in hepatocellular carcinoma (HCC). Thus, we attempted to assess the effect of LINC00511 and underlying mechanism in HCC progression. METHODS: TCGA and GEO database acted as supporters to provide us clinical samples data. Overall survival (OS) analyses were plotted using Kaplan-Meier method. Five cell lines were utilized to detect LINC00511 expression level and Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were conducted to examine the effects on cell behaviors. The correlations between LINC00511 and miR-195 or eyes absent homolog 1 (EYA1) were confirmed by luciferase reporter assay. Quantitative real-time PCR and western blotting were fulfilled to ascertain the mRNA and protein expression levels. RESULTS: In this study, we found that LINC00511 was high-regulated in HCC tissue samples and cell lines, which might be linked with unfavorable prognosis of HCCpatients and clinical parameters. Loss-of-function experiments determined that LINC00511 deficiency inhibited cell proliferation, colony formation and invasive activity in HepG2 cells, while gain-of-function experiments showed the counter impacts in Huh7 cells. Bioinformatics tools and luciferase reporter assays revealed that LINC00511 may act as a competing endogenous RNA (ceRNA) for miR-195 and positively correlate with EYA1, which was reinforced by rescue experiments. CONCLUSION: Taken together, these findings indicated that LINC00511 interacted with EYA1 promoted HCC development via mediating miR-195, proposing a promising therapeutic biomarker for HCC diagnosis and prognosis.