scholarly journals Sperm-associated antigen 9 is upregulated in hepatocellular carcinoma tissue and enhances QGY cell proliferation and invasion in�vitro

2017 ◽  
Author(s):  
Biqiong Ren ◽  
Guoying Zou ◽  
Junyu He ◽  
Yiran Huang ◽  
Guoan Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Carcinoma Tissue ◽  
Proliferation And Invasion ◽  
Hepatocellular Carcinoma Tissue

scholarly journals KLF7/VPS35 axis contributes to hepatocellular carcinoma progression through CCDC85C-activated β-catenin pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yarong Guo ◽  
Bao Chai ◽  
Junmei Jia ◽  
Mudan Yang ◽  
Yanjun Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Luciferase Reporter ◽  
Aberrant Expression ◽  
Proliferation And Invasion ◽  
Hcc Cells

Abstract Objective Dysregulation of KLF7 participates in the development of various cancers, but it is unclear whether there is a link between HCC and aberrant expression of KLF7. The aim of this study was to investigate the role of KLF7 in proliferation and migration of hepatocellular carcinoma (HCC) cells. Methods CCK8, colony growth, transwell, cell cycle analysis and apoptosis detection were performed to explore the effect of KLF7, VPS35 and Ccdc85c on cell function in vitro. Xenografted tumor growth was used to assess in vivo role of KLF7. Chip-qPCR and luciferase reporter assays were applied to check whether KLF7 regulated VPS35 at transcriptional manner. Co-IP assay was performed to detect the interaction between VPS35 and Ccdc85c. Immunohistochemical staining and qRT-PCR analysis were performed in human HCC sampels to study the clinical significance of KLF7, VPS35 and β-catenin. Results Firstly, KLF7 was highly expressed in human HCC samples and correlated with patients’ differentiation and metastasis status. KLF7 overexpression contributed to cell proliferation and invasion of HCC cells in vitro and in vivo. KLF7 transcriptional activation of VPS35 was necessary for HCC tumor growth and metastasis. Further, co-IP studies revealed that VPS35 could interact with Ccdc85c in HCC cells. Rescue assay confirmed that overexpression of VPS35 and knockdown of Ccdc85c abolished the VPS35-medicated promotion effect on cell proliferation and invasion. Finally, KLF7/VPS35 axis regulated Ccdc85c, which involved in activation of β-catenin signaling pathway, confirmed using β-catenin inhibitor, GK974. Functional studies suggested that downregulation of Ccdc85c partly reversed the capacity of cell proliferation and invasion in HCC cells, which was regulated by VPS35 upregulation. Lastly, there was a positive correlation among KLF7, VPS35 and active-β-catenin in human HCC patients. Conclusion We demonstrated that KLF7/VPS35 axis promoted HCC cell progression by activating Ccdc85c-medicated β-catenin pathway. Targeting this signal axis might be a potential treatment strategy for HCC.

Organization and expression of hepatitis B sequences cloned from hepatocellular carcinoma tissue DNA

1982 ◽  
Vol 20 (3) ◽  
pp. 293-301 ◽  
Author(s):  
Anne Dejean ◽  
Guido Carloni ◽  
Christian Bréchot ◽  
Pierre Tiollais ◽  
Simon Wain-Hobson
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B ◽  
Carcinoma Tissue ◽  
Hepatocellular Carcinoma Tissue

MicroRNA-493 suppresses cell proliferation and invasion by targeting ZFX in human hepatocellular carcinoma

2018 ◽  
Vol 22 (3) ◽  
pp. 427-434 ◽  
Author(s):  
Wei Ding ◽  
Hongbo Tan ◽  
Xuemei Li ◽  
Yue Zhang ◽  
Fang Fang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Human Hepatocellular Carcinoma ◽  
Proliferation And Invasion

scholarly journals lncRNA MIAT promotes proliferation and invasion of HCC cells via sponging miR-214

2018 ◽  
Vol 314 (5) ◽  
pp. G559-G565 ◽  
Author(s):  
Xinli Huang ◽  
Yun Gao ◽  
Jianjie Qin ◽  
Sen Lu
Keyword(s):  
Myocardial Infarction ◽  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Histone Acetylation ◽  
Noncoding Rna ◽  
Micro Rna ◽  
Western Blot Assay ◽  
Aberrant Expression ◽  
Proliferation And Invasion ◽  
Hcc Cells

The aberrant expression of long noncoding RNAs (lncRNAs) has been involved in various human tumors including hepatocellular carcinoma (HCC). Our study aimed to investigate the potential molecular mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in HCC. The expression of MIAT and micro-RNA (miR)-214 in HCC tissues and cells was examined by quantitative real-time PCR, and the levels of enhancer of zeste homolog 2 (EZH2) and β-catenin were detected by Western blot assay. Immunoprecipitation analysis was used to detect the level of H3/H4 histone acetylation. RNA pull-down assay was performed to confirm the targeting regulatory relationship between miR-214 and MIAT. Cell viability, proliferation, and invasion were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), [3H]thymidine incorporation, and Transwell assays, respectively. BALB/c nude mice were used to establish a hepatocellular carcinoma animal model with subcutaneous injection of SK-HEP-1 cells. Upregulation of MIAT is related to the proliferation and invasion of HCC, and downregulating MIAT expression inhibited HCC cell proliferation and invasion. The H3/H4 histone acetylation level of MIAT promoter in HCC tissues was higher than that in normal tissues. MIAT negatively regulated miR-214 in HCC cells. Inhibition of miR-214 reversed the influence of MIAT downregulation on HCC cell proliferation and invasion. In nude mouse xenograft models, downregulation of MIAT markedly suppressed the tumor growth of HCC via releasing miR-214. In conclusion, lncRNA MIAT promotes the proliferation and invasion of HCC cells through sponging miR-214, which brings a novel target for the therapy and prognosis of hepatocellular carcinoma. NEW & NOTEWORTHY This is the first research showing long noncoding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) to have a regulatory effect on hepatocellular carcinoma. Micro-RNA (miR)-214 could be sponged by MIAT to promote the proliferation and invasion of hepatocellular carcinoma cells. The lncRNA MIAT/miR-214 axis brings a novel insight for the therapy and prognosis of hepatocellular carcinoma.

scholarly journals Silencing of the TROP2 gene suppresses proliferation and invasion of hepatocellular carcinoma HepG2 cells

2019 ◽  
Vol 47 (3) ◽  
pp. 1319-1329 ◽  
Author(s):  
Jian Zhang ◽  
Hai Ma ◽  
Liu Yang ◽  
Hongchun Yang ◽  
Zhenxing He
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Human Trophoblast ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Proliferation And Invasion

Objectives Overexpression of human trophoblast cell surface antigen 2 (Trop2) has been observed in many cancers; however, its roles in proliferation, apoptosis, migration, and invasion of hepatocellular carcinoma (HCC) remain unclear. Thus, this study aimed to characterize the function of Trop2 in HCC. Methods Trop2 protein expression was detected by immunohistochemistry in HCC tissues. Cell proliferation, apoptosis, and invasion were respectively measured by CCK-8, flow cytometry, Transwell, and wound healing assays. Expression levels of epithelial–mesenchymal transition-related proteins and Trop2 protein in HCC cell lines were detected by western blotting after silencing of the TROP2 gene. Results Trop2 protein was highly expressed in HCC tissues and HCC cell lines. Trop2 mRNA and protein expression levels decreased in HepG2 and HCCLM3 cells after transfection with Trop2 siRNA. Silencing of the TROP2 gene in HepG2 and HCCLM3 cells strongly inhibited cell proliferation and migration, while enhancing cell apoptosis. Investigation of the molecular mechanism revealed that silencing of the TROP2 gene suppressed epithelial–mesenchymal transition of HepG2 and HCCLM3 cells. Conclusions The results of the present study may improve understanding of the role of Trop2 in regulation of cell proliferation and invasion, and may aid in development of novel therapy for HCC.

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