ArticleOncology letters2018
Hepatitis B virus X protein promotes epithelial-mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- The role of the hepatitis B virus genome and its integration in the hepatocellular carcinoma.Frontiers in microbiology · 2024Review
- The FirstMicroorganisms · 2022Article
- Hepatitis B virus X protein promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells by regulating SOCS1.BMB reports · 2022Article
- Article
- Hepatitis B virus X protein promotes vimentin expression via LIM and SH3 domain protein 1 to facilitate epithelial-mesenchymal transition and hepatocarcinogenesis.Cell communication and signaling : CCS · 2021Article
- Characterization of Hepatitis B Virus Integrations Identified in Hepatocellular Carcinoma Genomes.Viruses · 2021Article
- Potential lncRNA Biomarkers for HBV-Related Hepatocellular Carcinoma Diagnosis Revealed by Analysis on Coexpression Network.BioMed research international · 2021Article
- YAP1 Promotes Tumor Invasion and Metastasis in Nasopharyngeal Carcinoma with Hepatitis B Virus Infection.OncoTargets and therapy · 2020Article
- Article
- Long Non-Coding RNA EGOT Promotes the Malignant Phenotypes of Hepatocellular Carcinoma Cells and Increases the Expression of HMGA2 via Down-Regulating miR-33a-5p.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC), and HBV X protein (HBx) serves an essential role in the development of HCC. However, its mechanism remains to be elucidated. The aim of the present study was to investigate the role and mechanism of the HBx protein in the epithelial-mesenchymal transition (EMT) and metastasis of HCC. The HCCLM3 cell line was transfected with a HBx-expressing vector. The effects of HBx overexpression on proliferation, migration, invasion and EMT capacities of the HCCLM3 cell line were evaluated using MTT, migration and invasion assays, and western blotting, respectively. Furthermore, the impact of High mobility group AT-hook 2 (HMGA2) knockdown on HBx-mediated metastasis was investigated in the HCC cell line HCCLM3. The results demonstrated that HBx significantly upregulated HMGA2 expression, and enhanced the proliferation, EMT, invasion and migration in HCC cells. Furthermore, HMGA2 knockdown almost abolished HBx-induced EMT and metastasis in HCC. The results of the present study suggest that HBx promotes the proliferation, EMT, invasion and migration of HCC cells by targeting HMGA2. HMGB2 may serve as a potential therapeutic target for HBV-associated HCC.
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