ArticleThe Journal of biological chemistry2012
Overexpression of hyaluronan-binding protein 1 (HABP1/p32/gC1qR) in HepG2 cells leads to increased hyaluronan synthesis and cell proliferation by up-regulation of cyclin D1 in AKT-dependent pathway.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Unveiling the mysteries of C1QBP in gynecological tumors (Review).Molecular and clinical oncology · 2026Review
- C1QBP Associated With Immune Infiltration Predicts Poor Prognosis in Lung Adenocarcinoma.Cancer informatics · 2026Article
- p32 regulates glycometabolism and TCA cycle to inhibit ccRCC progression via copper-induced DLAT lipoylation oligomerization.International journal of biological sciences · 2024Article
- C1QBP Mediates Breast Cancer Cell Proliferation and Growth via Multiple Potential Signalling Pathways.International journal of molecular sciences · 2023Article
- gC1qR: A New Target for Cancer Immunotherapy.Frontiers in immunology · 2023Review
- An approach to p32/gC1qR/HABP1: a multifunctional protein with an essential role in cancer.Journal of cancer research and clinical oncology · 2022Review
- Prognostic and functional role of hyaluronan-binding protein 1 in pancreatic ductal adenocarcinoma.Oncology letters · 2022Article
- Overexpression of Multifunctional Protein p32 Promotes a Malignant Phenotype in Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- A low MW inhibitor of CD44 dimerization for the treatment of glioblastoma.British journal of pharmacology · 2020Article
- Overexpression of hyaluronan-binding protein 1 promotes the proliferation, migration, and invasion of malignant glioma.Translational cancer research · 2020Article
- Complement component 1q subcomponent binding protein in the brain of the rat.Scientific reports · 2019Article
- Article
- Multi-functional, multicompartmental hyaluronan-binding protein 1 (HABP1/p32/gC1qR): implication in cancer progression and metastasis.Oncotarget · 2018Review
- Hyaluronic acid binding protein 1 overexpression is an indicator for disease-free survival in cervical cancer.International journal of clinical oncology · 2017Article
- Antibody neutralization of cell-surface gC1qR/HABP1/SF2-p32 prevents lamellipodia formation and tumorigenesis.Oncotarget · 2016Article
- Elevated HABP1 protein expression correlates with progression and poor survival in patients with gastric cancer.OncoTargets and therapy · 2016Article
- Over expression of hyaluronan promotes progression of HCC via CD44-mediated pyruvate kinase M2 nuclear translocation.American journal of cancer research · 2016Article
- Restoration of miR-20a expression suppresses cell proliferation, migration, and invasion in HepG2 cells.OncoTargets and therapy · 2016Article
- Role of PXR in Hepatic Cancer: Its Influences on Liver Detoxification Capacity and Cancer Progression.PloS one · 2016Article
- Complement component 1, q subcomponent binding protein is a marker for proliferation in breast cancer.Experimental biology and medicine (Maywood, N.J.) · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of the mature form of hyaluronan-binding protein 1 (HABP1/gC1qR/p32), a ubiquitous multifunctional protein involved in cellular signaling, in normal murine fibroblast cells leads to enhanced generation of reactive oxygen species (ROS), mitochondrial dysfunction, and ultimately apoptosis with the release of cytochrome c. In the present study, human liver cancer cell line HepG2, having high intracellular antioxidant levels was chosen for stable overexpression of HABP1. The stable transformant of HepG2, overexpressing HABP1 does not lead to ROS generation, cellular stress, and apoptosis, rather it induced enhanced cell growth and proliferation over longer periods. Phenotypic changes in the stable transformant were associated with the increased "HA pool," formation of the "HA cable" structure, up-regulation of HA synthase-2, and CD44, a receptor for HA. Enhanced cell survival was further supported by activation of MAP kinase and AKT-mediated cell survival pathways, which leads to an increase in CYCLIN D1 promoter activity. Compared with its parent counterpart HepG2, the stable transformant showed enhanced tumorigenicity as evident by its sustained growth in low serum conditions, formation of the HA cable structure, increased anchorage-independent growth, and cell-cell adhesion. This study suggests that overexpression of HABP1 in HepG2 cells leads to enhanced cell survival and tumorigenicity by activating HA-mediated cell survival pathways.
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