ArticleJournal of cellular biochemistry2013
Methylation of the PTPRO gene in human hepatocellular carcinoma and identification of VCP as its substrate.
Article in Journal of cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Upregulation of PTPRO by WT1 alleviates podocyte injury in diabetic nephropathy through inhibiting the c-Abl/p53 pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Impact of Protein Phosphatase Expressions on the Prognosis of Hepatocellular Carcinoma Patients.ACS omega · 2024Article
- Age-related decline in hippocampal tyrosine phosphatase PTPRO is a mechanistic factor in chemotherapy-related cognitive impairment.JCI insight · 2023Article
- Valosin-Containing Protein (VCP)/p97: A Prognostic Biomarker and Therapeutic Target in Cancer.International journal of molecular sciences · 2021Review
- Regulatory Functions of Protein Tyrosine Phosphatase Receptor Type O in Immune Cells.Frontiers in immunology · 2021Review
- PTPRO is a therapeutic target and correlated with immune infiltrates in pancreatic cancer.Journal of Cancer · 2021Article
- PTPRO predicts patient prognosis and correlates with immune infiltrates in human clear cell renal cell carcinoma.Translational cancer research · 2020Article
- [Estrogen and its receptors in hepatitis B virus-related hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2019Review
- Review
- Increased PTPRA expression leads to poor prognosis through c-Src activation and G1 phase progression in squamous cell lung cancer.International journal of oncology · 2017Article
- Article
- Defining the Protein-Protein Interaction Network of the Human Protein Tyrosine Phosphatase Family.Molecular & cellular proteomics : MCP · 2016Article
- PTPROt-mediated regulation of p53/Foxm1 suppresses leukemic phenotype in a CLL mouse model.Leukemia · 2015Article
- Receptor-type protein tyrosine phosphatases in cancer.Chinese journal of cancer · 2015Review
- Downregulation of miR-221/222 enhances sensitivity of breast cancer cells to tamoxifen through upregulation of TIMP3.Cancer gene therapy · 2014Article
- Aberrant PTPRO methylation in tumor tissues as a potential biomarker that predicts clinical outcomes in breast cancer patients.BMC genetics · 2014Article
- Role of estrogen in hepatocellular carcinoma: is inflammation the key?Journal of translational medicine · 2014Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
We have previously reported that the gene encoding protein tyrosine phosphatase receptor type-O (PTPRO) is suppressed by promoter methylation in a rat model of hepatocellular carcinoma (HCC) and it functions as tumor suppressor in leukemia and lung cancer. Here, we explored the methylation and expression of PTPRO as well as its function in human HCC. MassARRAY analysis of primary human HCC and matching liver samples (n = 24) revealed significantly higher (P = 0.004) methylation density at the promoter CGI in tumors. Combined bisulfite restriction analysis (COBRA) of another set of human HCC samples (n = 17) demonstrated that the CGI was methylated in 29% of tumors where expression of PTPRO was lower than that in corresponding matching livers. A substrate-trapping mutant of PTPRO that stabilizes the bound substrates was used to identify its novel substrate(s). VCP/p97 was found to be a PTPRO substrate by mass spectrometry of the peptides pulled down by the substrate-trapping mutant of PTPRO. Tyrosyl dephosphorylation of VCP following ectopic expression of wild-type PTPRO in H293T and HepG2 cells confirmed that it is a bona fide substrate of PTPRO. Treatment of PTPRO overexpressing HepG2 cells with Doxorubicin, a DNA damaging drug commonly used in therapy of primary HCC, sensitized these cells to this potent anticancer drug that correlated with dephosphorylation of VCP. Taken together, these results demonstrate methylation and downregulation of PTPRO in a subset of primary human HCC and establish VCP as a novel functionally important substrate of this tyrosine phosphatase that could be a potential molecular target for HCC therapy.
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