ArticleExperimental & molecular medicine2016
RBP2 induces stem-like cancer cells by promoting EMT and is a prognostic marker for renal cell carcinoma.
Article in Experimental & molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 54 citations in OpenAlex.
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- miR-181d/RBP2/NF-κB p65 Feedback Regulation Promotes Chronic Myeloid Leukemia Blast Crisis.Frontiers in oncology · 2021Article
- FAT4 silencing promotes epithelial-to-mesenchymal transition and invasion via regulation of YAP and β-catenin activity in ovarian cancer.BMC cancer · 2020Article
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- HSPD1 repressed E-cadherin expression to promote cell invasion and migration for poor prognosis in oral squamous cell carcinoma.Scientific reports · 2019Article
- Controlling metastatic cancer: the role of phytochemicals in cell signaling.Journal of cancer research and clinical oncology · 2019Review
- Biology and targeting of the Jumonji-domain histone demethylase family in childhood neoplasia: a preclinical overview.Expert opinion on therapeutic targets · 2019Review
- Pathogenic and Therapeutic Role of H3K4 Family of Methylases and Demethylases in Cancers.Indian journal of clinical biochemistry : IJCB · 2019Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal cell carcinoma (RCC), one of the most common kidney cancers, has a poor prognosis. Epithelial to mesenchymal transition (EMT) is a hallmark of carcinoma invasion and metastasis. Several studies have examined the molecular regulation of EMT, but the relationship between histone demethylases and EMT is little understood. In this study, we investigated the role of retinoblastoma-binding protein-2 (RBP2), a histone demethylase that is highly expressed in RCC and is positively correlated with poor RCC prognosis in the regulation of EMT. We found that ectopic overexpression of RBP2 can induce cancer stem cell-like (CSC) phenotypes through EMT in RCC cells by converting them to a more mesenchymal phenotype. This results in increased resistance to apoptosis, which leads to enhanced tumor growth in xenograft models. Together, our data show that RBP2 is an epigenetic regulator that has an important role in the initiation of CSC phenotypes through EMT, leading to tumor progression. RBP2 is also a novel biomolecule for RCC diagnosis, and prognosis and may be a therapeutic target.
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