Background: Histone demethylase JARID1B plays several context dependent roles in epigenetic regulation of cellular differentiation in normal development and is highly expressed in multiple human cancers. The protein is a strong transcriptional repressor capable of downregulating numerous genes. There are three splicing isoforms of JARID1B, however the links between the protein structure and function are not clear. The expression pattern of JARID1B in human melanoma seems to be different from observed in other cancers. Moreover, up to now no data on the impact of JARID1B expression in cutaneous melanoma on the patients' prognosis have been reported.
Methods: We investigated immunohistochemically the association of intratumoral expression of total JARID1B protein and its RBP2-H1 isoform in primary and metastatic melanomas with prognosis for the patients.
Results: Expression of both total JARID1B protein and its RBP2-H1 variant was found in all the melanomas investigated. Our results indicate, however, that only high (above 90% of the cells) intratumoral expression of RBP2-H1 can be considered prognostic factor associated with worse overall survival of the patients.
Conclusions: Such results if considered together with data demonstrating a switch to enhanced expression of RBP2-H1 at early stages of malignant transformation of melanocytes are in agreement with hypothetical crucial role of JARID1B in the course of melanoma development and progression and suggest that altered splicing of JARID1B may be important factor increasing melanoma aggressiveness.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731204 | PMC |
| http://dx.doi.org/10.1186/s12885-017-3836-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Endothelial KDM5B Regulated by Piezo1 Contributes to Disturbed Flow Induced Atherosclerotic Plaque Formation.
J Cell Mol Med
December 2024
Cyrus Tang Medical Institute, Soochow University, Suzhou, China.
Epigenetic modifications play an important role in disturbed flow (d-flow) induced atherosclerotic plaque formation. By analysing a scRNA-seq dataset of the left carotid artery (LCA) under d-flow conditions, we found that Jarid1b (KDM5B) was upregulated primarily in a subcluster of endothelial cells in response to d-flow stimulation. We therefore investigated the mechanism of KDM5B expression and the role of KDM5B in endothelial cell.
View Article and Find Full Text PDFPGC1α as a downstream effector of KDM5B promotes the progression of androgen receptor-positive and androgen receptor-negative prostate cancers.
Am J Cancer Res
September 2024
Department of Pathology and Laboratory Medicine, University of Rochester Medical Center Rochester, NY 14642, USA.
PPARγ coactivator-1α (PGC1α), as a co-activator, is known to optimize the action of several transcription factors, including androgen receptor (AR). However, the precise functions of PGC1α in prostate cancer, particularly those via the non-AR pathways, remain poorly understood. Meanwhile, our bioinformatics search suggested that PGC1α could be a direct downstream target of lysine-specific demethylase 5B (KDM5B/JARID1B/PLU1).
View Article and Find Full Text PDFLncRNA HOXC-AS3 accelerates malignant proliferation of cervical cancer cells via stabilizing KDM5B.
J Cancer Res Clin Oncol
June 2024
Department of Obstetrics and Gynecology, Suzhou Wuzhong People's Hospital, Jiangsu Province, No. 61, Dongwu North Road, Suzhou City, 215128, China.
Background: Cervical cancer (CC) is a common malignancy amongst women globally. Ubiquitination plays a dual role in the occurrence and development of cancers. This study analyzed the mechanism of long noncoding RNA HOXC cluster antisense RNA 3 (lncRNA HOXC-AS3) in malignant proliferation of CC cells via mediating ubiquitination of lysine demethylase 5B (KDM5B/JARID1B).
View Article and Find Full Text PDFKDM5B promotes SMAD4 loss-driven drug resistance through activating DLG1/YAP to induce lipid accumulation in pancreatic ductal adenocarcinoma.
Cell Death Discov
May 2024
Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, P. R. China.
Inactivated suppressor of mothers against decapentaplegic homolog (SMAD) 4 significantly affects cancer development in pancreatic ductal adenocarcinoma (PDAC). However, the contribution of smad4 loss to drug resistance in PDAC is largely undetermined. In the present study, we reported that the loss of SMAD4 endows PDAC cells the ability to drug resistance through upregulating histone lysine demethylase, Lysine-Specific Demethylase 5B (KDM5B, also known as JARID1B or PLU1).
View Article and Find Full Text PDFJARID1B represses the osteogenic potential of human periodontal ligament mesenchymal cells.
Oral Dis
September 2024
School of Dentistry, Health Science Institute, Paulista University, São Paulo, Brazil.
Background: Here, we evaluated whether the histone lysine demethylase 5B (JARID1B), is involved in osteogenic phenotype commitment of periodontal ligament cells (PDLCs), by considering their heterogeneity for osteoblast differentiation.
Materials And Methods: Epigenetic, transcriptional, and protein levels of a gene set, involved in the osteogenesis, were investigated by performing genome-wide DNA (hydroxy)methylation, mRNA expression, and western blotting analysis at basal (without osteogenic induction), and at the 3rd and 10th days of osteogenic stimulus, in vitro, using PDLCs with low (l) and high (h) osteogenic potential as biological models.
Results: h-PDLCs showed reduced levels of JARID1B, compared to l-PDLCs, with significant inversely proportional correlations between RUNX2 and RUNX2/p57.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!