Advanced renal cell carcinoma (RCC) poses a threat to patient survival. Epigenetic remodelling is the pathogenesis of renal cancer. Histone demethylase 4B (KDM4B) is overexpressed in many cancers through various pathways. However, the role of KDM4B in clear cell renal carcinoma has not yet been elucidated. The differential expression of KDM4B was first verified by analysing public databases. The expression of KDM4B in fresh tissues and pathology slides was further analysed by western blotting and immunohistochemical staining. KDM4B overexpression and knockdown cell lines were also established. Cell Counting Kit-8 (CCK-8) assay was used to detect cell growth. Transwell assays were performed to assess cell migration. Xenografts were used to evaluate tumour growth and metastasis . Finally, KDM4B expression levels associated with copy number variation (CNV) and cell cycle stage were evaluated based on single-cell RNA sequencing data. KDM4B was expressed at higher levels in tumour tissues than in the adjacent normal tissues. High levels of KDM4B are associated with worse pathological features and poorer prognosis. KDM4B also promotes cell proliferation and migration , as well as tumour growth and metastasis . Tumour cells with high KDM4B expression exhibited higher CNV levels and a greater proportion of cells in the G1/S transition phase. Our results confirm that KDM4B promotes the progression of clear cell renal carcinoma, is correlated with poor prognosis, and may be related to high levels of CNV and cell cycle progression.
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http://dx.doi.org/10.1080/15592294.2023.2192319 | DOI Listing |
The integration of conventional omics data such as genomics and transcriptomics data into artificial intelligence models has advanced significantly in recent years; however, their low applicability in clinical contexts, due to the high complexity of models, has been limited in their direct use inpatients. We integrated classic omics, including DNA mutation and RNA gene expression, added a novel focus on promising omics methods based on A>I(G) RNA editing, and developed a drug response prediction model. We analyzed 104 patients from the Breast Cancer Genome-Guided Therapy Study (NCT02022202).
View Article and Find Full Text PDFNat Hum Behav
November 2024
Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Breast Cancer Res
October 2024
Department of Translational Oncology, St. Marianna University Graduate School of Medicine, 2-16-1, Sugao, Miyamae-ku, Kawasaki, 216-8511, Japan.
Background: Epigenetic dysregulation affecting oncogenic transcription and DNA damage response is a hallmark of cancer. The histone demethylase KDM4B, a factor regulating these processes, plays important roles in estrogen receptor-mediated transcription and DNA repair in breast cancer. However, how oncogenic phospho-signal transduction affects epigenetic regulation is not fully understood.
View Article and Find Full Text PDFSci Rep
October 2024
Department of Molecular Biology and Genomics, Institute for Molecular Biology in Medicine and Gene Therapy, Health Sciences University Center, University of Guadalajara, 44340, Guadalajara, Jalisco, Mexico.
NASH is characterized by hepatic lipid accumulation and inflammation; and JMJD2B-a histone demethylase-upregulation has been linked to its progression. Pirfenidone (PFD) is an antifibrotic agent with anti-inflammatory and antioxidant effects recognized to decrease NASH symptoms. Herein, our aim was to investigate PFD-induced epigenetics mechanisms involving JMJD2B and histone modifications in experimental NASH.
View Article and Find Full Text PDFInt J Nanomedicine
October 2024
Department of Endodontics and Periodontics, College of Stomatology, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
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