Cullin 4B (CUL4B) is a component of the Cullin4B-Ring E3 ligase complex (CRL4B) that functions in proteolysis and is implicated in tumorigenesis. Here, we report that CUL4B is associated with tumorigenesis by promoting proliferation and inhibiting apoptosis of human osteosarcoma cells. We performed RNA interference (RNAi) with a lentiviral vector system to silence the CUL4B gene using osteosarcoma SAOS-2 cells. The negative control included the normal target cells infected with the negative control virus whereas the knockdown cells included the normal target cells transfected with the RNAi target virus. We assessed the inhibition resulting from the decreased expression of the CUL4B gene on the proliferation rate of SAOS-2 cells, and also evaluated the cell cycle distribution, apoptosis and clonability. Compared with the negative control, the CUL4B gene expression was significantly inhibited in the SAOS-2 cells at the mRNA and protein levels in the knockdown group (P<0.01). Furthermore, in the knockdown group, the cell proliferation rate and clonability were also significantly inhibited (P<0.01). The apoptosis rate increased significantly (P<0.05). A significant decrease in the number of cells in the G1 phase (P<0.01) and significant increases in the S (P<0.01) and G2 phases (P<0.05) were observed. The silencing of CUL4B gene expression can effectively inhibit osteosarcoma cell proliferation and induce apoptosis. These findings may provide a novel biomarker for the treatment of osteosarcoma.
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http://dx.doi.org/10.3892/or.2014.3465 | DOI Listing |
Acta Neuropathol Commun
December 2024
The Key Laboratory of Experimental Teratology of the Ministry of Education and Department of Genetics, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Hemasphere
July 2024
Department of Hematology Hospital Universitario 12 de Octubre, Spanish National Cancer Research Center (CNIO), Complutense University Madrid Madrid Spain.
Multiple myeloma (MM) is a genetically heterogeneous disease and the management of relapses is one of the biggest clinical challenges. alterations are established high-risk markers and are included in the current disease staging criteria. is the most frequently mutated gene affecting around 20% of MM patients.
View Article and Find Full Text PDFInt Ophthalmol
June 2024
Department of Medical Genetics, Faculty of Medicine, Afyonkarahisar Health Sciences University, Afyonkarahisar, Turkey.
Purpose: Age-related cataract (ARC) is the most common cause of visual impairment and blindness in older adults. However, the role of CUL4B in the ARC remains unclear. Therefore, we investigated CUL4B expression and its effects on apoptosis.
View Article and Find Full Text PDFAm J Transl Res
May 2024
Department of Gastroenterology, Jinan Maternity and Child Care Hospital Affiliated to Shandong First Medical University Jinan 250218, Shandong, China.
Objectives: The purpose of this study is to decipher the role of Cullin family genes in colorectal cancer (CRC), drawing insights from comprehensive analyses encompassing multiple databases and experimental validations.
Methods: UALCAN, GEPIA2, Human Protein Atlas (HPA), KM plotter, cBioPortal, TISIDB, DAVID, colon cancer cell lines culturing, gene knockdown, CCK8 assay, colony formation, and Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) assays.
Results: Initial scrutiny of The Cancer Genome Atlas (TCGA) CRC datasets through the UALCAN and GEPIA databases unveiled significant alterations in Cullin family gene expressions.
Orphanet J Rare Dis
May 2024
Department of Children's Neuro-endocrinology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, Guangdong, China.
Background: Trio-based whole-exome sequencing (trio-WES) enables identification of pathogenic variants, including copy-number variants (CNVs), in children with unexplained neurodevelopmental delay (NDD) and neurodevelopmental comorbidities (NDCs), including autism spectrum disorder (ASD), epilepsy, and attention deficit hyperactivity disorder. Further phenotypic and genetic analysis on trio-WES-tested NDD-NDCs cases may help to identify key phenotypic factors related to higher diagnostic yield of using trio-WES and novel risk genes associated with NDCs in clinical settings.
Methods: In this study, we retrospectively performed phenotypic analysis on 163 trio-WES-tested NDD-NDCs children to determine the phenotypic differences between genetically diagnosed and non-genetically diagnosed groups.
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