Bmi1 gene silencing inhibits the proliferation and invasiveness of human hepatocellular carcinoma cells and increases their sensitivity to 5-fluorouracil.

Oncol Rep

Department of Hepato-Pancreato-Biliary Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, Guangdong Province, PR China.

Published: March 2013

The Bmi1 gene has been reported to play important roles in cancer initiation and progression. The aim of this study was to investigate the effects of RNA interference (RNAi)-mediated silencing of Bmi1 gene expression on the proliferation and invasiveness of hepatocellular carcinoma (HCC) cells and on the efficacy of chemotherapy in HCC patients. The Bmi1 gene was silenced by Bmi1-siRNA (small interfering RNA) in the human HCC cell lines HepG2 and Bel-7402, and the gene expression levels were assayed by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting. The proliferation and migration of Bmi1-silenced tumor cells and their sensitivity to 5-FU treatment were determined by Cell Counting Kit-8 (CCK-8), transwell assays and 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, respectively. Bmi1-siRNA inhibited the Bmi1 expression at both the mRNA and protein levels in HCC cells. Proliferation and migration of HCC cells treated with Bmi1-siRNA was significantly lower compared to that of the control cells. Moreover, Bmi1 gene silencing increased the percentage of apoptotic cells treated by 5-FU and decreased the IC50 values of 5-FU to a greater extent. Downregulation of the Bmi1 gene by RNAi can inhibit the proliferation and invasivesness of HCC cells and increase their sensitivity to 5-FU treatment.

Download full-text PDF

Source
http://dx.doi.org/10.3892/or.2012.2189DOI Listing

Publication Analysis

Top Keywords

bmi1 gene
24
hcc cells
16
gene silencing
8
proliferation invasiveness
8
hepatocellular carcinoma
8
cells
8
gene expression
8
proliferation migration
8
sensitivity 5-fu
8
5-fu treatment
8

Similar Publications

Salivary gland carcinomas encompass a broad group of malignant lesions characterized by varied prognoses. Stem cells have been associated with the potential for self-renewal and differentiation to various subpopulations, resulting in histopathological variability and diverse biological behavior, features that characterize salivary gland carcinomas. This study aims to provide a thorough systematic review of immunohistochemical studies regarding the expression and prognostic significance of stem cell markers between different malignant salivary gland tumors (MSGTs).

View Article and Find Full Text PDF

Introduction: Hematologic malignancies, originating from uncontrolled growth of hematopoietic and lymphoid tissues, constitute 6.5% of all cancers worldwide. Various risk factors including genetic disorders and single nucleotide polymorphisms play a role in the pathogenesis of hematologic malignancies.

View Article and Find Full Text PDF

Optimizing Stem Cell Expansion: The Role of Substrate Stiffness in Enhancing Dental Pulp Stem Cell Quiescence and Regeneration.

J Endod

January 2025

Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; Department of Dentistry, Mt. Sinai Hospital, Toronto, ON, Canada. Electronic address:

Introduction: Quiescent stem cells exhibit unique self-renewal and engraftment abilities vital for regenerative therapies, but these diminish during ex vivo culture. This study investigates how substrate stiffness regulates the balance between dental pulp stem cell (DPSC) quiescence, activation, and senescence and explores the role of extracellular matrix stiffness in modulating DPSC fate via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.

Methods: Polydimethylsiloxane substrates with varying stiffness in 2D (2 kPa, 50 kPa) and 3D (50 kPa) were fabricated.

View Article and Find Full Text PDF

Background: B-cell specific Moloney MLV insertion site-1 (Bmi-1) belongs to the polycomb group (PcG) gene and is a transcriptional suppressor to maintain appropriate gene expression patterns during development. To investigate whether the Bmi-1 gene has a corrective effect on bone senescence induced in Bmi-1 mice through regulating the bone microenvironment.

Methods: Littermate heterozygous male and female mice (Bmi-1) were used in this study.

View Article and Find Full Text PDF

Background: Glioblastoma (GBM) is the most common primary brain tumor in adults and has a median survival of less than 15 months. Advancements in the field of epigenetics have expanded our understanding of cancer biology and helped explain the molecular heterogeneity of these tumors. B-cell-specific Moloney murine leukemia virus insertion site-1 (Bmi-1) is a member of the highly conserved polycomb group (PcG) protein family that acts as a transcriptional repressor of multiple genes, including those that determine cell proliferation and differentiation.

View Article and Find Full Text PDF

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!