Multidrug resistance (MDR) is a major impediment to successful chemotherapy of gastric cancer. Our aim was to establish an epirubicin-resistant cell subline (AGS/EPI) and to elucidate the mechanisms involved in acquired EPI resistance. The AGS/EPI cell subline developed by exposing parental AGS cells to stepwise increasing concentrations of EPI demonstrated 2.52-fold resistance relative to the AGS cell line, and mRNA expression of the ATP-dependent drug-efflux pump P-glycoprotein (Pgp), more recently known as ABCB1 protein, was similarly upregulated. An AGS/EPI cell subline could thus be effectively established, and MDR mechanism of these cells was shown to be related to the overexpression of mRNA of the ABCB1 gene.
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http://dx.doi.org/10.7314/apjcp.2014.15.16.6849 | DOI Listing |
Cell Rep
December 2024
Department of Medicine and Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. Electronic address:
Androgen receptor (AR) splice variants, of which ARv7 is the most common, are increased in castration-resistant prostate cancer, but the extent to which they drive AR activity is unclear. We generated a subline of VCaP cells (VCaP16) that is resistant to the AR inhibitor enzalutamide (ENZ). AR activity in VCaP16 is driven by ARv7, independently of full-length AR (ARfl), and its cistrome and transcriptome mirror those of ARfl in VCaP cells.
View Article and Find Full Text PDFNPJ Precis Oncol
December 2024
Department of Molecular Biosciences, The University of Kansas, Lawrence, KS, USA.
Triple-negative breast cancer (TNBC) presents therapeutic challenges due to limited targeted treatment options and resistance to chemotherapy drugs, such as doxorubicin. This study investigated doxorubicin resistance mechanisms and a strategy to overcome it. A doxorubicin-resistant cell subline (231-DR) was developed from MDA-MB-231 TNBC cells, and enhanced expression of cellular FLICE-inhibitory protein (cFLIP) in 231-DR cells was identified as a potential driver of the resistance.
View Article and Find Full Text PDFCell Syst
December 2024
National Library of Medicine (NLM), National Institutes of Health (NIH), Bethesda, MD 20892, USA. Electronic address:
Cancer progression is an evolutionary process driven by the selection of cells adapted to gain growth advantage. We present a formal study on the adaptation of gene expression in subclonal evolution. We model evolutionary changes in gene expression as stochastic Ornstein-Uhlenbeck processes, jointly leveraging the evolutionary history of subclones and single-cell expression data.
View Article and Find Full Text PDFPoult Sci
November 2024
Department of Animal Science, Iowa State University, 806 Stange Road, 2255 Kildee Hall, Ames, IA 50011, USA. Electronic address:
The Major Histocompatibility Complex (MHC) is a cluster of genes with primarily immune-related functions. The MHC class I genes are responsible for self- versus non-self-recognition and viral antigen presentation to T lymphocytes. The chicken MHC class I protein binds its cognate antigen(s) over a repertoire spectrum ranging from promiscuous (generalist) to fastidious (specialist).
View Article and Find Full Text PDFCancer Drug Resist
November 2024
N.N. Blokhin National Medical Research Center of Oncology, the Ministry of Health of Russia, Moscow 115522, Russia.
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