Project description:Cajanin stilbene acid (CSA) was previously shown to induce cytotoxicity against cancer cells. We have employed microarray gene expression profiling to identify deregulated genes in MCF-7 breast cancer cells upon treatment with CSA and its synthetic derivatives (CSA6, CSA9, CSA19). TGM2 gene encoding transglutaminase 2 was commonly deregulated after treatment with all four CSA compounds. All compounds revealed strong effects on cell cycle progression and DNA damage response. Promoter motif analysis of the deregulated genes further supported the microarray results emphasizing the relevance of transcription factors regulating cell cycle and proliferation, MYC being among the most pronounced ones. Interestingly, cellular movement was among the top five affected cellular functions after treatment with the four derivatives. Gene expression profiling study with Whole Human Genome RNA chips (8M-CM-^W60K Agilent) was performed in MCF-7 breast cancer cells upon treatment with CSA and its synthetic derivatives (CSA6, CSA9, CSA19). Twelve chips were used; control (x2), CSA (x2), control (x2), CSA6 (x2), CSA9 (x2), CSA19 (x2). MCF-7 cells were treated with the compounds (IC50 concentrations) for 72 hours or left untreated (DMSO control). Two independent experiments were performed for each treatment.
Project description:Cajanin stilbene acid (CSA) was previously shown to induce cytotoxicity against cancer cells. We have employed microarray gene expression profiling to identify deregulated genes in MCF-7 breast cancer cells upon treatment with CSA and its synthetic derivatives (CSA6, CSA9, CSA19). TGM2 gene encoding transglutaminase 2 was commonly deregulated after treatment with all four CSA compounds. All compounds revealed strong effects on cell cycle progression and DNA damage response. Promoter motif analysis of the deregulated genes further supported the microarray results emphasizing the relevance of transcription factors regulating cell cycle and proliferation, MYC being among the most pronounced ones. Interestingly, cellular movement was among the top five affected cellular functions after treatment with the four derivatives.
Project description:Retinoic acid (RA) triggers growth-suppressive effects in tumor cells and therefore RA and its synthetic analogs have great potential as anti-carcinogenic agents. RA effects are mediated by retinoic acid receptors (RARs), which regulate gene expression in an RA-dependent manner. To define the genetic network regulated by RARs in breast cancer cells, we identified RAR genomic targets using chromatin immunoprecipitation and expression analysis in a model breast cancer cell line MCF-7. Furthermore, we identified genomic binding sites for two putative RAR coregulators FoxA1 and GATA3. Keywords: ChIP-Chip Analysis
Project description:MDA-MB-231 breast cancer cells and MCF-10A breast cells were exposed to 1 mT 50 Hz extremely low-frequency magnetic field (ELF-MF) for 4 hours
Project description:Time course of response to synthetic progestin ORG2058 in T-47D and ZR-75-1 breast cancer cell lines and in two PR positive clones of the MCF-10A cell line: AB9 and AB32. Transcriptional response to synthetic progestin, 10nM ORG2058, was compared between the four cell lines at three treatment times. T-47D breast cancer cells were treated in triplicate with 10nM ORG2058 or ethanol vehicle and harvested at 2, 6 and 24h after treatment for gene expression profiling
Project description:A fractional mathematical model of breast cancer competition model
Author links open overlay panelJ.E.Solís-PérezaJ.F.Gómez-Aguilar
bA.Atanganac
a
Tecnológico Nacional de México/CENIDET. Interior Internado Palmira S/N, Col. Palmira, C.P. 62490, Cuernavaca, Morelos, México
b
CONACyT-Tecnológico Nacional de México/CENIDET. Interior Internado Palmira S/N, Col. Palmira, C.P. 62490, Cuernavaca, Morelos, México
c
Institute for Groundwater Studies, Faculty of Natural and Agricultural Sciences, University of the Free State, Bloemfontein 9300, South Africa
Abstract
In this paper, a mathematical model which considers population dynamics among cancer stem cells, tumor cells, healthy cells, the effects of excess estrogen and the body’s natural immune response on the cell populations was considered. Fractional derivatives with power law and exponential decay law in Liouville–Caputo sense were considered. Special solutions using an iterative scheme via Laplace transform were obtained. Furthermore, numerical simulations of the model considering both derivatives were obtained using the Atangana–Toufik numerical method. Also, random model described by a system of random differential equations was presented. The use of fractional derivatives provides more useful information about the complexity of the dynamics of the breast cancer competition model.