SIU is as ABCG2 revealed placental syncytiotrophoblast expressed in the epithelium of the small intestine, and c Lon, liver kanalikul Re membranes and canals, and L le Bargains Of breast tissue. ABCG2 expression was observed in the luminal membrane of epithelial cells in the normal gall bladder, alveolar Ren pneumocytes, sebaceous glands, interstitial Brivanib BMS-540215 cells of the testes, prostate epithelium, endocervical cells in the building Rmutter who recognized the squamous cervical cells Many Langerhans and acinar cells of the pancreas, the adrenal zona reticularis layer tubules, hepatocytes and renal cortex. ABCG2 is also in the curves Sen and capillary endothelium. Furthermore, ABCG2 is Haupts Chlich in the plasma membranes of cells located in the tissues mentioned above HNT, many of whom harbor secretory or barrier function.
The distribution pattern of the specific ABCG2 is closely related to r The physiological human ABCG2. Erh Hte expression of ABCG2 is often seen in both resistant cell lines and clinical tumor tissues. The expression of ABCG2 in normal AV-951 cells and cancer cells apparently at different levels confinement, Lich gene amplification, epigenetic modifications, transcriptional and post-transcriptional regulation can be regulated. Gene amplification by polymerase chain reaction has long been considered one of the main reasons for the increased Recognized hte expression of ABCB1. It was therefore assumed that the increased be Hte expression of ABCG2 in resistant cancer cells, k Nnte also due to gene amplification.
The first report of the ABCG2 gene amplification was a study of some cell lines MCF-7 derived mitoxantroneselected by Southern blot analysis. This finding was verified with the latest comparative genomic hybridization and Southern blot of MCF-7 / MX cells and adriamycin in MCF 7/AdVp3000 labeled cells. The cell line MCF-7 parental mitoxantronesensitive had, however, no amplification Rkung or chromosomal translocation of the ABCG2 gene. It has also been shown that the Best RESISTANCE against SN 38 positively correlated in colon cancer cells with ABCG2 gene amplification, suggesting that gene amplification ABCG2 not restricted to MCF-7 cells Nkt breast cancer. With the gradual selected SF295 glioblastoma cell line hlten against mitoxantrone in combination with Southern blot and fluorescence in situ hybridization, Rao et al.
investigated the mechanisms of ABCG2 gene amplification in drug selection. It has been found that the double minute chromosomes for the ABCG2 gene amplification in resistant SF395 cell lines with a low concentration of mitoxantrone selected Hlt is. However, in the cell lines with a high concentration of mitoxantrone selected Is hlt, the ABCG2 gene amplification seems to be due to chromosomal reintegration of the amplicon to several chromosomes, to produce a more stable genotype. Moreover, epigenetic regulation of gene amplification found ABCG2 also genehas that are regulated epigenetically. Demethylation of the ABCG2 gene was found to affect the Erh Increase ABCG2 expression in human cells of multiple myeloma. Methylation of ABCG2 gene was found in renal cell carcinoma cell lines with demethylating agents and the treatment is obtained Ht ABCG2 expression. Chromatin Immunopr Zipitation shown that the methylated ABCG2 promoter with the methyl-CpG Islan interacted