Stem cells. BSI-201 Iniparib hsamiR 520H has also shown that ABCG2 down-regulated expression, resulting in inhibition of migration and invasion of pancreatic cancer cells. Another miRNA, miR 328, is also intended as ABCG2 gene and reduced the levels of ABCG2 mRNA and protein by cleavage of mRNA. The proximal element miRNA reaction ABCG2 is in position 3, ABCG2 mRNA UTR is in various cancer cell lines. Interestingly, it was found that the Mutma Went Lichen MREs lost of ABCG2 in the resistant cells and therefore resistant cancer cells, k Can ABCG2 mediated mRNA degradation and repression of the synthesis of escaped proteins by micro-RNAs, leading to an overexpression of ABCG2.
Although misfolded ABCG2 proteins, such as Cys592 and Cys608 mutants lacking the intramolecular disulfide bond and loss of membrane transport and correct the mutant Asn596 lose N-glycosylation site was shown to be removed from ER by retrograde translocation compartment cytosol, ubiquitinated by ubiquitin ligase and degraded by the proteasome, wild-type ABCG2 is degraded in the lysosomes. Endocytosis Flavopiridol and degradation of wild-type ABCG2 ABCG2 inhibitors can also be accelerated in the lysosome. Recently it was found that a new inhibitor of ABCG2, PZ 39, does not inhibit ABCG2 function only, but also causes conformational Changes and accelerates the degradation of ABCG2 by endocytosis and transport to lysosomes. Sp Ter it was found that there is a dynamic group of ABCG2 inhibitors nnte accelerate the degradation in lysosomes ABCG2 k. These inhibitors k Can also detract from newly synthesized ER ABCG2 and direct them to lysosomes for degradation or degradation of the ER-associated.
In fact, in a recent study found that Derlin 1, a protein that is part of a complex that mediates ERAD, the removal of the f wild-type ABCG2 Funded by the suppression of ER to Golgi transport. Although the human ABCG2 is widely expressed in normal tissues, the overexpression of ABCG2 h Frequently in various drugs was selected Found hlt cancer cell lines and tr Gt to the clinical MDR h Hematopoietic malignancies Ethical and solid tumors. Gain Markets expression of ABCG2 has also been linked to cancer stem cells in combination. ABCG2 in MDR cancer cell lines above mentioned HNT was ABCG2 originally from a cell line MCF breast cancer adriamycin weight Hlten 7/AdVp3000, the Best RESISTANCE Against a variety detected by cytotoxic agents, confinement Cloned Lich including normal mitoxantrone, doxorubicin and daunorubicin , but not to an increase increase the expression of ABCB1 or ABCC1.
An overexpression of ABCG2 has been found in and correlated with the MDR Ph Genotypes of many drugs selected Cancer cell lines, elected by different tumor types, including normal topotecan ovarian tumor cell line selected Hlt T8, mitoxantrone selected Hlt cell lines c cancer lon S1 M1 80 and HT29, SN 38 selected hlt human small cell lung cancer cells PC 6/SN2 5, mitoxantrone selected hlt human gastric carcinoma cell line EPG85 257RNOV, gefitinib-resistant non-small cell lung cancer, epirubicin resistant human hepatocytes HLE PPE-carcinoma , and topotecan and doxorubicin human multiple myeloma cells. However, the difference between the resistance profiles of ABCG2-mediated drug found in these cell lines, which are at various cell origin or the involvement of other factors, drug resistance due to the different weight Attributed hlt. Recently, several other guy