dam Digter GSK1292263 proteins Or degrading them are connected. Heat shock proteins Were also embroidered with cell growth and resistance to various cancer treatments that induce apoptosis, associated with it. For example, HSP90 interacts with several key proteins in the F Promotion of the progress of prostate cancer, including normal wild-type and mutated AR, HER2 ErbB2, Src, Abl, Akt and Raf. GRP78 BiP is expressed in high concentrations in a variety of tumors confers resistance to drugs in both cell proliferation and cancer cell dormant. Genetically MODIFIED animal model with reduced GRP78 level barrier fa Significantly to tumor growth. Erh hte tumor cell proliferation, protection against apoptosis, and the F promotion of tumor angiogenesis: The three main mechanisms for GRP78 mediated tumor progression has been proposed. ER stress was placed on the various stages of tumor development in the context. The proposed mechanism is dd in tumorigenesis and angiogenesis occurs before the activation of the UPR cell cycle arrest in G1 and induced activation of p38, which both f to a state Rdern dormancy. When the signals from the apoptotic UPR w During this stage of tumor development induced k Can cancer cells with mutated elements of the apoptotic death escape fate alternative. ER stress induces anti-apoptotic NF B and inhibits p53-dependent-Dependent apoptotic signals.
If the balance of the early development of cancer leans against cell death, ER stress can the dynamic growth of cancer cells by the Erh Increase of angiogenesis to improve. An example is the increased secretion of VEGF induction GRP170 a protein chaperone BiP, which acts as VEGF. Third The unfolded protein response and its effects on GRP78 prognosis of the disease is a marker of UPR activation. A high degree of GRP78 is usually correlates with high histological grade, recurrence and survival in patients with poor breast, liver, prostate, colon and stomach cancer, but there are conflicting reports about the lung. Neuroblastoma is an apparent exception to the abundance of GRP78 more dd and correlates with a better prognosis. A retrospective cohort study of 127 patients with stage II and III breast cancer who were treated with doxorubicin-based chemotherapy showed the relationship between GRP78 positivity t And time to recurrence. Another study showed that breast cancer is the UPR in the majority of F Lle of breast cancer and is activated. Resistance to chemotherapy and hormone therapy Estrogen is known to stimulate the UPR in vitro. UPR activation interacts with Strogenantwort elements and can control the growth of tumors. Overexpression of GRP94 and GRP78 was h more frequently observed in patients with lung cancer and in poorly differentiated tumors or m differentiated strength. A study of adenocarcinoma Esophagus, were GRP78 and GRP94 mRNA h Forth in all tumors. Erh Hte expression can be downloaded from GRP78 and l local tumor growth embroidered in the early tumor stages, w While high expression of GRP78 and GRP94 in advanced stages was as dependent Ngig cellular different Ren stress reactions such as glucose deprivation, hypoxia, or h Your immune response. Has up-regulated expression of GRP78 and GRP94 also reported in the stomach