Ene expression changes within the course of normal brain aging are
Ene expression changes in the course of standard brain aging are sexually PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28499442 L-685458 L-685,458 dimorphic. BMC Cancer (2015) 15:224 DOI 10.1186/s12885-015-1239-RESEARCH ARTICLEOpen AccessChemoresistance is associated with improved cytoprotective autophagy and diminished apoptosis in bladder cancer cells treated together with the BH3 mimetic (-)-Gossypol (AT-101)Jens Mani1, Stefan Vallo1, Stefanie Rakel2, Patrick Antonietti2, Florian Gessler2, Roman Blaheta1, Georg Bartsch1, Martin Michaelis3,4, Jindrich Cinatl3, Axel Haferkamp1 and Donat K el2*AbstractBackground: Acquired resistance to normal chemotherapy causes therapy failure in sufferers with metastatic bladder cancer. 2008;105:15605?0. 14. Nitta RT, Del Vecchio CA, Chu AH, Mitra SS, Godwin AK, Wong AJ. The role on the c-Jun N-terminal kinase 2-alpha-isoform in non-small cell lung carcinoma tumorigenesis. Oncogene. 2011;30:234?4. 15. Strasak AM, Rapp K, Brant LJ, Hilbe W, Gregory M, Oberaigner W, et al. Association of gamma-glutamyltransferase and danger of cancer incidence in males: a prospective study. Cancer Res. 2008;68:3970?. 16. Lee SB, Kim JJ, Chung JS, Lee MS, Lee KH, Kim BS, et al. Romo1 can be a negative-feedback regulator of Myc. J Cell Sci. 2011;124:1911?four. 17. Behrend L, Henderson G, Zwacka RM. Reactive oxygen species in oncogenic transformation. Biochem Soc Trans. 2003;31:1441?. 18. Wei H. Activation of oncogenes and/or inactivation of anti-oncogenes by reactive oxygen species. Med Hypotheses. 1992;39:267?0. 19. Waris G, Ahsan H. Reactive oxygen species: role within the development of cancer and different chronic situations. J Carcinog. 2006;five:14. 20. Day RM, Suzuki YJ. Cell proliferation, reactive oxygen and cellular glutathione. Dose Response. 2005;3:425?2. 21. Zhang H, Forman HJ, Choi J. Gamma-glutamyl transpeptidase in glutathione biosynthesis. Methods Enzymol. 2005;401:468?3. 22. Lin J, Manson JE, Selhub J, Buring PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27693494 JE, Zhang SM. Plasma cysteinylglycine levels and breast cancer danger in females. Cancer Res. 2007;67:11123?. 23. Spear N, Aust SD. Thiol-mediated NTA-Fe(III) reduction and lipid peroxidation. Arch Biochem Biophys. 1994;312:198?02. 24. Franzini M, Corti A, Lorenzini E, Paolicchi A, Pompella A, De CM, et al. Modulation of cell development and cisplatin sensitivity by membrane gamma-glutamyltransferase in melanoma cells. Eur J Cancer. 2006;42:2623?0. Mani et al. BMC Cancer (2015) 15:224 DOI 10.1186/s12885-015-1239-RESEARCH ARTICLEOpen AccessChemoresistance is related with elevated cytoprotective autophagy and diminished apoptosis in bladder cancer cells treated using the BH3 mimetic (-)-Gossypol (AT-101)Jens Mani1, Stefan Vallo1, Stefanie Rakel2, Patrick Antonietti2, Florian Gessler2, Roman Blaheta1, Georg Bartsch1, Martin Michaelis3,4, Jindrich Cinatl3, Axel Haferkamp1 and Donat K el2*AbstractBackground: Acquired resistance to typical chemotherapy causes remedy failure in patients with metastatic bladder cancer. Overexpression of pro-survival Bcl-2 loved ones proteins has been linked using a poor chemotherapeutic response, suggesting that Bcl-2-targeted therapy might be a feasible technique in patients with these tumors. The small-molecule pan-Bcl-2 inhibitor (-)-gossypol (AT-101) is known to induce apoptotic cell death, but may also induce autophagy by way of release with the pro-autophagic BH3 only protein Beclin-1 from Bcl-2. The possible therapeutic effects of (-)-gossypol in chemoresistant bladder cancer and the role of autophagy within this context are hitherto unknown. Methods: Cisplatin (5637rCDDP1000, RT4rCDDP1000) and gemcitabine (5637rGEMCI20, RT4rGEMCI20) chemoresistant sub-lines from the chemo-sensitive bladder cancer cell lines 5637 and RT4 had been established for the investigation of acquired resistance mechanisms.