Cisplatin

Inhibitor of signal transducer and activator of transcription 3 (STAT3) suppresses ovarian cancer growth, migration and invasion and enhances the effect of cisplatin in vitro

Y. J. Tang, Sun, Z. L., Wu, W. G., Xing, J., He, Y. F., Xin, D. M., and Han, P., “Inhibitor of signal transducer and activator of transcription 3 (STAT3) suppresses ovarian cancer growth, migration and invasion and enhances the effect of cisplatin in vitro”, vol. 14, pp. 2450-2460, 2015.

The aim of the present study was to investigate the anti-ovarian cancer effect of the inhibitor of signal transducer and activator of transcription 3 (STAT3), WP1066. Western blot was used to detect the phosphorylation of STAT3 in ovarian cancer cell line SKOV3 and cisplatin-resistant ovarian cancer cell line SKOV3/DDP. MTT and colony-forming assays were performed to evaluate the viability and growth of ovarian cancer cells. The apoptosis of ovarian cancer cells was determined by flow cytometry.

Well-balanced commensal microbiota contributes to anti-cancer response in a lung cancer mouse model

Q. - F. Gui, Lu, H. - F., Zhang, C. - X., Xu, Z. - R., and Yang, Y. - H., “Well-balanced commensal microbiota contributes to anti-cancer response in a lung cancer mouse model”, vol. 14, pp. 5642-5651, 2015.

The intestinal microflora affects inflammation and immunity, not only locally at the mucosal level but also systemically, raising the question of whether the microflora affects inflammatory processes that contribute to cancer and its therapy. Prebiotics have also been found to play an antitumor role that is not limited to the gut. We investigated the antitumor roles of the intestinal microbiota using the Lewis lung cancer mouse model.

Recombinant adenovirus-mediated overexpression of PTEN and KRT10 improves cisplatin resistance of ovarian cancer in vitro and in vivo

H. Wu, Wang, K., Liu, W., and Hao, Q., “Recombinant adenovirus-mediated overexpression of PTEN and KRT10 improves cisplatin resistance of ovarian cancer in vitro and in vivo”, vol. 14, pp. 6591-6597, 2015.

Drug resistance is a major cause of treatment failure in ovarian cancer patients, and novel therapeutic strategies are urgently needed. Overexpression of phosphatase and tensin homolog (PTEN) has been shown to preserve the cisplatin-resistance of ovarian cancer cells, while cisplatin-induced keratin 10 (KRT10) overexpression mediates the resistance-reversing effect of PTEN. However, whether overexpression of PTEN or KRT10 can improve the cisplatin resistance of ovarian cancer in vivo has not been investigated.

Azithromycin enhances the favorable results of paclitaxel and cisplatin in patients with advanced non-small cell lung cancer

D. J. Chu, Yao, D. E., Zhuang, Y. F., Hong, Y., Zhu, X. C., Fang, Z. R., Yu, J., and Yu, Z. Y., “Azithromycin enhances the favorable results of paclitaxel and cisplatin in patients with advanced non-small cell lung cancer”, vol. 13, pp. 2796-2805, 2014.

Although new chemotherapeutic drugs have been applied constantly, their efficacy for non-small cell lung cancer (NSCLC) is still not satisfactory. In recent years, epidemiological investigations have shown that lung cancer may be induced by chronic Chlamydia pneumoniae (Cpn) infection, since stable high titers of Cpn antibodies, especially IgA, are a hallmark of chronic infections.

Effects of cisplatin and panobinostat on human mesothelial (Met-5A) and malignant pleural mesothelioma (MSTO-211H) cells

K. E. Gultekin, Yurdakonar, M. K., Yaman, E., Yuce, U. S., Yilmaz, A., Alp, E., Celik, A., Demiroz, S. M., and Onen, H. I., “Effects of cisplatin and panobinostat on human mesothelial (Met-5A) and malignant pleural mesothelioma (MSTO-211H) cells”, vol. 12, pp. 5405-5413, 2013.

New therapeutic approaches are still needed for effective malignant pleural mesothelioma treatment. The use of classical chemotherapy agents in combination with newly developed molecules may shed light on new therapeutic approaches. We aimed to determine the efficacy of panobinostat, alone and in combination with cisplatin, on cell survival and mRNA expression of FOXO3A, CCND1, and CASP9 genes in both mesothelioma and healthy mesothelial cell lines. Cells were treated with 1-100 μM cisplatin and 25-1000 nM panobinostat.

Pre-treatment with glutamine reduces genetic damage due to cancer treatment with cisplatin

R. J. Oliveira, Sassaki, E. S., Monreal, A. C. D., Monreal, M. T. F. D., Pesarini, J. R., Mauro, M. O., Matuo, R., Silva, A. F., Zobiole, N. N., Siqueira, J. M., Ribeiro, L. R., and Mantovani, M. S., “Pre-treatment with glutamine reduces genetic damage due to cancer treatment with cisplatin”, vol. 12, pp. 6040-6051, 2013.

Cisplatin is an effective antineoplastic drug. However, it provokes considerable collateral effects, including genotoxic and clastogenic activity. It has been reported that a diet rich in glutamine can help inhibit such collateral effects.

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