Oncogene 2002, 21:7001–7010 PubMedCrossRef 14 Xi S, Zhang Q, Dye

Oncogene 2002, 21:7001–7010.PubMedCrossRef 14. Xi S, Zhang Q, Dyer KF, Lerner EC, Smithgall TE, Gooding WE, Kamens J, Grandis JR: Src

kinases RXDX-101 order mediate STAT growth pathways in squamous cell carcinoma of the head and neck. J Biol Chem 2003, 278:31574–31583.PubMedCrossRef 15. Koppikar P, Choi SH, Egloff AM, Cai Selleckchem AZD5363 Q, Suzuki S, Freilino M, Nozawa H, Thomas SM, Gooding WE, Siegfried JM, Grandis JR: Combined inhibition of c-Src and epidermal growth factor receptor abrogates growth and invasion of head and neck squamous cell carcinoma. Clin Cancer Res 2008, 14:4284–4291.PubMedCrossRef 16. Nozawa H, Howell G, Suzuki S, Zhang Q, Qi Y, Klein-Seetharaman J, Wells A, Grandis JR, Thomas SM: Combined inhibition of PLCγ-1 and c-Src abrogates epidermal growth factor receptor-mediated selleck screening library head and neck squamous cell carcinoma invasion. Clin Cancer Res 2008, 14:4336–4344.PubMedCrossRef 17. Loganzo F, Dosik JS, Zhao Y, Vidal MJ, Nanus DM, Sudol M, Albino AP: Elevated expression of protein tyrosine kinase c-Yes, but not c-Src, in human malignant melanoma. Oncogene 1993, 8:2637–2644.PubMed 18. Marchetti D, Parikh N, Sudol M, Gallick GE: Stimulation of the protein tyrosine kinase c-Yes but not c-Src by neurotrophins in human brain-metastatic melanoma cells. Oncogne 1998, 16:3253–3260.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions JHL, MKC

designed the study and SHN, SHL, YJL carried out western blotting. DWK, MYP and DJJ carried out immunohistochemistry and JHL, MKC drafted the manuscript. J-KP, CHK, SGK participated in the manuscript drafting and performed the statistical analysis. All authors read and approved the final manuscript.”
“Background The current treatment of hepatocellular carcinoma, especially hepatocellular carcinoma in middle and advanced stages, is a comprehensive therapy using a combination of surgery and chemotherapy.

Chemotherapy plays a critical role in the treatment of hepatocellular carcinoma. Nevertheless, multi-drug resistance (MDR) [1, 2] of hepatocellular carcinoma cells to multiple chemotherapeutics renders chemotherapy for hepatoma insufficient. Therefore, the target of drug resistance and its reverse strategy is one of the hotspots of www.selleck.co.jp/products/Rapamycin.html hepatocellular carcinoma research. Establishing a reliable tumor MDR model is the foundation for the study of tumor MDR and its reversal. In this study, we established three different human hepatocellular carcinoma drug-resistance cell sub-lines of Bel-7402/ADM by applying ADM by three normal methods. We compared the biological characteristics the three cell sub-lines to acquire a comparatively ideal drug-resistance model which paved the way for revealing the clinical multidrug resistance phenomenon and the screening of a reversal agent. Materials and methods Cells and Animals Human hepatocellular carcinoma cell line Bel-7402 was purchased from Shanghai Institute of Biological Products.

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