Article citationsMore>>

Villanueva, J., Vultur, A., Lee, J.T., Somasundaram, R., Fukunaga-Kalabis, M., Cipolla, A.K., et al. (2010) Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K. Cancer Cell, 18, 683695. doi:10.1016/j.ccr.2010.11.023

has been cited by the following article:

• TITLE: Different effects of the inhibition of Src activity on Akt/PKB in melanoma cells with wild BRAF and mutated BRAF V600E

  AUTHORS: Zdena Tuháčková, Jiří Réda, Lubica Ondrušová, Petra Žáková

  KEYWORDS: HBL Melanoma Cells;SK-MEL-5 Melanoma Cells; BRAF V600E mutation; Src Kinase Activity; Akt/PKB Signaling

  JOURNAL NAME: Advances in Biological Chemistry, Vol.3 No.3A, June 21, 2013

  ABSTRACT: Src regulates cell adhesion, invasiveness, motility and growth in cancer cells. In melanoma, accumulating data show that Src inhibition can be effective and may enhance the effects of other agents. Increased Src expression and activity thus has recently become a target for drug therapy. Several melanoma cell lines were exposed to inhibitors of Src activity despite their broad specificity. To examine the particular activity of Src in human melanoma cells, we used SU6656, the selective inhibitor of Src family protein kinases. The activity of Src and cell proliferation were suppressed in HBL human cells, wild type melanoma cells and in SK-MEL-5 human melanoma cells harboring mutant BRAF V600E, upon their treatment with SU6656. The suppression of Src kinase activity had not inhibitory effects on Akt/PKB activity in SK-MEL-5 cells, which we have previously found in HBL cells. This may indicate that changes of Src involvement in the control of Akt/PKB activity and its downstream signaling could be induced by BRAF V600E mutation in SK-MEL-5 cells.