Tang Bor Luen
Department of Biochemistry, Yong Loo Lin School of Medicine, National University Health Service, National University of Singapore, 8 Medical Drive, Singapore, 117597, Singapore.
Tumour Biol. 2010 Aug;31(4):359-61. doi: 10.1007/s13277-010-0030-z. Epub 2010 Apr 8.
Conflicting reports in the literature suggest that Rab25 could either be a context dependent promoter or suppressor of tumorigenesis. We hypothesized that whether Rab25 acts as a promoter or suppressor in tumor progression depends on the expression status of its effector, the Rab coupling protein (RCP). An elevated expression of RCP resulting from genomic amplification may enhance Rab25's tumor progression activity. Elevation of Rab25 alone may sequester endogenous RCP, and attenuates its activating effect on other oncogenic products, such as mutant Ras.
文献中的相互矛盾的报道表明，Rab25可能是肿瘤发生的背景依赖性促进因子或抑制因子。我们推测，Rab25在肿瘤进展中是作为促进因子还是抑制因子，取决于其效应器Rab偶联蛋白（RCP）的表达状态。基因组扩增导致的RCP表达升高可能会增强Rab25的肿瘤进展活性。单独升高Rab25可能会隔离内源性RCP，并减弱其对其他致癌产物（如突变型Ras）的激活作用。
