Is Rab25 a tumor promoter or suppressor--context dependency on RCP status?
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.
Tang
Bor Luen
BL
Department of Biochemistry, Yong Loo Lin School of Medicine, National University Health Service, National University of Singapore, 8 Medical Drive, Singapore, 117597, Singapore. bchtbl@nus.edu.sg
D048868:Adaptor Proteins, Signal Transducing / Q000502:physiology*; D002273:Carcinogens; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology*; D009857:Oncogenes / Q000502:physiology*; D025521:Tumor Suppressor Proteins / Q000502:physiology*; D020691:rab GTP-Binding Proteins / Q000502:physiology*
D048868:Adaptor Proteins, Signal Transducing; D002273:Carcinogens; D008565:Membrane Proteins; C488966:RAB11FIP1 protein, human; C509763:Rab25 protein, human; D025521:Tumor Suppressor Proteins; D020691:rab GTP-Binding Proteins