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- W2230620121 abstract "Proc Amer Assoc Cancer Res, Volume 46, 20052330 There is increasing evidence that activation of the cGMP-dependent enzyme protein kinase G (PKG) can play an important role in inhibiting cell proliferation and inducing apoptosis. The intracellular level of cGMP is regulated through a dynamic balance between its rate of synthesis by guanylyl cyclases (GCs) and its degradation by specific cGMP-phosphodiesterases (PDEs), especially PDEs 2 and 5. In previous studies we found that cGMP-PDE inhibitors, a GC activator, and constitutively activated mutants of PKG Iβ induced apoptosis in SW480 human colon cancer cells (Deguchi et al., Mol. Cancer Ther. 1, 803-809, 2002, and Cancer Res. 64, 3966-3973, 2004). However, the actual profile of components of the cGMP/PKG signaling pathway in human cancers has not been previously studied in detail. In this study, we examined by western blot analysis cellular levels of PDE5, PKG Iβ and phospho-VASP (vasodilator-stimulated phosphoprotein), a marker of PKG activation, in 19 pairs of primary human colon carcinomas and paired adjacent normal colonic mucosa. PKG Iβ was decreased in 54%, PDE5 was increased in 58%, and phospho-VASP was decreased in 89% of the colon tumors. We also did similar assays in several cell lines. When compared to the normal human fetal colon cell line CCD841CoN cells, PDE5 was increased and phospho-VASP was decreased in the colon cancer cell lines SW480, SW620, and DLD1. When compared to MCF-10F normal human mammary epithelial cells, MCF7 human breast cancer cells also displayed an increase in expression of PDE5 and decreased levels of PKG Iβ and phospho-VASP. Furthermore, ras- and raf-transformed Rat6 fibroblasts displayed decreased levels of PKG Iβ and increased levels of PDE5 when compared with the parental Rat6 cells. Taken together, these findings suggest that down-regulation of cGMP/PKG-mediated signaling pathways often occurs during tumorigenesis and cell transformation. These results are consistent with previous evidence indicating that agents that increase the activation of PKG can inhibit growth and induce apoptosis in cancer cells, and provide a rationale for the further development of such agents as a novel strategy for cancer therapy." @default.
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- W2230620121 date "2005-05-01" @default.
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- W2230620121 title "Down-regulation of the cGMP/PKG pathway in primary human colon cancers and cancer cell lines" @default.
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