Table 1.
Role of Nitric Oxide (NO) in Various Cancer Types.
Cancer type | Role of NO | Outcome | Reference |
---|---|---|---|
Prostate | Positive | In vivo tumor inhibition: This study validates the significance of NO on inhibition of castration-resistant prostate cancer (CRPC) tumors through tumor microenvironment (TME) | Arora et al. (2018) |
Shows the ability of NO to attenuate hypoxia-induced progression of prostate cancer | Siemens et al. (2009) | ||
Small molecules able to inhibit WNT and androgen receptor (AR) signaling via NO release represent a promising platform for the development of new compounds for the treatment of CRPC | Laschak et al. (2012) | ||
Inhibits epithelial–mesenchymal transition. Treatment of human prostate metastatic cell lines with the NO donor, DETANONOate, inhibits epithelial–mesenchymal transition and reverses both the mesenchymal phenotype and the cell-invasive properties | Baritaki et al. (2010) | ||
Inhibits cellular proliferation. GIT-27NO, an NO donor, inhibited in vivo prostate cancer cell growth of PC3 and LnCap cells | Donia et al. (2009) | ||
Lung | Positive | Decrease in epithelial–mesenchymal transition. NO serves a critical role in preserving an epithelial phenotype and in attenuating epithelial–mesenchymal transition in alveolar epithelial cells | Vyas-Read et al. (2007) |
Negative | Promotes angiogenesis. In vivo, NO has a role in maintaining tumor blood supply, and we provide early clinical evidence that inhibition of NO synthesis has tumor antivascular activity | Ng et al. (2007) | |
Gastric | Positive | Inhibits cellular proliferation. Cell growth suppression via NO may be mediated through Akt signaling | Sang et al. (2011) |
Ovarian | Negative | Promotes cellular proliferation. While NO was reduced, there was inhibited cell proliferation in HOC-7 cells | Keith Bechtel and Bonavida (2001) |
Breast | Negative | Promotes cellular proliferation. Via inactivation of RAS, there is an NO-induced increase in proliferation | Pervin et al. (2007) |
Hepatic | Positive | Promotes apoptosis. In high doses, NO was able to promote apoptosis via p38MAP-kinase | Wang et al. (2011) |
Negative | Inhibits apoptosis. In low doses, NO inhibited apoptosis via iNOS/akt/surviving axis | Wang et al. (2011) |