Abstract
Metastasis is known as the most life-threatening event in cancer patients. In principle, the immune system can prevent tumor development. However, dysfunctional T cells may fail to eliminate the tumor cells effectively and provide additional survival advantages for tumor proliferation and metastasis. Constitutive activation of Ras-associated protein1 (Rap1) has not only led to T cell anergy, but also inhibited autophagy and supported cancer progression through various oncogenic events. Inhibition of Rap1 activity with its negative regulator, Rap1GAP, impairs tumor progression. However, active Rap1 reduces tumor invasion in some cancers, indicating that the pleiotropic effects of Rap1 signaling in cancers could be cancer-specific. All in all, targeting Rap1 signaling and its regulators could potentially control carcinogenesis, metastasis, chemoresistance and immune evasion. Rap1GAP could be a promising therapeutic target in combating cancer.
Highlights
Cancer has been identified as a major public health problem and the leading cause of death in developed and developing countries
The overexpression of Rap1GAP in pancreatic cancer cells enhances the basal apoptotic rates and increases drug sensitivity such as 5-fluorouracil (5-FU) and etoposide [59]. These results suggest that the downregulation of Rap1GAP in pancreatic cancer cells may protect the cells from drug-induced apoptosis
The Ras-associated protein1 (Rap1) signaling is clearly shown to play a role in tumor promotion, through the activation of other signaling pathways such as MAPK/ERK, steroid receptor coactivator (Src)/FAK, or other novel pathways which have not been elucidated
Summary
Cancer has been identified as a major public health problem and the leading cause of death in developed and developing countries. Activated in orderinto to kill the cancer cells Cellularcells adhesion such as integrins and the Ttumors cells infiltrate tumors in order to [12,13]. Requires twothen signals to become fully antigens activated; via MHC class I molecules (CTL)complex, requires two signals to become first, the interaction of T cell receptor (TCR) with. In vivo study showed that increased active Rap in T lymphocytes was associated with enhanced T cell receptor (TCR)-mediated response and increased integrin activation [20]. These findings clearly indicate that Rap plays a crucial role in mediating integrin activation in T cells via inside-out signaling cascades. The dysregulation of Rap signal has been evidenced in tumor invasion and metastasis
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