Camp, also known as cyclic adenosine monophosphate, is the first discovered second messenger. It plays pivotal roles in cell signaling, regulating numerous physiological and pathological processes [1]. Camp mainly exerts its function through the cAMP-PKA-CREB signaling pathway, where it can regulate the transcription of various target genes via protein kinase A (PKA) and its downstream effector cAMP-responsive element binding protein (CREB). Additionally, PKA can phosphorylate many kinases such as Raf, GSK3 and FAK [1].

Aberrant cAMP-PKA signaling is involved in various human tumors, with cAMP signaling potentially having both tumor-suppressive and tumor-promoting roles depending on tumor types and context. It can regulate cancer cell growth, migration, invasion and metabolism [1]. In the tumor microenvironment (TME), cAMP has pleiotropic effects. Its downstream effectors include PKA, exchange protein activated by cAMP (EPAC) and ion channels. While it can promote cancer cell growth in some cases, it can also inhibit cell proliferation and survival in a context-and cancer type-dependent manner. Targeting cAMP signaling in the TME shows therapeutic benefits in cancer [2].

In conclusion, Camp is a crucial second messenger that regulates a wide range of biological processes, especially those related to cell signaling. Its role in cancer, particularly in the context of the TME, has been revealed through research. Understanding Camp and its associated signaling pathways could provide new insights into tumorigenesis mechanisms and potentially lead to the development of novel cancer therapies.

References:

1. Zhang, Hongying, Kong, Qingbin, Wang, Jiao, Jiang, Yangfu, Hua, Hui. 2020. Complex roles of cAMP-PKA-CREB signaling in cancer. In Experimental hematology & oncology, 9, 32. doi:10.1186/s40164-020-00191-1. https://pubmed.ncbi.nlm.nih.gov/33292604/

2. Zhang, Hongying, Liu, Yongliang, Liu, Jieya, Hua, Hui, Jiang, Yangfu. 2024. cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment. In Journal of hematology & oncology, 17, 5. doi:10.1186/s13045-024-01524-x. https://pubmed.ncbi.nlm.nih.gov/38233872/