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. 2018 Oct 4;19(10):3027. doi: 10.3390/ijms19103027

Table 2.

Putative receptors stimulated by cordycepin and their downstream targets.

Receptors Downstream Targets References
Adenosine receptors (ADORAs) ADORA2A Induced apoptosis via ADORA2A receptor-p53-caspase-7-PARP pathway in C6 glioma cells. [27]
ADORA3 Inhibition of the tumor growth was antagonized by a selective adenosine A3 receptor agonist, MRS1191 1, in mouse melanoma and lung carcinoma cells via the radioligand binding assay. The involvement of adenosine A3 receptors was confirmed with the use of MRS1523 2 and MRS1220 3. [28,29,30]
Death receptors (DRs) DR3 Induced apoptosis of the human colon cancer cell HT-29 via the elevation of DR3, caspase-8, caspase-1, cleaved caspase-3 and cleaved PARP expression. [31]
DR5 Caused an elevation of the levels of Fas, death receptor 5 (DR5), proapoptotic BAX, and decreased anti-apoptotic Bcl-2 level. [32]
Epidermal growth factor receptor (EGFR) Inhibited cell proliferation and induced apoptosis via the EGFR signaling pathway in the human lung cancer cell H1975. The caspase-3 and BAX protein levels were increased, while phosphorylated expression levels of EGFR, AKT, and ERK1/2 were decreased. [47,55]

1 T3-ethyl 5-benzyl 2-methyl-6-phenyl-4-phenylethynyl-1,4-(±)-dihydropyridine-3,5-dicarboxylate; 2 3-Propyl-6-ethyl-5-[(ethylthio)carbonyl]-2 phenyl-4-propyl-3-pyridine carboxylate; 3 N-[9-Chloro-2-(2-furanyl)[1,2,4]-triazolo[1,5-c]quinazolin-5-yl]benzene acetamide.