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SUMMARY
Phosphatidylinositol 3-kinase (PI3-K) is an essential signaling molecule that is up‐regulated in various cancers. In this research, we examined the molecular mechanisms by which PI3-K expressions is regulated and the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in the early stages of experimental colon carcinogenesis. Group 1 served as the control, group 2 was the negative control, group 3 was treated with the standard drug Xeloda, group 4 and 5 was the extract treated groups including hydroethanol and ethanol respectively. Xeloda treatment resulted significant apoptotic cell death while showing low PI3-K expression as well as Spondias mombin decreases the expression of PI3-K. This study identified that Spondias mombin and Xeloda constitute remarkable chemopreventive targets in mediating apoptosis in the 1,2- dimethyl hydrazine (DMH) induced early Wistar rat colon carcinogenesis via PI3-K/PTEN signaling pathway. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a tumor suppressor gene whose expression is frequently lost in malignancies as seen on induction of carcinogenesis using DMH in the Wistar rats. On treatment with Spondias mombin extracts (hydroethanol and ethanol) led to a significant increase in PTEN expression as well as the standard chemotherapeutic drug, Xeloda.
