Isovitexin attenuates tumor growth in human colon cancer cells through the modulation of apoptosis and epithelial-mesenchymal transition via PI3K/Akt/mTOR signaling pathway.

Abstract

Isovitexin, a biologically active flavone C-glycosylated derivative, has a variety of biological activities. We aimed to identify the effect of isovitexin (Isov) on colon cancer. Human colonic epithelial cells (HCECs) and cancer cells were treated with Isov and Cell Counting Kit-8 (CCK8) was used to detect cell proliferation and calculate the half-inhibitory concentration (IC50). The biological activity of cancer cells was assessed. The tumor size and volume were recorded. Protein expression levels were analyzed by western blotting. Isov inhibited cancer cell proliferation but had little cytotoxicity on HCECs. Isov significantly attenuated cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and induced cell apoptosis., This trend was blocked by insulin-like growth factor-1 (IGF-1) treatment. The expression levels of phosphorylated phosphatidylinositol 3-kinasep (p-PI3K), phosphorylated protein kinase B (p-Akt), phosphorylated mammalian target of rapamycin (p-mTOR), and B cell lymphoma-2 (Bcl-2) decreased when treated with Isov, while the levels of Bcl2-associated X (Bax) and caspase-3 significantly increased. After Isov treatment, the tumor volume and weight were decreased, and the levels of p-PI3K, p-Akt, p-mTOR, and Bcl-2 significantly decreased in tumor tissues. Our findings demonstrated that Isov inhibited cancer cell migration, invasion, and EMT. Isov may be a new potential treatment for colon cancer.

• Authors: Hao Zhu, Na Zhao, Maozhu Jiang
• Journal: Biochemistry and cell biology = Biochimie et biologie cellulaire (Biochem Cell Biol) Vol. 99 Issue 6 Pg. 741-749 (12 2021) ISSN: 1208-6002 [Electronic] Canada
• PMID: 34219464 (Publication Type: Journal Article)

Chemical References

• Apigenin
• MTOR protein, human
• Proto-Oncogene Proteins c-akt
• TOR Serine-Threonine Kinases
• isovitexin

Topics

• Apigenin
• Apoptosis
• Cell Line, Tumor
• Cell Movement
• Cell Proliferation
• Colonic Neoplasms (drug therapy)
• Epithelial-Mesenchymal Transition
• Humans
• Phosphatidylinositol 3-Kinases (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• Signal Transduction
• TOR Serine-Threonine Kinases (metabolism)