Kirenol inhibited the cell survival and induced apoptosis in human thyroid cancer cells by altering PI3K/AKT and MAP kinase signaling pathways.

Abstract

The thyroid cancer, especially papillary thyroid cancers are very common among population with high intake of iodine or iodine uptake. Even though several treatment options are available, there is still complication and side effects are still persistent. The role of signaling molecules in cancer signaling is very vast and their significance in progression of disease was increasing which leads to mortality of the patient. The major key players are PI3K, AKT and MAP kinase, involves in cell survival, proliferation, and inhibition of apoptosis and are the promising candidate for cancer treatment target, several researchers focuses these molecule to treat various acute and chronic diseases like cancer. On the other side, various literatures propose that natural compounds derived from plant source are shown potent anticancer property against several cancers. In our study we are looking in to one such active principle obtained from plant source, a diterpenoid compound kirenol, and its role thyroid cancer. Here, we report that kirenol role on various cellular mechanisms like induction of apoptosis, enhancing ROS indirectly by inhibiting antioxidants, altering the signaling mechanism of cell survival and apoptosis. Our study proposes that kirenol involved in the cancer cell cytotoxicity by inducing apoptosis and inhibition of cancer cell survival. Thus, targeting this signaling molecule with kirenol definitely favors and may lead to a therapeutic modality for thyroid cancer.

• Authors: Yulong Wang, Jia Xu, Saud Alarifi, Huanjun Wang
• Journal: Environmental toxicology (Environ Toxicol) Vol. 36 Issue 5 Pg. 811-820 (May 2021) ISSN: 1522-7278 [Electronic] United States
• PMID: 33331091 (Publication Type: Journal Article)
• Copyright: © 2020 Wiley Periodicals LLC.

Chemical References

• Diterpenes
• kirenol
• Proto-Oncogene Proteins c-akt

Topics

• Apoptosis
• Cell Line, Tumor
• Cell Proliferation
• Cell Survival
• Diterpenes (pharmacology)
• Humans
• MAP Kinase Signaling System
• Phosphatidylinositol 3-Kinases (metabolism)
• Proto-Oncogene Proteins c-akt (genetics, metabolism)
• Thyroid Neoplasms (drug therapy)