Kim, S.-A.; Kang, O.-H.; Kwon, D.-Y. Cryptotanshinone Induces Cell Cycle Arrest and Apoptosis of NSCLC Cells through the PI3K/Akt/GSK-3β Pathway. Int. J. Mol. Sci.2018, 19, 2739.
Kim, S.-A.; Kang, O.-H.; Kwon, D.-Y. Cryptotanshinone Induces Cell Cycle Arrest and Apoptosis of NSCLC Cells through the PI3K/Akt/GSK-3β Pathway. Int. J. Mol. Sci. 2018, 19, 2739.
Kim, S.-A.; Kang, O.-H.; Kwon, D.-Y. Cryptotanshinone Induces Cell Cycle Arrest and Apoptosis of NSCLC Cells through the PI3K/Akt/GSK-3β Pathway. Int. J. Mol. Sci.2018, 19, 2739.
Kim, S.-A.; Kang, O.-H.; Kwon, D.-Y. Cryptotanshinone Induces Cell Cycle Arrest and Apoptosis of NSCLC Cells through the PI3K/Akt/GSK-3β Pathway. Int. J. Mol. Sci. 2018, 19, 2739.
Abstract
Cryptotanshinone (CTT) is a natural product and a quinoid diterpene isolated from the root of the Asian medicinal plant, Salvia miltiorrhiza bunge. Notably, CTT has a variety of anti-cancer actions, including the activation of apoptosis, anti-proliferation, and a reduction in angiogenesis. We further investigated the anti-cancer effects of CTT in A549 and H460 which are NSCLC cell lines. CTT treatment in NSCLC cells reduced cell growth through PI3K/Akt/GSK3β pathway inhibition, G0 / G1 cell cycle arrest, and the activation of apoptosis. CTT induced increase of Bax and cleavage of apoptosis-related signaling such as caspase-3, caspase-9, poly-ADP-ribose polymerase (PARP), and Bax, as well as inhibition of anti-apoptosis related signaling such as Bcl-2, survivin, and cellular-inhibitor of apoptosis protein 1 and 2 (cIAP-1 and -2). It also induced G0/G1 phase cell cycle arrest by decreasing the expression of cyclin A, cyclin D, cyclin E, Cdk 2, and Cdk 4. In addition, CTT reduced the protein expression of the PI3K/Akt/GSK3β signaling pathway related to cell proliferation. These results highlight the latent potential of CTT as natural therapeutic agent for NSCLC.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
