A Mechanism for Apoptotic Effects of a Planar Catechin Analog on Cancer Cells
Hiromu Ito,
Yoshimi Shoji,
Ken-ichiro Matsumoto,
Kiyoshi Fukuhara,
Ikuo Nakanishi
Affiliations
Hiromu Ito
Quantum RedOx Chemistry Team, Quantum Life Spin Group, Institute for Quantum Life Science (iQLS), National Institutes for Quantum Science and Technology (QST), Inage-ku, Chiba 263-8555, Japan
Yoshimi Shoji
Quantum RedOx Chemistry Team, Quantum Life Spin Group, Institute for Quantum Life Science (iQLS), National Institutes for Quantum Science and Technology (QST), Inage-ku, Chiba 263-8555, Japan
Ken-ichiro Matsumoto
Quantitative RedOx Sensing Group, Department of Radiation Regulatory Science Research, Institute for Radiological Science (NIRS), National Institutes for Quantum Science and Technology (QST), Inage-ku, Chiba 263-8555, Japan
Kiyoshi Fukuhara
Quantum RedOx Chemistry Team, Quantum Life Spin Group, Institute for Quantum Life Science (iQLS), National Institutes for Quantum Science and Technology (QST), Inage-ku, Chiba 263-8555, Japan
Ikuo Nakanishi
Quantum RedOx Chemistry Team, Quantum Life Spin Group, Institute for Quantum Life Science (iQLS), National Institutes for Quantum Science and Technology (QST), Inage-ku, Chiba 263-8555, Japan
Catechin is one of the representative antioxidants that shows physiological activities such as an anti-cancer effect. We have developed a chemically modified catechin analog possessing a planar structure, which shows an enhanced radical-scavenging activity as well as inhibitory effects on the proliferation and migration of cancer cells, compared to the parent (+)-catechin. In this study, the mechanism for cancer cell inhibition by the planar catechin was partly elucidated using a gastric cancer cell line. The planar catechin treatment induced an enhanced expression of an apoptotic marker, cleaved caspase-3, in addition to the mitigation of the intracellular accumulation of reactive oxygen species (ROS) and NF-κB expression. Furthermore, γH2AX, a marker of double-strand breaks in DNA, was also induced by the planar catechin treatment in a dose-dependent manner. These findings suggest that the removal of ROS by the planar catechin with a higher antioxidant ability executed NF-κB suppression and/or the planar catechin-injured DNA, leading to the induction of apoptosis in cancer cells.