Dr. Sci. Tsuneo ISHIDA

Zinc(II) induced oncological suppressive effects on prostate cancer (PCa) prevention and development with PCa Stage 1, Stage 2, and Stage 3 have been investigated, subsequently, the zinc-ions binding prostate anti-cancer molecular mechanism is clarified.

For PCa prevention, adequate dietary zinc intake status can prevent the prostate cancer disease through restoration of high zinc levels, protective preventative PCa progressing by using chemotherapeutic agents.

At PCa Stage 1, zinc can inhibit PCa proliferation and cell growth, and can prevent PCa progressing that Zn2+ ions can diminish androgen receptor (AR), proliferating cell nuclear antigen (PCNA), proliferation index. At PCa Stage 2, zinc suppresses the progression of PCa by proliferation, migration, and invasiveness that zinc is confirmed to function as a tumor suppressor in PCa cells, in which zinc, zinc transporters, and zinc and ZRT-and Irt-like proteins1 (ZIP1) can suppress tumor growth, invasive and migratory tumor malignant cell, and regional lymph nodes in PCa cancer. At PCa Stage 3, metastatic prostate cancer is composed of prolife-ration, neovascularization, extravasation, and bone or bone marrow metastasis with angiogenesis that MAZ regulates PCa bone metastasis, intercellular zinc levels inhibit metastatic and angiogenic malignant cells, and ZMYND8 inhibits tumor angiogenesis.

Zinc induced ROS generation in PCa cell is involved that ROS-mediated oxidative stress on prostate cancer can be modulated by rich antioxidants and accumulated zinc, resulting paclitaxed (PTX) to mitochondrial dysfunction, leading to apoptotic tumor cells.

Zinc coordinated molecular apoptosis mechanism in PCa cells is involved that Zn2+ ions having Zn2+ ions-centered tetrahedral geometric coordination pattern bind with each PCa stage tumor proteins, causing Zn2+ ions-several protein complex formation and apoptosis of PCa cells, leading to molecular apoptosis of prostate cancer tumor cells.

Keywords : Zinc(II), PCa proliferation and growth, Invasive and migratory malignant cell, Regional lymph nodes, Bone and bone marrow metastasis, Tumor angiogenesis, ROS and oxidative stress.

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