People with cancer always have low zinc.

Cellular zinc homeostasis is altered in cancer. Zinc levels in serum are typically decreased in patients with tumors, including breast, head and neck, lung, liver, prostate, pancreatic and gynecological tumors, compared to normal serum levels.

Sig Transduct Target Ther 2, 17029 (2017).

The emerging role of zinc transporters in cellular homeostasis and cancer.

Bafaro, E., Liu, Y., Xu, Y. et al.


Zinc is an essential micronutrient that plays a role in the structural or enzymatic functions of many cellular proteins. Cellular zinc homeostasis involves the opposing action of two families of metal transporters: the ZnT (SLC30) family that functions to reduce cytoplasmic zinc concentrations and the ZIP (SLC39) family that functions to increase cytoplasmic zinc concentrations. Fluctuations in intracellular zinc levels mediated by these transporter families affect signaling pathways involved in normal cell development, growth, differentiation and death. Consequently, changes in zinc transporter localization and function resulting in zinc dyshomeostasis have pathophysiological effects. Zinc dyshomeostasis has been implicated in the progression of cancer. Here we review recent progress toward understanding the structural basis for zinc transport by ZnT and ZIP family proteins, as well as highlight the roles of zinc as a signaling molecule in physiological conditions and in various cancers. As zinc is emerging as an important signaling molecule in the development and progression of cancer, the ZnT and ZIP transporters that regulate cellular zinc homeostasis are promising candidates for targeted cancer therapy.


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Bacteria produce an oily protective coating, Lipo-Poly-Saccharide - LPS, also know as, "biofilm", like a slime coating for protection. This LPS will trigger a zinc wave from leukocyctes as an attack on the biofilm and bacteria. 

Further reading: Biofilm disruptors