Peptide
Ammonium Tetrathiomolybdate (TBM)

 

Ammonium Tetrathiomolybdate (TBM)

Ammonium tetrathiomolybdate (TM) was developed as a non-toxic treatment for Wilson’s disease, which is a condition that results in copper buildup in the body. Tetrathiomolybdate binds both food copper and endogenously produced copper and prevents their absorption when taken with food. When taken without food it enters the blood and binds with available copper to prevent it being used by cells. Tetrathiomolybdate has also shown to be a promising treatment for cancer. Copper is involved in turning on the growth of new blood vessels that tumors depend on for growth. By depriving the tumors of the copper supply that is needed for new blood vessels, the growth may be slowed or stabilized. It has also been shown to target the copper transporter ATP7A and enhance the sensitivity of breast cancer to Cisplatin treatment, as well as, decreasing the development of resistance to cisplatin.

CLINICAL RESEARCH:

Ammonium Tetrathiomolybdate treatment targets the copper transporter ATP7A and enhances sensitivity of breast cancer to cisplatin.
Cisplatin is an effective breast cancer drug but resistance often develops over prolonged chemotherapy. Therefore, we performed a candidate approach RNAi screen in combination with cisplatin treatment to identify molecular pathways conferring survival advantages. The screen identified ATP7A as a therapeutic target. ATP7A is a copper ATPase transporter responsible for intercellular movement and sequestering of cisplatin. Pharmaceutical replacement for ATP7A by ammonium tetrathiomolybdate (TM) enhanced cisplatin treatment in breast cancer cells. Allograft and xenograft models in athymic nude mice treated with cisplatin/TM exhibited retarded tumor growth, reduced accumulation of cancer stem cells and decreased cell proliferation as compared to mono-treatment with cisplatin or TM. Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis. Microarray analysis of gene ontology pathways that responded uniquely to cisplatin/ TM double treatment depicted changes in cell cycle regulation, specifically in the G1/S transition. These findings offer the potential to combat platinum-resistant tumors and sensitize patients to conventional breast cancer treatment by identifying and targeting the resistant tumors’ unique molecular adaptations.

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