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Effect of melamine on [Ca(2+)]i and viability in PC3 human prostate cancer cells
Chia-Cheng Yu1, Chiang-Ting Chou2, Te-Kung Sun3
1Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
Abstract:
Melamine is thought to be an endocrine disrupter that affects physiology in cells. This study examined the effect of melamine on cytosolic free Ca(2+) concentrations ([Ca(2+)]i) and viability in PC3 human prostate cancer cells. Melamine evoked [Ca(2+)]i rises concentration-dependently. Melamine-evoked Ca(2+) entry was inhibited by nifedipine, econazole, SKF96365, GF109203X and phorbol 12-myristate 13 acetate. In Ca(2+)-free medium, treatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin inhibited melamine-evoked [Ca(2+)]i rise. Conversely, treatment with melamine abolished thapsigargin-evoked [Ca(2+)]i rise. Inhibition of phospholipase C with U73122 did not alter melamine-evoked [Ca(2+)]i rise. Melamine at 500-800μM decreased cell viability, which was not reversed by pretreatment with the Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Collectively, our data suggest that in PC3 cells, melamine induced [Ca(2+)]i rises by evoking phospholipase C-independent Ca(2+) release from the endoplasmic reticulum, and Ca(2+) entry via protein kinase C-regulated store-operated Ca(2+) entry. Melamine also caused Ca(2+)-independent cell death.
Insights
Melamine disrupts calcium signaling in prostate cancer cells by releasing it from the endoplasmic reticulum and enhancing calcium entry. This chemical also induces cell death, independent of calcium levels.
Area of Science:
- Cell Biology
- Toxicology
- Biochemistry
Background:
- Melamine is recognized as a potential endocrine disruptor impacting cellular physiology.
- Prostate cancer cells (PC3) are utilized to investigate cellular responses to chemical exposure.
Purpose of the Study:
- To investigate the effects of melamine on intracellular calcium concentrations ([Ca(2+)]i) and cell viability in PC3 human prostate cancer cells.
- To elucidate the mechanisms underlying melamine-induced calcium changes and cell death.
Main Methods:
- Measurements of cytosolic free Ca(2+) concentrations ([Ca(2+)]i) in response to melamine.
- Utilized various inhibitors targeting specific calcium channels, pumps, and signaling pathways (e.g., nifedipine, thapsigargin, U73122, GF109203X).
- Assessed cell viability using relevant assays following melamine treatment.
Main Results:
- Melamine induced a concentration-dependent rise in [Ca(2+)]i.
- Melamine-evoked calcium release from the endoplasmic reticulum was phospholipase C-independent.
- Calcium entry via store-operated calcium channels, regulated by protein kinase C, was involved in the melamine response.
- High concentrations of melamine (500-800μM) reduced cell viability through a calcium-independent mechanism.
Conclusions:
- Melamine triggers intracellular calcium release from the endoplasmic reticulum and enhances store-operated calcium entry in PC3 cells.
- The observed cell death induced by melamine is not directly mediated by alterations in intracellular calcium levels.
- These findings contribute to understanding melamine's toxicological profile and its impact on cancer cell physiology.
