ArticleThe Journal of physiology2005
Expression of Na+-dependent citrate transport in a strongly metastatic human prostate cancer PC-3M cell line: regulation by voltage-gated Na+ channel activity.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Boosting the Activity of Melanoma-Targeting CAR-T Cells in the Presence of Citrate by the Application of Gluconate.Pharmaceutics · 2026Article
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Citrate chemistry and biology for biomaterials design.Biomaterials · 2018Review
- Combination of Mitochondrial and Plasma Membrane Citrate Transporter Inhibitors Inhibits De Novo Lipogenesis Pathway and Triggers Apoptosis in Hepatocellular Carcinoma Cells.BioMed research international · 2018Article
- Is there a role for voltage-gated Na+ channels in the aggressiveness of breast cancer?Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Review
- Dual roles of voltage-gated sodium channels in development and cancer.The International journal of developmental biology · 2015Review
- Tumor microenvironment promotes dicarboxylic acid carrier-mediated transport of succinate to fuel prostate cancer mitochondria.American journal of cancer research · 2015Article
- The sodium channel β1 subunit mediates outgrowth of neurite-like processes on breast cancer cells and promotes tumour growth and metastasis.International journal of cancer · 2014Article
- Regulation of voltage-gated sodium channel expression in cancer: hormones, growth factors and auto-regulation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Membrane potential and cancer progression.Frontiers in physiology · 2013Article
- Molecular origin of plasma membrane citrate transporter in human prostate epithelial cells.EMBO reports · 2010Article
- An emerging role for voltage-gated Na+ channels in cellular migration: regulation of central nervous system development and potentiation of invasive cancers.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2008Review
- Nerve growth factor enhances voltage-gated Na+ channel activity and Transwell migration in Mat-LyLu rat prostate cancer cell line.Journal of cellular physiology · 2007Article
- The neonatal splice variant of Nav1.5 potentiates in vitro invasive behaviour of MDA-MB-231 human breast cancer cells.Breast cancer research and treatment · 2007Article
- Activity-dependent regulation of voltage-gated Na+ channel expression in Mat-LyLu rat prostate cancer cell line.The Journal of physiology · 2006Article
- Neuronal characteristics of small-cell lung cancer.British journal of cancer · 2005Review
- Voltage-gated sodium channels and metastatic disease.Channels (Austin, Tex.)Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Prostate is a unique organ which synthesizes and releases large amounts of citrate. It has been shown that in metastatic prostate cancer, the amount of citrate in prostatic fluid is significantly reduced, approaching the level normally found in blood. In our previous study, we characterized electrophysiologically the mechanism of citrate transport in a normal prostatic epithelial (PNT2-C2) cell line. It was concluded that the cells expressed a novel transporter carrying 1 citrate3- together with 4 K+, primarily out of cells. In the present study, we aimed similarly to characterize the mechanism(s) of citrate transport in a strongly metastatic human prostate cancer (PC-3M) cell line and to compare this with the previous data. Citrate transport in PC-3M cells was found to be both Na+ and K+ dependent. Intracellular application of citrate produced an outward current that was primarily K+ dependent whilst extracellular citrate elicited an inward current that was mainly Na+ dependent. The electrophysiological and pharmacological characteristics of the citrate outward current were similar to the K+-dependent citrate transporter found in the PNT2-C2 cells. On the other hand, the inward citrate current had a markedly different reversal potential, ionic characteristics, inhibitor profile and pH sensitivity. Preincubation of the PC-3M cells (24 or 48 h) with the voltage-gated Na+ channel (VGSC) blocker tetrodotoxin (TTX) significantly reduced the Na+ sensitivity of the citrate current, up-regulated VGSC mRNA expression but did not change the partial permeability of the membrane to Na+. It was concluded (a) that PC-3M cells express a K+-dependent transporter (carrying citrate outward), similar to that found in normal prostate epithelial cells, as well as (b) a Na+-dependent transporter (carrying citrate inward). The molecular nature of the latter was investigated by RT-PCR; the three known Na+-dependent citrate/dicarboxylate transporters could not be detected. VGSC activity, which itself has been associated with metastatic prostate cancer, had a differential effect on the two citrate transporters, down-regulating the expression of the Na+-dependent component whilst enhancing the K+-dependent citrate transporter.
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