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We began analyzing https://link.springer.com/article/10.1007/s00424-003-1205-x, but it redirected us to https://link.springer.com/article/10.1007/s00424-003-1205-x. The analysis below is for the second page.

Title[redir]:
Voltage-gated Na+ channels confer invasive properties on human prostate cancer cells | Pflügers Archiv - European Journal of Physiology
Description:
Prostate cancer is the second leading cause of cancer deaths in American males, resulting in an estimated 37,000 deaths annually, typically the result of metastatic disease. A consequence of the unsuccessful androgen ablation therapy used initially to treat metastatic disease is the emergence of androgen-insensitive prostate cancer, for which there is currently no prescribed therapy. Here, three related human prostate cancer cell lines that serve as a model for this dominant form of prostate cancer metastasis were studied to determine the correlation between voltage-gated sodium channel expression/function and prostate cancer metastatic (invasive) potential: the non-metastatic, androgen-dependent LNCaP LC cell line and two increasingly tumorogenic, androgen-independent daughter cell lines, C4 and C4-2. Fluorometric in vitro invasion assays indicated that C4 and C4-2 cells are more invasive than LC cells. Immunoblot analysis showed that voltage-gated sodium channel expression increases with the invasive potential of the cell line, and this increased invasive potential can be blocked by treatment with the specific voltage-gated sodium channel inhibitor, tetrodotoxin (TTX). These data indicate that increased voltage-gated sodium channel expression and function are necessary for the increased invasive potential of these human prostate cancer cells. When the human adult skeletal muscle sodium channel Nav1.4 was expressed transiently in each cell line, there was a highly significant increase in the numbers of invading LC, C4, and C4-2 cells. This increased invasive potential was reduced to control levels by treatment with TTX. These data are the first to indicate that the expression of voltage-gated sodium channels alone is sufficient to increase the invasive potential of non-metastatic (LC cells) as well as more aggressive cells (i.e., C4 and C4-2 cells). Together, the data suggest that increased voltage-gated sodium channel expression alone is necessary and sufficient to increase the invasive potential of a set of human prostate cancer cell lines that serve as a model for prostate cancer metastasis.

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Keywords {🔍}

cancer, prostate, google, scholar, article, cas, pubmed, cell, channel, human, cells, voltagegated, channels, sodium, invasive, potential, expression, lines, bennett, physiol, data, metastatic, line, djamgoz, privacy, cookies, content, ion, lncap, invasion, increased, access, calcium, tumor, res, prostatic, fraser, publish, research, search, androgenindependent, vitro, usa, mba, lond, analysis, information, log, journal, properties,

Topics {✒️}

voltage-gated sodium channels voltage-activated na+ channels androgen-independent prostrate cancer androgen-insensitive prostate cancer voltage-activated na+ currents ca2+-permeable cation channel t-type calcium channel sodium channel gating prostate cancer metastasis month download article/chapter channel cytoplasmic regions potassium current properties voltage-gated prostate cancer cells prostate cancer patients full article pdf cell lines derived prostate cancer metastatic calcium-selective channel related subjects cold spring harbor prostate-specific gene privacy choices/manage cookies rat prostate cancer increased invasive potential mediated ca2+ entry american cancer society endothelial cell invasion + channel activity grimes ja isoform specific manner article bennett prostate cancer treat metastatic disease prostatic cancer cell line highly significant increase intracellular calcium oscillations european economic area mitogenic signal transduction s5-s6 loop shares high homology south florida college lncap cells check access instant access isoform-specific effects conditions privacy policy voltage dependence basement membrane complexes

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