Suppression of ClC-3 channel expression reduces migration of nasopharyngeal carcinoma cells
Biochemical Pharmacology, ISSN: 0006-2952, Vol: 75, Issue: 9, Page: 1706-1716
2008
- 76Citations
- 14Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations76
- Citation Indexes76
- 76
- CrossRef57
- Captures14
- Readers14
- 14
Article Description
Recent studies suggest that chloride (Cl − ) channels regulate tumor cell migration. In this report, we have used antisense oligonucleotides specific for ClC-3, the most likely molecular candidate for the volume-activated Cl − channel, to investigate the role of ClC-3 in the migration of nasopharyngeal carcinoma cells (CNE-2Z) in vitro. We found that suppression of ClC-3 expression inhibited the migration of CNE-2Z cells in a concentration-dependent manner. Whole-cell patch-clamp recordings and image analysis further demonstrated that ClC-3 suppression inhibited the volume-activated Cl − current ( I Cl,vol ) and regulatory volume decrease (RVD) of CNE-2Z cells. The expression of ClC-3 positively correlated with cell migration, I Cl,vol and RVD. These results strongly suggest that ClC-3 is a component or regulator of the volume-activated Cl − channel. ClC-3 may regulate CNE-2Z cell migration by modulating cell volume. ClC-3 may be a new target for cancer therapies.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006295208000609; http://dx.doi.org/10.1016/j.bcp.2008.01.008; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=41949119163&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/18359479; https://linkinghub.elsevier.com/retrieve/pii/S0006295208000609; https://dx.doi.org/10.1016/j.bcp.2008.01.008
Elsevier BV
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