ArticleInternational journal of molecular sciences2014
Serum starvation-induced voltage-gated potassium channel Kv7.5 expression and its regulation by Sp1 in canine osteosarcoma cells.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Remodeling of Kv7.1 and Kv7.5 Expression in Vascular Tumors.International journal of molecular sciences · 2020Article
- Kv7 Channels in Lung Diseases.Frontiers in physiology · 2020Review
- Regulation of voltage-gated potassium channels attenuates resistance of side-population cells to gefitinib in the human lung cancer cell line NCI-H460.BMC pharmacology & toxicology · 2017Article
- The Role of KV7.3 in Regulating Osteoblast Maturation and Mineralization.International journal of molecular sciences · 2016Article
- Silencing of voltage-gated potassium channel KV9.3 inhibits proliferation in human colon and lung carcinoma cells.Oncotarget · 2015Article
- Gene function analysis in osteosarcoma based on microarray gene expression profiling.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
The KCNQ gene family, whose members encode Kv7 channels, belongs to the voltage-gated potassium (Kv) channel group. The roles of this gene family have been widely investigated in nerve and muscle cells. In the present study, we investigated several characteristics of Kv7.5, which is strongly expressed in the canine osteosarcoma cell line, CCL-183. Serum starvation upregulated Kv7.5 expression, and the Kv7 channel opener, flupirtine, attenuated cell proliferation by arresting cells in the G0/G1 phase. We also showed that Kv7.5 knockdown helps CCL-183 cells to proliferate. In an effort to find an endogenous regulator of Kv7.5, we used mithramycin A to reduce the level of the transcription factor Sp1, and it strongly inhibited the induction of Kv7.5 in CCL-183 cells. These results suggest that the activation of Kv7.5 by flupirtine may exert an anti-proliferative effect in canine osteosarcoma. Therefore, Kv7.5 is a possible molecular target for canine osteosarcoma therapy.
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