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KCNH1 activates cell population proliferation. 77 / 83
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77
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"The importance of studying molecules contained in the venom of different animals that interact with Kv10.1 potassium channels rose after the finding by Dr. Pardo and collaborators in 1999 that inhibition of Kv10.1 channels causes reduced cell proliferation in different cancer cell lines [29]."
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"Proanthocyanidin B1, a natural compound extracted from grape seeds, is a specific inhibitor of Kv10.1 channels, and inhibition of Kv10.1 currents can inhibit migration, proliferation, and xenograft tumor development in the hepatoma cell line Hh-7 cells as well as HepG2 cells (72)."
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"Based on the findings in previous studies that potassium voltage gated channel subfamily H member 1 (KCNH1) was overexpressed in osteosarcoma and promoted the proliferation and invasion of osteosarcoma [XREF_BIBR - XREF_BIBR] and on our profile of the miRanda, PITA, RNAhybrid databases to explore the corresponding circRNAs of KCNH1, we speculated that hsa-circ-0016347 may be a potential regulator of osteosarcoma progression."
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"On the contrary, Kv10.1 is overexpressed in a variety of cell lines derived from human malignancies and in different cancers including head and neck, gastric, colon, hepatocellular pancreatic, renal or prostate carcinoma [XREF_BIBR - XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR] within which Kv10.1 enhances the proliferation of the cells and is required for the maintenance of growth."
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"Inhibition of Eag1 expression by siRNA or shRNA decreases proliferation and migration in SaOS-2 and GM-63 [11,19], however, the effects produced by the blockade of Eag1 on Ca deposition have not been investigated yet.Based on these, we designed experiments to test the functional expression of hEag1 K channels in SaOS-2 osteosarcoma cells and to determine if pharmacological modulation of the channel may play a role in the regulation of osteogenic differentiation."
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"They reported that silencing Eag1 reduced the viability and proliferation of the U87MG glioblastoma cell line and increased the apoptotic rate triggered by temozolomide (TMZ) [148], clearly pointing out and confirming a role for potassium channels (Eag1) in modulation apoptosis in a glioma context."