IndraLab

Statements



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"TNF-alpha induces the expression of Nav1.6 and induces the proliferation, migration and invasion of glioma cells."

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"Knockdown of Nav1.6 significantly inhibited the proliferation, epithelial-mesenchymal transition and invasiveness of FTC cells."

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"Hence , we targeted the JAK-STAT pathway and demonstrated that Nav1.6 enhanced FTC cell proliferation , epithelial-mesenchymal transition , and invasion by phosphorylating JAK2 to activate STAT3 ."

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"THP-1 invasion also was inhibited by small hairpin RNA knockdown of SCN8A."

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"Pharmacological inhibition of Nav1.5, Nav1.6, and Nav1.7 suppresses migration and invasion in experimental models, although the precise underlying mechanisms remain incompletely understood [6]."

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"The inhibition of SCN8A in primary cultured CC cells using Cn2 toxin and tetrodotoxin significantly reduces the invasiveness of these cancer cells [93]."

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"Carrithers and colleagues have reported that SCN8A contributes to cell invasion via podosome and invadopodia formation in macrophages derived from human monocytic leukemia and melanoma cancer cells (25)."

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"Lung cancer studies have determined that Nav1.6 and Nav1.7 mediate invasion, and β1 and β3 are expressed in cancer cells using H23, H460, and Calu-1 cell lines [68–70]."

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"Voltage-gated sodium channels (Nav) have also been proposed to contribute to cellular motility and migration in several types of immune cells including lymphocytes [39] and macrophages [40] and intracellularly localized Nav1.6 supports invasiveness of human breast cancer cells[41]."

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"The upregulation of SCN8A-mediated invasiveness of cervical cancer cells involves MMP-2 activity, and SCN8A channels are considered therapeutic targets against cancer metastasis (25,26)."

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"7 The overexpression of SCN8A (Nav1.6) can promote tumor invasion of CC."