IndraLab

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SCN5A activates Neoplasm Invasiveness. 28 / 28
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"SCN5A silencing also decreased the invasiveness of HCT116 cells by 50%."
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"In an orthotopic breast cancer model, functionally active Nav1.5 contributed to tumor growth, local invasion, and metastasis to liver, lungs and spleen (17)."
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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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"Additionally, in SW480 and DLD1 cell lines, it has been suggested that Nav1.5 mediates proliferation, migration, and invasion, and increases chemosensitivity through the cell cycle, epithelial-mesenchymal transition, and Ras signaling pathways [45–49]."
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"Studies have found that ropivacaine, an inhibitor of NaV1.5, can attenuate the invasion ability of colon cancer cells (Baptista-Hon et al., 2014)."
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"Moreover, ropivacaine, lidocaine, TTX, and a siRNA specifically targeting Nav1.5 could inhibit Nav1.5 channel function and invasion of metastatic colon cancer SW620 cells, and the Nav1.5 channel activator veratridine promoted SW620 cell invasion (9,18)."
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"In CRC cells, SCN5A knockdown reduced the proliferation, migration and invasion."
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"Nav1.5 promotes BCa invasiveness by promoting H efflux via Na /H exchange [13]."
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"In addition, siRNA knockdown of Nav1.5 could reduce invasion of endocrine-resistant breast cancer cells, in part through reducing ERK1/2 phosphorylation and total MMP activity (22)."
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"We have shown previously that NaV1.5 promotes MDA-MB-231 breast cancer cells invasiveness by potentiating the activity of Na (+)/H (+) exchanger type 1 (NHE-1), the major regulator of H (+) efflux in these cells."
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"In colon cancer, Nav1.5 was also shown to enhance the invasion of cancer cells."
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"Nav1.5 maintains the expression of the transcription factor SNAI1 by EMT, obtains mesenchymal phenotypes, and enhances invasion (Gradek et al., 2019)."
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"Elevated Nav1.5 expression promotes cell invasion and breakdown of extracellular matrix proteins, maintains actin polymerisation to produce F-actin stress fibres, and allows cancer cells to acquire a fibroblast morphology, suggesting a role for Nav1.5 in “mesenchymal invasion”."
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"The ion channel NaV1.5 has been shown to promote MDA-MB-231 breast cancer cells invasiveness by potentiating the activity of NHE1 [260,261] ."
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"While there are several subtypes of VGSC found upregulated in a number of carcinomas, breast cancer in particular, there is distinctively high expression of the ‘neonatal’ splice variant of the cardiac VGSC isoform, Nav1.5 (nNav1.5) that potentiates motility, migration, and invasion of aggressive human breast cancer cells in vitro and metastasis in vivo [10]."
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"BmK AGAP inhibits Nav1.5 and further downregulates PTX3 via the NF-kB and Wnt/β-catenin signaling pathways, thereby suppressing stemness, epithelial–mesenchymal transition, migration, and invasion of breast cancer cells (Table 4)."
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"Similarly, Gillet et al. demonstrated that TTX blocked continuous sodium influx in MDA-MB-231 breast cancer cells, and knockdown of NaV1.5 expression reduced cell invasiveness, while using sodium channel activator veratridine had the opposite effects."
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"Knockdown of Nav1.5 inhibits cell proliferation , migration and invasion via Wnt / beta-catenin signaling pathway in oral squamous cell carcinoma ."
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"Nav1.5 promotes invasion through the CD44-src-cortactin signaling pathway [ 70,104,105,106 ] ."
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"Reduced expression of the voltage gated Nav1.5 channel suppressed cell proliferation and invasiveness and induced apoptosis in astrocytoma cells [11] ."
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"SCN5A codes for a subunit of a voltage-gated Na -channel that is elevated in aggressive breast cancer and enhances breast cancer growth and metastatic dissemination; its silencing by siRNA in MDA-MB-231 cells reduces invasion (87, 88)."
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"The fact that neither pharmacologic nor genetic knockdown of SCN5A inhibited cell invasion completely may be explained by the presence of other mechanisms that contribute to cell invasion, existence of additional functional isoforms (such as Na v 1.8, encoded by SCN10A, the most TTX resistant isoform; see XREF_SUPPLEMENTARY), or simply incomplete gene knockdown."
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"Taken together, our inhibitor and knockdown experiments suggest that veratridine stimulated invasion by SW620 colon cancer cells is mediated by an SCN5A dependent pathway involving PKA/RAP1B/MEK/ERK (predominant pathway)."
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"SCN5A gene encodes voltage-gated sodium channels aberrantly expressed in breast cancer and promotes EMT and invasiveness [76]."
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"In breast cancer cells with significantly downregulated SIK1 levels, Nav1.5 overexpression has been observed, promoting Na -mediated invasiveness (76-78)."
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"It has been previously shown that NaV1.5 activity enhances breast cancer cell invasiveness through perimembrane acidification and subsequent degradation of the extracellular matrix by cysteine cathepsins."
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"In CRC cells , SCN5A knockdown reduced the proliferation , migration and invasion ."
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"SCN5A silencing reduced the invasiveness of SW620 by 50% and neither compound 1 nor compound 4 caused a further decrease, suggesting that these compounds reduce cancer cell invasiveness by selectively targeting Na 1.5."
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