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10.1007/s00204-020-02674-w http://scihub22266oqcxt.onion/10.1007/s00204-020-02674-w 32080757!?!32080757 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32080757&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Arch+Toxicol 2020 ; 94 (3): 735-747 Nephropedia Template TP {{tp|p=32080757|t=2020. Cadmium exposure enhances cell migration and invasion through modulated TRPM7 channel expression |pdf=|usr=}}{{32080757}} gab.com Text Cadmium exposure enhances cell migration and invasion through modulated TRPM7 channel expression JO: Arch Toxicol http://www.kidney.de/pget.php?&tw=1&pmid=32080757 #FOAvip Cadmium is a xenobiotic involved in neoplastic transformation. Cadmium enters the cells through divalent cation transporters including the Transient Receptor Potential Melastatin-related 7 (TRPM7) which is known to be involved in cancer cell fate. This work aimed to study the role of TRPM7 in neoplastic transformation induced by cadmium exposure in non-cancer epithelial cells. Non-cancer epithelial cells were chronically exposed to low-dose of cadmium. TRPM7 expression and function were studied by Western-Blot, Patch-Clamp and calcium and magnesium imaging. Finally, cell migration and invasion were studied by Boyden chamber assays. Chronic cadmium exposure induced TRPM7 overexpression and increased the membrane currents (P < 0.001). Cells exposed to cadmium had higher intracellular calcium and magnesium levels (P < 0.05). TRPM7 silencing restored calcium levels but strongly decreased intracellular magnesium concentration (P < 0.001). Moreover, cadmium exposure enhanced both cell migration and invasion, but TRPM7 silencing strongly decreased these features (P < 0.001). Furthermore, mammary epithelial cells exposed to cadmium became rounded and had less cell-to-cell junctions. Cadmium exposure decreased epithelial markers while the mesenchymal ones were increased. Importantly, TRPM7 silencing was able to reverse these phenotypic modifications (P < 0.05). To summarize, our data show that chronic cadmium exposure enhanced TRPM7 expression and activity in non-cancer epithelial cells. TRPM7 overexpression induced intracellular magnesium increase and stimulated cell migration and invasion. These neoplastic properties could be linked to a TRPM7-dependent epithelial-to-mesenchymal transition reprogramming in cell exposed to cadmium. These findings provide new insights into the regulation of cell fates by cadmium exposure. Twit Text FOAVip Cadmium exposure enhances cell migration and invasion through modulated TRPM7 channel expression ????Arch Toxicol http://www.kidney.de/pget.php?&tw=1&pmid=32080757 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32080757 #FOAvip English Wikipedia <ref>{{Cite pmid|32080757}}</ref> Cadmium exposure enhances cell migration and invasion through modulated TRPM7 channel expression #MMPMID32080757 Vanlaeys A; Fouquet G; Kischel P; Hague F; Pasco-Brassart S; Lefebvre T; Rybarczyk P; Dhennin-Duthille I; Brassart B; Ouadid-Ahidouch H; Gautier M Arch Toxicol 2020[Mar]; 94 (3): 735-747 PMID32080757show ga Cadmium is a xenobiotic involved in neoplastic transformation. Cadmium enters the cells through divalent cation transporters including the Transient Receptor Potential Melastatin-related 7 (TRPM7) which is known to be involved in cancer cell fate. This work aimed to study the role of TRPM7 in neoplastic transformation induced by cadmium exposure in non-cancer epithelial cells. Non-cancer epithelial cells were chronically exposed to low-dose of cadmium. TRPM7 expression and function were studied by Western-Blot, Patch-Clamp and calcium and magnesium imaging. Finally, cell migration and invasion were studied by Boyden chamber assays. Chronic cadmium exposure induced TRPM7 overexpression and increased the membrane currents (P < 0.001). Cells exposed to cadmium had higher intracellular calcium and magnesium levels (P < 0.05). TRPM7 silencing restored calcium levels but strongly decreased intracellular magnesium concentration (P < 0.001). Moreover, cadmium exposure enhanced both cell migration and invasion, but TRPM7 silencing strongly decreased these features (P < 0.001). Furthermore, mammary epithelial cells exposed to cadmium became rounded and had less cell-to-cell junctions. Cadmium exposure decreased epithelial markers while the mesenchymal ones were increased. Importantly, TRPM7 silencing was able to reverse these phenotypic modifications (P < 0.05). To summarize, our data show that chronic cadmium exposure enhanced TRPM7 expression and activity in non-cancer epithelial cells. TRPM7 overexpression induced intracellular magnesium increase and stimulated cell migration and invasion. These neoplastic properties could be linked to a TRPM7-dependent epithelial-to-mesenchymal transition reprogramming in cell exposed to cadmium. These findings provide new insights into the regulation of cell fates by cadmium exposure. |Cadmium/*toxicity[MESH] |Cell Movement/*drug effects[MESH] |Epithelial-Mesenchymal Transition[MESH] |Hazardous Substances/*toxicity[MESH] |Humans[MESH]Cadmium exposure enhances cell migration and invasion through modulate(epmc).pdf DeepDyve Pubget Overpricing