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10.1093/abbs/gmw005 http://scihub22266oqcxt.onion/10.1093/abbs/gmw005 C4886244!4886244 !26922319     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26922319 &cmd=llinks): Failed to open stream: HTTP request failed! 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Insufficient radiofrequency ablation promotes the growth of non-small cell lung cancer cells through PI3K/Akt/HIF-1? signals |pdf=|usr=}}{{26922319 }} gab.com Text Insufficient radiofrequency ablation promotes the growth of non-small cell lung cancer cells through PI3K/Akt/HIF-1 signals JO: Acta Biochim Biophys Sin (Shanghai) http://www.kidney.de/pget.php?&tw=1&pmid=26922319 #FOAvip Accelerated progression of residual non-small cell lung cancer (NSCLC) after incomplete radiofrequency ablation (RFA) has frequently been reported. In this study, NSCLC cells A549, CCL-185, and H358 were treated using a water bath at 47°C for 5, 10, 15, 20, and 25 min gradually to establish the sublines A549-H, CCL-185-H, and H358-H, respectively. A549-H, CCL-185-H, and H358-H cells showed a significant increase in proliferation rate when compared with their corresponding parental cellsin vitro The expression of hypoxia-inducible factor-1? (HIF-1?) was obviously upregulated in both A549-H and CCL-185-H cells. Silencing of HIF-1? abolished the insufficient RFA-induced proliferation in A549-H and CCL-185-H cells. Furthermore, insufficient RFA treatment markedly elevated the phosphorylation of ERK1/2 and Akt, but not of p38 MAPK or JNK, in A549-H and CCL-185-H cells. The inhibitor of Akt, LY294002, but not the inhibitor of ERK1/2, PD98059, suppressed the upregulation of HIF-1? and the proliferation of A549-H and CCL-185-H cellsin vitro Thein vivoresults confirmed that insufficient RFA could trigger the tumor growth, upregulate the HIF-1? expression, and activate Akt in A549 xenograft tumors. Our data suggest that insufficient RFA can promote thein vitroandin vivogrowth of NSCLC via upregulating HIF-1? through the PI3K/Akt signals. Twit Text FOAVip Insufficient radiofrequency ablation promotes the growth of non-small cell lung cancer cells through PI3K/Akt/HIF-1 signals ????Acta Biochim Biophys Sin (Shanghai) http://www.kidney.de/pget.php?&tw=1&pmid=26922319 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26922319 #FOAvip English Wikipedia <ref>{{Cite pmid|26922319 }}</ref> Insufficient radiofrequency ablation promotes the growth of non-small cell lung cancer cells through PI3K/Akt/HIF-1? signals #MMPMID26922319 Wan J ; Wu W ; Chen Y ; Kang N ; Zhang R Acta Biochim Biophys Sin (Shanghai) 2016[Apr]; 48 (4 ): 371-7 PMID26922319 show ga Accelerated progression of residual non-small cell lung cancer (NSCLC) after incomplete radiofrequency ablation (RFA) has frequently been reported. In this study, NSCLC cells A549, CCL-185, and H358 were treated using a water bath at 47°C for 5, 10, 15, 20, and 25 min gradually to establish the sublines A549-H, CCL-185-H, and H358-H, respectively. A549-H, CCL-185-H, and H358-H cells showed a significant increase in proliferation rate when compared with their corresponding parental cellsin vitro The expression of hypoxia-inducible factor-1? (HIF-1?) was obviously upregulated in both A549-H and CCL-185-H cells. Silencing of HIF-1? abolished the insufficient RFA-induced proliferation in A549-H and CCL-185-H cells. Furthermore, insufficient RFA treatment markedly elevated the phosphorylation of ERK1/2 and Akt, but not of p38 MAPK or JNK, in A549-H and CCL-185-H cells. The inhibitor of Akt, LY294002, but not the inhibitor of ERK1/2, PD98059, suppressed the upregulation of HIF-1? and the proliferation of A549-H and CCL-185-H cellsin vitro Thein vivoresults confirmed that insufficient RFA could trigger the tumor growth, upregulate the HIF-1? expression, and activate Akt in A549 xenograft tumors. Our data suggest that insufficient RFA can promote thein vitroandin vivogrowth of NSCLC via upregulating HIF-1? through the PI3K/Akt signals. |*Cell Proliferation [MESH] |*Signal Transduction [MESH] |Animals [MESH] |Carcinoma, Non-Small-Cell Lung/enzymology/metabolism/pathology/*radiotherapy [MESH] |Cell Line, Tumor [MESH] |Heterografts [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism [MESH] |Lung Neoplasms/enzymology/metabolism/pathology/*radiotherapy [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Phosphatidylinositol 3-Kinases/*metabolism [MESH]Insufficient radiofrequency ablation promotes the growth of non-small (epmc).pdf DeepDyve Pubget Overpricing