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10.1016/j.lungcan.2015.09.014 http://scihub22266oqcxt.onion/10.1016/j.lungcan.2015.09.014 C4619129!4619129 !26410177     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26410177 &cmd=llinks): Failed to open stream: HTTP request failed! 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Small-molecule targeting of signal transducer and activator of transcription (STAT) 3 to treat non-small cell lung cancer |pdf=|usr=}}{{26410177 }} gab.com Text Small-molecule targeting of signal transducer and activator of transcription (STAT) 3 to treat non-small cell lung cancer JO: Lung Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26410177 #FOAvip OBJECTIVE: Lung cancer is the leading cause of cancer death in both men and women. Non-small cell lung cancer (NSCLC) has an overall 5-year survival rate of 15%. While aberrant STAT3 activation has previously been observed in NSCLC, the scope of its contribution is uncertain and agents that target STAT3 for treatment are not available clinically. METHODS: We determined levels of activated STAT3 (STAT3 phosphorylated on Y705, pSTAT3) and the two major isoforms of STAT3 (? and ?) in protein extracts of 8 NSCLC cell lines, as well as the effects of targeting STAT3 in vitro and in vivo in NSCLC cells using short hairpin (sh) RNA and two novel small-molecule STAT3 inhibitors, C188-9 and piperlongumine (PL). RESULTS: Levels of pSTAT3, STAT3?, and STAT? were increased in 7 of 8 NSCLC cell lines. Of note, levels of pSTAT3 were tightly correlated with levels of STAT3?, but not STAT3?. Targeting of STAT3 in A549 cells using shRNA decreased tSTAT3 by 75%; this was accompanied by a 47-78% reduction in anchorage-dependent and anchorage-independent growth and a 28-45% reduction in mRNA levels for anti-apoptotic STAT3 gene targets. C188-9 and PL (@30 ?M) each reduced pSTAT3 levels in all NSCLC cell lines tested by ?50%, reduced anti-apoptotic protein mRNA levels by 25-60%, and reduced both anchorage-dependent and anchorage-independent growth of NSCLC cell lines with IC50 values ranging from 3.06 to 52.44 ?M and 0.86 to 11.66 ?M, respectively. Treatment of nude mice bearing A549 tumor xenografts with C188-9 or PL blocked tumor growth and reduced levels of pSTAT3 and mRNA encoding anti-apoptotic proteins. CONCLUSION: STAT3 is essential for growth of NSCLC cell lines and tumors and its targeting using C188-9 or PL may be a useful strategy for treatment. Twit Text FOAVip Small-molecule targeting of signal transducer and activator of transcription (STAT) 3 to treat non-small cell lung cancer ????Lung Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26410177 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26410177 #FOAvip English Wikipedia <ref>{{Cite pmid|26410177 }}</ref> Small-molecule targeting of signal transducer and activator of transcription (STAT) 3 to treat non-small cell lung cancer #MMPMID26410177 Lewis KM ; Bharadwaj U ; Eckols TK ; Kolosov M ; Kasembeli MM ; Fridley C ; Siller R ; Tweardy DJ Lung Cancer 2015[Nov]; 90 (2 ): 182-90 PMID26410177 show ga OBJECTIVE: Lung cancer is the leading cause of cancer death in both men and women. Non-small cell lung cancer (NSCLC) has an overall 5-year survival rate of 15%. While aberrant STAT3 activation has previously been observed in NSCLC, the scope of its contribution is uncertain and agents that target STAT3 for treatment are not available clinically. METHODS: We determined levels of activated STAT3 (STAT3 phosphorylated on Y705, pSTAT3) and the two major isoforms of STAT3 (? and ?) in protein extracts of 8 NSCLC cell lines, as well as the effects of targeting STAT3 in vitro and in vivo in NSCLC cells using short hairpin (sh) RNA and two novel small-molecule STAT3 inhibitors, C188-9 and piperlongumine (PL). RESULTS: Levels of pSTAT3, STAT3?, and STAT? were increased in 7 of 8 NSCLC cell lines. Of note, levels of pSTAT3 were tightly correlated with levels of STAT3?, but not STAT3?. Targeting of STAT3 in A549 cells using shRNA decreased tSTAT3 by 75%; this was accompanied by a 47-78% reduction in anchorage-dependent and anchorage-independent growth and a 28-45% reduction in mRNA levels for anti-apoptotic STAT3 gene targets. C188-9 and PL (@30 ?M) each reduced pSTAT3 levels in all NSCLC cell lines tested by ?50%, reduced anti-apoptotic protein mRNA levels by 25-60%, and reduced both anchorage-dependent and anchorage-independent growth of NSCLC cell lines with IC50 values ranging from 3.06 to 52.44 ?M and 0.86 to 11.66 ?M, respectively. Treatment of nude mice bearing A549 tumor xenografts with C188-9 or PL blocked tumor growth and reduced levels of pSTAT3 and mRNA encoding anti-apoptotic proteins. CONCLUSION: STAT3 is essential for growth of NSCLC cell lines and tumors and its targeting using C188-9 or PL may be a useful strategy for treatment. |Animals [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Apoptosis/drug effects/genetics [MESH] |Carcinoma, Non-Small-Cell Lung/*drug therapy/genetics [MESH] |Cell Line [MESH] |Cell Line, Tumor [MESH] |Cell Survival/drug effects/genetics [MESH] |Gene Expression Regulation, Neoplastic/drug effects/genetics [MESH] |Humans [MESH] |Lung Neoplasms/*drug therapy/genetics [MESH] |Lung/drug effects [MESH] |Mice [MESH] |Mice, Nude [MESH] |Phosphorylation/drug effects/genetics [MESH] |RNA, Small Interfering/genetics [MESH] |STAT3 Transcription Factor/*genetics [MESH] |Signal Transduction/*drug effects/genetics [MESH]Small-molecule targeting of signal transducer and activator of transcr(epmc).pdf DeepDyve Pubget Overpricing