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10.18632/oncotarget.5799 http://scihub22266oqcxt.onion/10.18632/oncotarget.5799 C4742184!4742184 !26415230     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26415230 &cmd=llinks): Failed to open stream: HTTP request failed! 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SP600125 has a remarkable anticancer potential against undifferentiated thyroid cancer through selective action on ROCK and p53 pathways |pdf=|usr=}}{{26415230 }} gab.com Text SP600125 has a remarkable anticancer potential against undifferentiated thyroid cancer through selective action on ROCK and p53 pathways JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26415230 #FOAvip Thyroid cancer is the most common endocrine malignancy with increasing incidence worldwide.The majority of thyroid cancer cases are well differentiated with favorable outcome. However, undifferentiated thyroid cancers are one of the most lethal human malignancies because of their invasiveness, metastatization and refractoriness even to the most recently developed therapies.In this study we show for the first time a significant hyperactivation of ROCK/HDAC6 pathway in thyroid cancer tissues, and its negative correlation with p53 DNA binding ability.We demonstrate that a small compound, SP600125 (SP), is able to induce cell death selectively in undifferentiated thyroid cancer cell lines by specifically acting on the pathogenic pathways of cancer development. In detail, SP acts on the ROCK/HDAC6 pathway involved in dedifferentiation and invasiveness of undifferentiated human cancers, by restoring its physiological activity level. As main consequence, cancer cell migration is inhibited and, at the same time, cell death is induced through the mitotic catastrophe. Moreover, SP exerts a preferential action on the mutant p53 by increasing its DNA binding ability. In TP53-mutant cells that survive mitotic catastrophe this process results in p21 induction and eventually lead to premature senescence. In conclusion, SP has been proved to be able to simultaneously block cell replication and migration, the two main processes involved in cancer development and dissemination, making it an ideal candidate for developing new drugs against anaplastic thyroid cancer. Twit Text FOAVip SP600125 has a remarkable anticancer potential against undifferentiated thyroid cancer through selective action on ROCK and p53 pathways ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26415230 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26415230 #FOAvip English Wikipedia <ref>{{Cite pmid|26415230 }}</ref> SP600125 has a remarkable anticancer potential against undifferentiated thyroid cancer through selective action on ROCK and p53 pathways #MMPMID26415230 Grassi ES ; Vezzoli V ; Negri I ; Lábadi Á ; Fugazzola L ; Vitale G ; Persani L Oncotarget 2015[Nov]; 6 (34 ): 36383-99 PMID26415230 show ga Thyroid cancer is the most common endocrine malignancy with increasing incidence worldwide.The majority of thyroid cancer cases are well differentiated with favorable outcome. However, undifferentiated thyroid cancers are one of the most lethal human malignancies because of their invasiveness, metastatization and refractoriness even to the most recently developed therapies.In this study we show for the first time a significant hyperactivation of ROCK/HDAC6 pathway in thyroid cancer tissues, and its negative correlation with p53 DNA binding ability.We demonstrate that a small compound, SP600125 (SP), is able to induce cell death selectively in undifferentiated thyroid cancer cell lines by specifically acting on the pathogenic pathways of cancer development. In detail, SP acts on the ROCK/HDAC6 pathway involved in dedifferentiation and invasiveness of undifferentiated human cancers, by restoring its physiological activity level. As main consequence, cancer cell migration is inhibited and, at the same time, cell death is induced through the mitotic catastrophe. Moreover, SP exerts a preferential action on the mutant p53 by increasing its DNA binding ability. In TP53-mutant cells that survive mitotic catastrophe this process results in p21 induction and eventually lead to premature senescence. In conclusion, SP has been proved to be able to simultaneously block cell replication and migration, the two main processes involved in cancer development and dissemination, making it an ideal candidate for developing new drugs against anaplastic thyroid cancer. |Anthracenes/*pharmacology [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Histone Deacetylase 6 [MESH] |Histone Deacetylases/metabolism [MESH] |Humans [MESH] |Protein Kinase Inhibitors/pharmacology [MESH] |Signal Transduction/drug effects [MESH] |Thyroid Neoplasms/*drug therapy/enzymology/metabolism/pathology [MESH] |Tumor Suppressor Protein p53/*metabolism [MESH]SP600125 has a remarkable anticancer potential against undifferentiate(epmc).pdf DeepDyve Pubget Overpricing