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10.18632/oncotarget.7062 http://scihub22266oqcxt.onion/10.18632/oncotarget.7062 C4891038!4891038 !26843616     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26843616 &cmd=llinks): Failed to open stream: HTTP request failed! 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In vitro and in vivo inhibition of breast cancer cell growth by targeting the Hedgehog/GLI pathway with SMO (GDC-0449) or GLI (GANT-61) inhibitors |pdf=|usr=}}{{26843616 }} gab.com Text In vitro and in vivo inhibition of breast cancer cell growth by targeting the Hedgehog/GLI pathway with SMO (GDC-0449) or GLI (GANT-61) inhibitors JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26843616 #FOAvip Aberrant Hedgehog (Hh)/glioma-associated oncogene (GLI) signaling has been implicated in cancer progression. Here, we analyzed GLI1, Sonic Hedgehog (Shh) and NF-?B expression in 51 breast cancer (ductal carcinoma) tissues using immunohistochemistry. We found a positive correlation between nuclear GLI1 expression and tumor grade in ductal carcinoma cases. Cytoplasmic Shh staining significantly correlated with a lower tumor grade. Next, the in vitro effects of two Hh signaling pathway inhibitors on breast cancer cell lines were evaluated using the Smoothened (SMO) antagonist GDC-0449 and the direct GLI1 inhibitor GANT-61. GDC-0449 and GANT-61 exhibited the following effects: a) inhibited breast cancer cell survival; b) induced apoptosis; c) inhibited Hh pathway activity by decreasing the mRNA expression levels of GLI1 and Ptch and inhibiting the nuclear translocation of GLI1; d) increased/decreased EGFR and ErbB2 protein expression, reduced p21-Ras and ERK1/ERK2 MAPK activities and inhibited AKT activation; and e) decreased the nuclear translocation of NF-?B. However, GANT-61 exerted these effects more effectively than GDC-0449. The in vivo antitumor activities of GDC-0449 and GANT-61 were analyzed in BALB/c mice that were subcutaneously inoculated with mouse breast cancer (TUBO) cells. GDC-0449 and GANT-61 suppressed tumor growth of TUBO cells in BALB/c mice to different extents. These findings suggest that targeting the Hh pathway using antagonists that act downstream of SMO is a more efficient strategy than using antagonists that act upstream of SMO for interrupting Hh signaling in breast cancer. Twit Text FOAVip In vitro and in vivo inhibition of breast cancer cell growth by targeting the Hedgehog/GLI pathway with SMO (GDC-0449) or GLI (GANT-61) inhibitors ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26843616 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26843616 #FOAvip English Wikipedia <ref>{{Cite pmid|26843616 }}</ref> In vitro and in vivo inhibition of breast cancer cell growth by targeting the Hedgehog/GLI pathway with SMO (GDC-0449) or GLI (GANT-61) inhibitors #MMPMID26843616 Benvenuto M ; Masuelli L ; De Smaele E ; Fantini M ; Mattera R ; Cucchi D ; Bonanno E ; Di Stefano E ; Frajese GV ; Orlandi A ; Screpanti I ; Gulino A ; Modesti A ; Bei R Oncotarget 2016[Feb]; 7 (8 ): 9250-70 PMID26843616 show ga Aberrant Hedgehog (Hh)/glioma-associated oncogene (GLI) signaling has been implicated in cancer progression. Here, we analyzed GLI1, Sonic Hedgehog (Shh) and NF-?B expression in 51 breast cancer (ductal carcinoma) tissues using immunohistochemistry. We found a positive correlation between nuclear GLI1 expression and tumor grade in ductal carcinoma cases. Cytoplasmic Shh staining significantly correlated with a lower tumor grade. Next, the in vitro effects of two Hh signaling pathway inhibitors on breast cancer cell lines were evaluated using the Smoothened (SMO) antagonist GDC-0449 and the direct GLI1 inhibitor GANT-61. GDC-0449 and GANT-61 exhibited the following effects: a) inhibited breast cancer cell survival; b) induced apoptosis; c) inhibited Hh pathway activity by decreasing the mRNA expression levels of GLI1 and Ptch and inhibiting the nuclear translocation of GLI1; d) increased/decreased EGFR and ErbB2 protein expression, reduced p21-Ras and ERK1/ERK2 MAPK activities and inhibited AKT activation; and e) decreased the nuclear translocation of NF-?B. However, GANT-61 exerted these effects more effectively than GDC-0449. The in vivo antitumor activities of GDC-0449 and GANT-61 were analyzed in BALB/c mice that were subcutaneously inoculated with mouse breast cancer (TUBO) cells. GDC-0449 and GANT-61 suppressed tumor growth of TUBO cells in BALB/c mice to different extents. These findings suggest that targeting the Hh pathway using antagonists that act downstream of SMO is a more efficient strategy than using antagonists that act upstream of SMO for interrupting Hh signaling in breast cancer. |Active Transport, Cell Nucleus/drug effects [MESH] |Anilides/*therapeutic use [MESH] |Animals [MESH] |Apoptosis/drug effects [MESH] |Breast Neoplasms/*drug therapy/pathology [MESH] |Carcinoma, Ductal/*drug therapy/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cell Survival/drug effects [MESH] |Enzyme Activation/drug effects [MESH] |ErbB Receptors/biosynthesis [MESH] |Extracellular Signal-Regulated MAP Kinases/metabolism [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic/*drug effects [MESH] |Hedgehog Proteins/antagonists & inhibitors [MESH] |Humans [MESH] |MCF-7 Cells [MESH] |Mammary Neoplasms, Experimental/*drug therapy/pathology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |NF-kappa B/biosynthesis [MESH] |Patched-1 Receptor/biosynthesis [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Proto-Oncogene Proteins p21(ras)/metabolism [MESH] |Pyridines/*therapeutic use [MESH] |Pyrimidines/*therapeutic use [MESH] |RNA, Messenger/biosynthesis [MESH] |Receptor, ErbB-2/biosynthesis [MESH] |Signal Transduction/drug effects [MESH] |Smoothened Receptor/*antagonists & inhibitors [MESH]In vitro and in vivo inhibition of breast cancer cell growth by target(epmc).pdf DeepDyve Pubget Overpricing