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10.1038/onc.2016.307 http://scihub22266oqcxt.onion/10.1038/onc.2016.307 C5348575!5348575 !27593933     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27593933 &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       Oncogene 2017 ; 36 (10 ): 1404-1416 Nephropedia Template TP {{tp|p=27593933 |t=2017. DLX1 acts as a crucial target of FOXM1 to promote ovarian cancer aggressiveness by enhancing TGF-?/SMAD4 signaling |pdf=|usr=}}{{27593933 }} gab.com Text DLX1 acts as a crucial target of FOXM1 to promote ovarian cancer aggressiveness by enhancing TGF- /SMAD4 signaling JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=27593933 #FOAvip Recent evidence from a comprehensive genome analysis and functional studies have revealed that FOXM1 is a crucial metastatic regulator that drives cancer progression. However, the regulatory mechanism by which FOXM1 exerts its metastatic functions in cancer cells remains obscure. Here, we report that DLX1 acts as a FOXM1 downstream target, exerting pro-metastatic function in ovarian cancers. Both FOXM1 isoforms (FOXM1B or FOXM1C) could transcriptionally upregulate DLX1 through two conserved binding sites, located at +61 to +69bp downstream (TFBS1) and -675 to -667bp upstream (TFBS2) of the DLX1 promoter, respectively. This regulation was further accentuated by the significant correlation between the nuclear expression of FOXM1 and DLX1 in high-grade serous ovarian cancers. Functionally, the ectopic expression of DLX1 promoted ovarian cancer cell growth, cell migration/invasion and intraperitoneal dissemination of ovarian cancer in mice, whereas small interfering RNA-mediated DLX1 knockdown in FOXM1-overexpressing ovarian cancer cells abrogated these oncogenic capacities. In contrast, depletion of FOXM1 by shRNAi only partially attenuated tumor growth and exerted almost no effect on cell migration/invasion and the intraperitoneal dissemination of DLX1-overexpressing ovarian cancer cells. Furthermore, the mechanistic studies showed that DLX1 positively modulates transforming growth factor-? (TGF-?) signaling by upregulating PAI-1 and JUNB through direct interaction with SMAD4 in the nucleus upon TGF-?1 induction. Taken together, these data strongly suggest that DLX1 has a pivotal role in FOXM1 signaling to promote cancer aggressiveness through intensifying TGF-?/SMAD4 signaling in high-grade serous ovarian cancer cells. Twit Text FOAVip DLX1 acts as a crucial target of FOXM1 to promote ovarian cancer aggressiveness by enhancing TGF- /SMAD4 signaling ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=27593933 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27593933 #FOAvip English Wikipedia <ref>{{Cite pmid|27593933 }}</ref> DLX1 acts as a crucial target of FOXM1 to promote ovarian cancer aggressiveness by enhancing TGF-?/SMAD4 signaling #MMPMID27593933 Chan DW ; Hui WW ; Wang JJ ; Yung MM ; Hui LM ; Qin Y ; Liang RR ; Leung TH ; Xu D ; Chan KK ; Yao KM ; Tsang BK ; Ngan HY Oncogene 2017[Mar]; 36 (10 ): 1404-1416 PMID27593933 show ga Recent evidence from a comprehensive genome analysis and functional studies have revealed that FOXM1 is a crucial metastatic regulator that drives cancer progression. However, the regulatory mechanism by which FOXM1 exerts its metastatic functions in cancer cells remains obscure. Here, we report that DLX1 acts as a FOXM1 downstream target, exerting pro-metastatic function in ovarian cancers. Both FOXM1 isoforms (FOXM1B or FOXM1C) could transcriptionally upregulate DLX1 through two conserved binding sites, located at +61 to +69bp downstream (TFBS1) and -675 to -667bp upstream (TFBS2) of the DLX1 promoter, respectively. This regulation was further accentuated by the significant correlation between the nuclear expression of FOXM1 and DLX1 in high-grade serous ovarian cancers. Functionally, the ectopic expression of DLX1 promoted ovarian cancer cell growth, cell migration/invasion and intraperitoneal dissemination of ovarian cancer in mice, whereas small interfering RNA-mediated DLX1 knockdown in FOXM1-overexpressing ovarian cancer cells abrogated these oncogenic capacities. In contrast, depletion of FOXM1 by shRNAi only partially attenuated tumor growth and exerted almost no effect on cell migration/invasion and the intraperitoneal dissemination of DLX1-overexpressing ovarian cancer cells. Furthermore, the mechanistic studies showed that DLX1 positively modulates transforming growth factor-? (TGF-?) signaling by upregulating PAI-1 and JUNB through direct interaction with SMAD4 in the nucleus upon TGF-?1 induction. Taken together, these data strongly suggest that DLX1 has a pivotal role in FOXM1 signaling to promote cancer aggressiveness through intensifying TGF-?/SMAD4 signaling in high-grade serous ovarian cancer cells. |*Signal Transduction [MESH] |Animals [MESH] |Binding Sites [MESH] |Cell Line, Tumor [MESH] |Cell Movement/genetics [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Female [MESH] |Forkhead Box Protein M1/*metabolism [MESH] |Heterografts [MESH] |Homeodomain Proteins/*genetics [MESH] |Humans [MESH] |Mice [MESH] |Neoplasm Grading [MESH] |Neoplasm Metastasis [MESH] |Nucleotide Motifs [MESH] |Ovarian Neoplasms/*genetics/*metabolism/pathology [MESH] |Promoter Regions, Genetic [MESH] |Protein Binding [MESH] |Smad4 Protein/*metabolism [MESH] |Transcription Factors/*genetics [MESH] |Transcriptional Activation [MESH]DLX1 acts as a crucial target of FOXM1 to promote ovarian cancer aggre(epmc).pdf DeepDyve Pubget Overpricing