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10.1186/s13046-017-0593-2 http://scihub22266oqcxt.onion/10.1186/s13046-017-0593-2 C5602941!5602941!28915924     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Exp+Clin+Cancer+Res 2017 ; 36 (ä): ä Nephropedia Template TP {{tp|p=28915924|t=2017. PDL1 And LDHA act as ceRNAs in triple negative breast cancer by regulating miR-34a |pdf=|usr=}}{{28915924}} gab.com Text PDL1 And LDHA act as ceRNAs in triple negative breast cancer by regulating miR-34a JO: J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28915924 #FOAvip Backgroud: The purpose of this study was to elucidate the regulation of programmed death ligand 1 (PDL1), lactate dehydrogenase A (LDHA) and miR-34a in triple negative breast cancer (TNBC) and to explore the function and mechanism of PDL1 and LDHA as competitive endogenous RNAs (ceRNAs) in TNBC via regulation of miR-34a. Methods: Western blotting, quantitative RT-PCR (qRT-PCR) and immunohistochemistry (IHC) assays were conducted to explore the expression of PDL1, LDHA and miR-34a in TNBC and correlations between them. MTS cell viability, Transwell migration, glucose consumption and lactate production assays and flow cytometry were performed and mouse xenograft models were constructed to explore the functions and regulation of the PDL1 3?UTR and LDHA 3?UTR and miR-34a in TNBC. Results: We found that PDL1 and LDHA were synchronously upregulated in TNBC cell lines and tissues. Co-expression of PDL1 and LDHA was correlated with poor outcome in TNBC. Both PDL1 and LDHA are targets of miR-34a, and the 3?UTRs of PDL1 and LDHA both have binding sites for miR-34a. The functions of PDL1 and LDHA were inhibited by miR-34a. In addition, PDL1 and LDHA acted as ceRNAs to promote the expression and function of each other through regulation of miR-34a in TNBC. Conclusions: This study provides a new theoretical basis for a novel TNBC therapeutic strategy. Simultaneously targeting PDL1 and LDHA, which would combine immunotherapy and metabolically targeted treatments, might shed some light on the treatment of breast cancer, especially TNBC. Twit Text FOAVip PDL1 And LDHA act as ceRNAs in triple negative breast cancer by regulating miR-34a ????J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=28915924 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28915924 #FOAvip English Wikipedia <ref>{{Cite pmid|28915924}}</ref> PDL1 And LDHA act as ceRNAs in triple negative breast cancer by regulating miR-34a #MMPMID28915924 Huang X; Xie X; Wang H; Xiao X; Yang L; Tian Z; Guo X; Zhang L; Tang H; Xie X J Exp Clin Cancer Res 2017[]; 36 (ä): ä PMID28915924show ga Backgroud: The purpose of this study was to elucidate the regulation of programmed death ligand 1 (PDL1), lactate dehydrogenase A (LDHA) and miR-34a in triple negative breast cancer (TNBC) and to explore the function and mechanism of PDL1 and LDHA as competitive endogenous RNAs (ceRNAs) in TNBC via regulation of miR-34a. Methods: Western blotting, quantitative RT-PCR (qRT-PCR) and immunohistochemistry (IHC) assays were conducted to explore the expression of PDL1, LDHA and miR-34a in TNBC and correlations between them. MTS cell viability, Transwell migration, glucose consumption and lactate production assays and flow cytometry were performed and mouse xenograft models were constructed to explore the functions and regulation of the PDL1 3?UTR and LDHA 3?UTR and miR-34a in TNBC. Results: We found that PDL1 and LDHA were synchronously upregulated in TNBC cell lines and tissues. Co-expression of PDL1 and LDHA was correlated with poor outcome in TNBC. Both PDL1 and LDHA are targets of miR-34a, and the 3?UTRs of PDL1 and LDHA both have binding sites for miR-34a. The functions of PDL1 and LDHA were inhibited by miR-34a. In addition, PDL1 and LDHA acted as ceRNAs to promote the expression and function of each other through regulation of miR-34a in TNBC. Conclusions: This study provides a new theoretical basis for a novel TNBC therapeutic strategy. Simultaneously targeting PDL1 and LDHA, which would combine immunotherapy and metabolically targeted treatments, might shed some light on the treatment of breast cancer, especially TNBC. äPDL1 And LDHA act as ceRNAs in triple negative breast cancer by regula(epmc).pdf DeepDyve Pubget Overpricing