Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1158/0008-5472.CAN-15-2265 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-2265 C4775337!4775337!26837760     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2016 ; 76 (5): 1204-13 Nephropedia Template TP {{tp|p=26837760|t=2016. G0S2 suppresses oncogenic transformation by repressing a Myc-regulated transcriptional program |pdf=|usr=}}{{26837760}} gab.com Text G0S2 suppresses oncogenic transformation by repressing a Myc-regulated transcriptional program JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26837760 #FOAvip Methylation-mediated silencing of G0S2 has been detected in a variety of solid tumors, whereas G0S2 induction is associated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may possess tumor suppressor activity. In this study, we clearly demonstrate that G0S2 opposes oncogene-induced transformation using G0S2-null immortalized mouse embryonic fibroblasts (MEFs). G0S2-null MEFs were readily transformed with HRAS or EGFR treatment compared to wildtype MEFs. Importantly, restoration of G0S2 reversed HRAS-driven transformation. G0S2 is known to regulate fat metabolism by attenuating adipose triglyceride lipase (ATGL), but repression of oncogene-induced transformation by G0S2 was independent of ATGL inhibition. Gene expression analysis revealed that an upregulation of gene signatures associated with transformation, proliferation, and MYC targets in G0S2-null MEFs. RNAi-mediated ablation and pharmacologic inhibition of MYC abrogated oncogene-induced transformation of G0S2-null MEFs. Furthermore, we found that G0S2 was highly expressed in normal breast tissues compared to malignant tissue. Intriguingly, high levels of G0S2 were also associated with a decrease in breast cancer recurrence rates, especially in estrogen receptor-positive subtypes, and overexpression of G0S2 repressed the proliferation of breast cancer cells in vitro. Taken together, these findings indicate that G0S2 functions as a tumor suppressor in part by opposing MYC activity, prompting further investigation of the mechanisms by which G0S2 silencing mediates MYC-induced oncogenesis in other malignancies. Twit Text FOAVip G0S2 suppresses oncogenic transformation by repressing a Myc-regulated transcriptional program ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26837760 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26837760 #FOAvip English Wikipedia <ref>{{Cite pmid|26837760}}</ref> G0S2 suppresses oncogenic transformation by repressing a Myc-regulated transcriptional program #MMPMID26837760 Yim CY; Sekula DJ; Hever-Jardine MP; Liu X; Warzecha JM; Tam J; Freemantle SJ; Dmitrovsky E; Spinella MJ Cancer Res 2016[Mar]; 76 (5): 1204-13 PMID26837760show ga Methylation-mediated silencing of G0S2 has been detected in a variety of solid tumors, whereas G0S2 induction is associated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may possess tumor suppressor activity. In this study, we clearly demonstrate that G0S2 opposes oncogene-induced transformation using G0S2-null immortalized mouse embryonic fibroblasts (MEFs). G0S2-null MEFs were readily transformed with HRAS or EGFR treatment compared to wildtype MEFs. Importantly, restoration of G0S2 reversed HRAS-driven transformation. G0S2 is known to regulate fat metabolism by attenuating adipose triglyceride lipase (ATGL), but repression of oncogene-induced transformation by G0S2 was independent of ATGL inhibition. Gene expression analysis revealed that an upregulation of gene signatures associated with transformation, proliferation, and MYC targets in G0S2-null MEFs. RNAi-mediated ablation and pharmacologic inhibition of MYC abrogated oncogene-induced transformation of G0S2-null MEFs. Furthermore, we found that G0S2 was highly expressed in normal breast tissues compared to malignant tissue. Intriguingly, high levels of G0S2 were also associated with a decrease in breast cancer recurrence rates, especially in estrogen receptor-positive subtypes, and overexpression of G0S2 repressed the proliferation of breast cancer cells in vitro. Taken together, these findings indicate that G0S2 functions as a tumor suppressor in part by opposing MYC activity, prompting further investigation of the mechanisms by which G0S2 silencing mediates MYC-induced oncogenesis in other malignancies. äG0S2 suppresses oncogenic transformation by repressing a Myc-regulated(epmc).pdf DeepDyve Pubget Overpricing