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10.1152/ajpgi.00419.2015 http://scihub22266oqcxt.onion/10.1152/ajpgi.00419.2015 C4836134!4836134 !26867566     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26867566 &cmd=llinks): Failed to open stream: HTTP request failed! 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Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24 |pdf=|usr=}}{{26867566 }} gab.com Text Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24 JO: Am J Physiol Gastrointest Liver Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26867566 #FOAvip The Na(+)/H(+) exchanger regulatory factor (NHERF) family of proteins is scaffolds that orchestrate interaction of receptors and cellular proteins. Previous studies have shown that NHERF1 functions as a tumor suppressor. The goal of this study is to determine whether the loss of NHERF2 alters colorectal cancer (CRC) progress. We found that NHERF2 expression is elevated in advanced-stage CRC. Knockdown of NHERF2 decreased cancer cell proliferation in vitro and in a mouse xenograft tumor model. In addition, deletion of NHERF2 in Apc(Min/+) mice resulted in decreased tumor growth in Apc(Min/+) mice and increased lifespan. Blocking NHERF2 interaction with a small peptide designed to bind the second PDZ domain of NHERF2 attenuated cancer cell proliferation. Although NHERF2 is known to facilitate the effects of lysophosphatidic acid receptor 2 (LPA2), transcriptome analysis of xenograft tumors revealed that NHERF2-dependent genes largely differ from LPA2-regulated genes. Activation of ?-catenin and ERK1/2 was mitigated in Apc(Min/+);Nherf2(-/-) adenomas. Moreover, Stat3 phosphorylation and CD24 expression levels were suppressed in Apc(Min/+);Nherf2(-/-) adenomas. Consistently, NHERF2 knockdown attenuated Stat3 activation and CD24 expression in colon cancer cells. Interestingly, CD24 was important in the maintenance of Stat3 phosphorylation, whereas NHERF2-dependent increase in CD24 expression was blocked by inhibition of Stat3, suggesting that NHERF2 regulates Stat3 phosphorylation through a positive feedback mechanism between Stat3 and CD24. In summary, this study identifies NHERF2 as a novel oncogenic protein and a potential target for cancer treatment. NHERF2 potentiates the oncogenic effects in part by regulation of Stat3 and CD24. Twit Text FOAVip Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24 ????Am J Physiol Gastrointest Liver Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26867566 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26867566 #FOAvip English Wikipedia <ref>{{Cite pmid|26867566 }}</ref> Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24 #MMPMID26867566 Yoshida M ; Zhao L ; Grigoryan G ; Shim H ; He P ; Yun CC Am J Physiol Gastrointest Liver Physiol 2016[Apr]; 310 (8 ): G586-98 PMID26867566 show ga The Na(+)/H(+) exchanger regulatory factor (NHERF) family of proteins is scaffolds that orchestrate interaction of receptors and cellular proteins. Previous studies have shown that NHERF1 functions as a tumor suppressor. The goal of this study is to determine whether the loss of NHERF2 alters colorectal cancer (CRC) progress. We found that NHERF2 expression is elevated in advanced-stage CRC. Knockdown of NHERF2 decreased cancer cell proliferation in vitro and in a mouse xenograft tumor model. In addition, deletion of NHERF2 in Apc(Min/+) mice resulted in decreased tumor growth in Apc(Min/+) mice and increased lifespan. Blocking NHERF2 interaction with a small peptide designed to bind the second PDZ domain of NHERF2 attenuated cancer cell proliferation. Although NHERF2 is known to facilitate the effects of lysophosphatidic acid receptor 2 (LPA2), transcriptome analysis of xenograft tumors revealed that NHERF2-dependent genes largely differ from LPA2-regulated genes. Activation of ?-catenin and ERK1/2 was mitigated in Apc(Min/+);Nherf2(-/-) adenomas. Moreover, Stat3 phosphorylation and CD24 expression levels were suppressed in Apc(Min/+);Nherf2(-/-) adenomas. Consistently, NHERF2 knockdown attenuated Stat3 activation and CD24 expression in colon cancer cells. Interestingly, CD24 was important in the maintenance of Stat3 phosphorylation, whereas NHERF2-dependent increase in CD24 expression was blocked by inhibition of Stat3, suggesting that NHERF2 regulates Stat3 phosphorylation through a positive feedback mechanism between Stat3 and CD24. In summary, this study identifies NHERF2 as a novel oncogenic protein and a potential target for cancer treatment. NHERF2 potentiates the oncogenic effects in part by regulation of Stat3 and CD24. |*Gene Deletion [MESH] |Adenoma/genetics/*metabolism/pathology [MESH] |Adenomatous Polyposis Coli Protein/genetics [MESH] |Animals [MESH] |CD24 Antigen/genetics/*metabolism [MESH] |Cell Proliferation [MESH] |Colonic Neoplasms/genetics/*metabolism/pathology [MESH] |Feedback, Physiological [MESH] |Female [MESH] |HCT116 Cells [MESH] |HT29 Cells [MESH] |Humans [MESH] |Mice [MESH] |Mice, Nude [MESH] |Mitogen-Activated Protein Kinase 1/metabolism [MESH] |Mitogen-Activated Protein Kinase 3/metabolism [MESH] |Phosphoproteins/genetics/*metabolism [MESH] |STAT3 Transcription Factor/genetics/*metabolism [MESH] |Sodium-Hydrogen Exchangers/genetics/*metabolism [MESH]Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cance(epmc).pdf DeepDyve Pubget Overpricing