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Role of STAT3 in lung cancer. STAT3在肺癌中的作用
JAK-STAT Pub Date : 2015-01-20 eCollection Date: 2014-01-01 DOI: 10.1080/21623996.2014.999503
Pranabananda Dutta, Nafiseh Sabri, Jinghong Li, Willis X Li
{"title":"Role of STAT3 in lung cancer.","authors":"Pranabananda Dutta,&nbsp;Nafiseh Sabri,&nbsp;Jinghong Li,&nbsp;Willis X Li","doi":"10.1080/21623996.2014.999503","DOIUrl":"https://doi.org/10.1080/21623996.2014.999503","url":null,"abstract":"<p><p>Lung cancer remains a challenging disease. It is responsible for the high cancer mortality rates in the US and worldwide. Elucidation of the molecular mechanisms operative in lung cancer is an important first step in developing effective therapies. Accumulating evidence over the last 2 decades suggests a critical role for Signal Transducer and Activator of Transcription 3 (STAT3) as a point of convergence for various signaling pathways that are dysregulated in the disease. In this review, we discuss possible molecular mechanisms involving STAT3 in lung tumorigenesis based on recent literature. We consider possible roles of STAT3 in cancer cell proliferation and survival, in the tumor immune environment, and in epigenetic regulation and interaction of STAT3 with other transcription factors. We also discuss the potential role of STAT3 in tumor suppression, which complicates strategies of targeting STAT3 in cancer therapy. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 4","pages":"e999503"},"PeriodicalIF":0.0,"publicationDate":"2015-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/21623996.2014.999503","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34210321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 70
STAT4 is required for IL-23 responsiveness in Th17 memory cells and NKT cells. 在Th17记忆细胞和NKT细胞中，STAT4是IL-23响应性所必需的。
JAK-STAT Pub Date : 2014-10-30 eCollection Date: 2014-01-01 DOI: 10.4161/21623988.2014.955393
Nicole L Glosson-Byers, Sarita Sehra, Mark H Kaplan
{"title":"STAT4 is required for IL-23 responsiveness in Th17 memory cells and NKT cells.","authors":"Nicole L Glosson-Byers,&nbsp;Sarita Sehra,&nbsp;Mark H Kaplan","doi":"10.4161/21623988.2014.955393","DOIUrl":"https://doi.org/10.4161/21623988.2014.955393","url":null,"abstract":"<p><p>STAT4 is a critical mediator of inflammatory immunity and is required for all known IL-12 biological responses, including the induction of IFN-γ and development of Th1 cells. We demonstrate that IL-23, an IL-12-related cytokine, also requires STAT4 for optimal IL-17 secretion from memory T helper cells and NKT cells. Although IL-23 stimulation had modest effects on STAT4 activation, STAT4-deficiency results in reduced Il23r expression. These data demonstrate a restricted requirement for STAT4 in innate and adaptive IL-17-secreting T cell responses that might contribute to inflammatory immunity. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 3","pages":"e955393"},"PeriodicalIF":0.0,"publicationDate":"2014-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/21623988.2014.955393","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34210315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
JAK2 mutations to the fore in hereditary thrombocythemia. JAK2突变在遗传性血小板增多症中的作用。
JAK-STAT Pub Date : 2014-10-30 eCollection Date: 2014-01-01 DOI: 10.4161/21623988.2014.957618
Stephen E Langabeer
{"title":"JAK2 mutations to the fore in hereditary thrombocythemia.","authors":"Stephen E Langabeer","doi":"10.4161/21623988.2014.957618","DOIUrl":"https://doi.org/10.4161/21623988.2014.957618","url":null,"abstract":"<p><p>Acquired mutations of the gene that encodes the intracellular signalling molecule JAK2 are the most frequently observed disease-driving events of the common myeloproliferative neoplasms. A number of germline JAK2 mutations have recently been described in several kindred with the rare disease of hereditary thrombocythemia, also known as familial thrombocythemia or familial thrombocytosis. These inherited mutations are all located within the pseudo-kinase and kinase domains of JAK2 and have been shown to directly contribute to the thrombocythemic phenotype. Molecular characterisation of the resulting, aberrant signalling signatures may provide insights into genotype-phenotype relationships of both hereditary thrombocythemia and the common myeloproliferative neoplasms. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 3","pages":"e957618"},"PeriodicalIF":0.0,"publicationDate":"2014-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/21623988.2014.957618","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34210316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Contribution of chaperones to STAT pathway signaling. 伴侣蛋白在STAT通路信号传导中的作用。
JAK-STAT Pub Date : 2014-10-30 eCollection Date: 2014-01-01 DOI: 10.4161/21623988.2014.970459
Claire E Bocchini, Moses M Kasembeli, Soung-Hun Roh, David J Tweardy
{"title":"Contribution of chaperones to STAT pathway signaling.","authors":"Claire E Bocchini,&nbsp;Moses M Kasembeli,&nbsp;Soung-Hun Roh,&nbsp;David J Tweardy","doi":"10.4161/21623988.2014.970459","DOIUrl":"https://doi.org/10.4161/21623988.2014.970459","url":null,"abstract":"<p><p>Aberrant STAT signaling is associated with the development and progression of many cancers and immune related diseases. Recent findings demonstrate that proteostasis modulators under clinical investigation for cancer therapy have a significant impact on STAT signaling, which may be critical for mediating their anti-cancer effects. Chaperones are critical for protein folding, stability and function and, thus, play an essential role in the maintenance of proteostasis. In this review we discuss the role of chaperones in STAT and tyrosine kinase (TK) protein folding, modulation of STAT and TK activity, and degradation of TKs. We highlight the important role of chaperones in STAT signaling, and how this knowledge has provided a framework for the development of new therapeutic avenues of targeting STAT signaling related pathologies. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 3","pages":"e970459"},"PeriodicalIF":0.0,"publicationDate":"2014-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/21623988.2014.970459","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34210319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 27
A new mechanism for growth hormone receptor activation of JAK2, and implications for related cytokine receptors. JAK2生长激素受体激活的新机制及其对相关细胞因子受体的影响。
JAK-STAT Pub Date : 2014-06-16 eCollection Date: 2014-01-01 DOI: 10.4161/jkst.29569
Michael J Waters, Andrew J Brooks, Yash Chhabra
{"title":"A new mechanism for growth hormone receptor activation of JAK2, and implications for related cytokine receptors.","authors":"Michael J Waters,&nbsp;Andrew J Brooks,&nbsp;Yash Chhabra","doi":"10.4161/jkst.29569","DOIUrl":"https://doi.org/10.4161/jkst.29569","url":null,"abstract":"<p><p>The growth hormone receptor was the first cytokine receptor to be cloned and crystallized, and provides a valuable exemplar for activation of its cognate kinase, JAK2. We review progress in understanding its activation mechanism, in particular the molecular movements made by this constitutively dimerized receptor in response to ligand binding, and how these lead to a separation of JAK-binding Box1 motifs. Such a separation leads to removal of the pseudokinase inhibitory domain from the kinase domain of a partner JAK2 bound to the receptor, and vice versa, leading to apposition of the kinase domains and transactivation. This may be a general mechanism for class I cytokine receptor action. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 ","pages":"e29569"},"PeriodicalIF":0.0,"publicationDate":"2014-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.29569","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32566672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 32
Effects of JAK2-STAT3 signaling after cerebral insults. 脑损伤后JAK2-STAT3信号的影响
JAK-STAT Pub Date : 2014-06-12 eCollection Date: 2014-01-01 DOI: 10.4161/jkst.29510
Daniel J Raible, Lauren C Frey, Amy R Brooks-Kayal
{"title":"Effects of JAK2-STAT3 signaling after cerebral insults.","authors":"Daniel J Raible,&nbsp;Lauren C Frey,&nbsp;Amy R Brooks-Kayal","doi":"10.4161/jkst.29510","DOIUrl":"https://doi.org/10.4161/jkst.29510","url":null,"abstract":"<p><p>The JAK2-STAT3 signaling pathway has been shown to regulate the expression of genes involved in cell survival, cell proliferation, cell-cycle progression, and angiogenesis in development and after cerebral insults. Until recently, little has been known about the effects of this pathway activation after cerebral insults and if blocking this pathway leads to better recovery. This review exams the role of this pathway after 3 cerebral insults (traumatic brain injury, stroke, and status epilepticus). </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 ","pages":"e29510"},"PeriodicalIF":0.0,"publicationDate":"2014-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.29510","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32570681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 42
Propofol mediates signal transducer and activator of transcription 3 activation and crosstalk with phosphoinositide 3-kinase/AKT. 异丙酚介导磷酸化肌醇3-激酶/AKT的转录3激活和串扰的信号传导和激活因子。
JAK-STAT Pub Date : 2014-06-12 eCollection Date: 2014-01-01 DOI: 10.4161/jkst.29554
Jayant Shravah, Baohua Wang, Marijana Pavlovic, Ujendra Kumar, David Dy Chen, Honglin Luo, David M Ansley
{"title":"Propofol mediates signal transducer and activator of transcription 3 activation and crosstalk with phosphoinositide 3-kinase/AKT.","authors":"Jayant Shravah,&nbsp;Baohua Wang,&nbsp;Marijana Pavlovic,&nbsp;Ujendra Kumar,&nbsp;David Dy Chen,&nbsp;Honglin Luo,&nbsp;David M Ansley","doi":"10.4161/jkst.29554","DOIUrl":"https://doi.org/10.4161/jkst.29554","url":null,"abstract":"<p><p>We previously demonstrated that propofol, an intravenous anesthetic with anti-oxidative properties, activated the phosphoinositide 3-kinase (PI3K)/AKT pathway to increase the expression of B cell lymphoma (Bcl)-2 and, therefore the anti-apoptotic potential on cardiomyocytes. Here, we wanted to determine if propofol can also activate the Janus kinase (JAK) 2/signal transducer and activator of transcription (STAT) 3 pathway, another branch of cardioprotective signaling. The cellular response of nuclear factor kappa B (NFκB) and STAT3 was also evaluated. Cardiac H9c2 cells were treated by propofol alone or in combination with pretreatment by inhibitors for JAK2/STAT3 or PI3K/AKT pathway. STAT3 and AKT phosphorylation, and STAT3 translocation were measured by western blotting and immunofluorescence staining, respectively. Propofol treatment significantly increased STAT3 phosphorylation at both tyrosine 705 and serine 727 residues. Sustained early phosphorylation of STAT3 was observed with 25~75 μM propofol at 10 and 30 min. Nuclear translocation of STAT3 was seen at 4 h after treatment with 50 μM propofol. In cultured H9c2 cells, we further demonstrated that propofol-induced STAT3 phosphorylation was reduced by pretreatment with PI3K/AKT pathway inhibitors wortmannin or API-2. Conversely, pretreatment with JAK2/STAT3 pathway inhibitor AG490 or stattic inhibited propofol-induced AKT phosphorylation. In addition, propofol induced NFκB p65 subunit perinuclear translocation. Inhibition or knockdown of STAT3 was associated with increased levels of the NFκB p65 subunit. Our results suggest that propofol induces an adaptive response by dual activation and crosstalk of cytoprotective PI3K/AKT and JAK2/STAT3 pathways. Rationale to apply propofol clinically as a preemptive cardioprotectant during cardiac surgery is supported by our findings. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 ","pages":"e29554"},"PeriodicalIF":0.0,"publicationDate":"2014-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.29554","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32570683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 35
STAT3 and epithelial-mesenchymal transitions in carcinomas. STAT3与癌中上皮-间质转化。
JAK-STAT Pub Date : 2014-01-01 Epub Date: 2014-04-29 DOI: 10.4161/jkst.28975
Michael K Wendt, Nikolas Balanis, Cathleen R Carlin, William P Schiemann
{"title":"STAT3 and epithelial-mesenchymal transitions in carcinomas.","authors":"Michael K Wendt,&nbsp;Nikolas Balanis,&nbsp;Cathleen R Carlin,&nbsp;William P Schiemann","doi":"10.4161/jkst.28975","DOIUrl":"https://doi.org/10.4161/jkst.28975","url":null,"abstract":"<p><p>Cellular programs coupled to cycles of epithelial-mesenchymal transitions (EMTs) play critical roles during embryogenesis, as well as during tissue development, remodeling, and repair. Research over the last decade has established the importance of an ever-expanding list of master EMT transcription factors, whose activity is regulated by STAT3 and function to stimulate the rapid transition of cells between epithelial and mesenchymal phenotypes. Importantly, inappropriate reactivation of embryonic EMT programs in carcinoma cells underlies their metastasis to distant organ sites, as well as their acquisition of stem cell-like and chemoresistant phenotypes operant in eliciting disease recurrence. Thus, targeted inactivation of master EMT transcription factors may offer new inroads to alleviate metastatic disease. Here we review the molecular, cellular, and microenvironmental factors that contribute to the pathophysiological activities of STAT3 during its regulation of EMT programs in human carcinomas. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 1","pages":"e28975"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.28975","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32353160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 173
The involvement of JAK-STAT3 in cell motility, invasion, and metastasis. JAK-STAT3参与细胞运动、侵袭和转移。
JAK-STAT Pub Date : 2014-01-01 Epub Date: 2014-02-20 DOI: 10.4161/jkst.28086
Yong Teng, James L Ross, John K Cowell
{"title":"The involvement of JAK-STAT3 in cell motility, invasion, and metastasis.","authors":"Yong Teng,&nbsp;James L Ross,&nbsp;John K Cowell","doi":"10.4161/jkst.28086","DOIUrl":"https://doi.org/10.4161/jkst.28086","url":null,"abstract":"<p><p>JAK-STAT3 signaling, while regulating many aspects of cancer development and progression, promotes invasion and metastasis through activation of key metastasis promoting genes such as WASF3. STAT3 promotes WASF3 expression and JAK2 independently activates it, which is required for invasion. JAK-STAT3 signaling is dependent on WASF3 function, since its inactivation in cells expressing JAK-STAT3 suppresses invasion. WASF3 overexpression leads to activation of NFκB and ZEB1 which also promote invasion through regulation of target genes involved in metastasis. NFκB frequently cooperates with STAT3 to upregulate metastasis promoting genes such as matrix metalloproteinases and cytokines, as well as to suppress microRNAs which can suppresses invasion. This better understanding of the complex role played by JAK-STAT3 in the regulation of cell movement, invasion, and metastasis provides opportunities to suppress this lethal aspect of cancer progression by not only targeting the JAK and STAT3 proteins directly, but also some of the downstream effectors of JAK-STAT3 signaling. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 1","pages":"e28086"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.28086","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32299291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 123
Protein tyrosine phosphatases as wardens of STAT signaling. 蛋白酪氨酸磷酸酶作为STAT信号的监管人。
JAK-STAT Pub Date : 2014-01-01 Epub Date: 2014-02-20 DOI: 10.4161/jkst.28087
Frank-D Böhmer, Karlheinz Friedrich
{"title":"Protein tyrosine phosphatases as wardens of STAT signaling.","authors":"Frank-D Böhmer,&nbsp;Karlheinz Friedrich","doi":"10.4161/jkst.28087","DOIUrl":"https://doi.org/10.4161/jkst.28087","url":null,"abstract":"<p><p>Signaling by signal transducers and activators of transcription (STATs) is controlled at many levels of the signaling cascade. Protein tyrosine phosphatases (PTPs) regulate STAT activation at several layers, including direct pSTAT dephosphorylation in both cytoplasm and nucleus. Despite the importance of this regulation mode, many aspects are still incompletely understood, e.g., the identity of PTPs acting on certain members of the STAT family. After a brief introduction into the STAT and PTP families, we discuss here the current knowledge on PTP mediated regulation of STAT activity, focusing on the interaction of individual STATs with specific PTPs. Finally, we highlight open questions and propose important tasks of future research. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"3 1","pages":"e28087"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.28087","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32299292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 84
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