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Cancer letters 20건

  1. [해외논문]   TAp73 inhibits cell invasion and migration by directly activating KAI1 expression in colorectal carcinoma   SCI SCIE

    Bae, Woo-Kyun (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Hong, Chang-Soo (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Park, Mi-Ra (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Sun, Eun-Gene (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Lee, Ji-Hee (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Kang, Keunsoo (Department of Microbiology, Dankook University, Cheonan, South Korea ) , Ryu, Kyung-Hyun (Department of Biological Science, Sookmyung Women's University, Seoul, South Korea ) , Shim, Hyun-Jeong (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Hwang, Jun-Eul (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Cho, Sang-Hee (Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea ) , Chung, Ik-Joo (Department of Hemato-Oncology, Chonnam National University H)
    Cancer letters v.415 ,pp. 106 - 116 , 2018 , 0304-3835 ,

    초록

    Abstract p73 is a member of the p53 family of transcription factors and, like p53, plays a role as a tumor suppressor. p73 is involved in development, proliferation, apoptosis and metastasis. However, the precise molecular mechanisms underlying its function in inhibiting metastasis remain largely unknown. Here, we show that induction of TAp73 decreased invasion and migration activity of colorectal cancer cells, whereas knockdown of TAp73 led to increased invasion and migration activity. KAI1 was identified as a transcriptional target of TAp73 and its expression is indispensable for TAp73-mediated inhibition of cell invasion and migration. Furthermore, induction of TAp73 in colorectal cancer cells elevated KAI1 expression and decreased the frequency of hepatic metastasis in vivo . Whereas, the decreased invasion and migration activities caused by TAp73 induction were abrogated by knockdown of KAI1. Interestingly, TAp73 and KAI1 are overexpressed in primary colorectal cancers and a significant correlation between TAp73 and KAI1 expression was detected, but their expressions were significantly down-regulated in metastatic cancers. Taken together, our results support a novel role for TAp73 in controlling colorectal cancer cell invasion, migration and metastasis by regulating transcription of KAI1. Highlights TAp73 inhibits invasion, migration and metastasis of colorectal cancer cells. TAp73 directly binds to the KAI1 promoter and induces its expression. KAI1 is indispensable for TAp73-mediated inhibition of cell invasion and migration. TAp73 and KAI1 expression levels are positively correlated in human colorectal cancer.

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  2. [해외논문]   The role of STAT3 in leading the crosstalk between human cancers and the immune system   SCI SCIE

    Wang, Yu (Department of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China ) , Shen, Yicheng (University of Texas Medical Branch School of Medicine, Galveston, TX 77555, USA ) , Wang, Sinan (Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin Gastroenterology and Hepatology Institute, Tianjin 300070, China ) , Shen, Qiang (Department of Clinical Cancer Prevention, Division of Cancer Prevention and Population Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA ) , Zhou, Xuan (Department of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China)
    Cancer letters v.415 ,pp. 117 - 128 , 2018 , 0304-3835 ,

    초록

    Abstract The development and progression of human cancers are continuously and dynamically regulated by intrinsic and extrinsic factors. As a converging point of multiple oncogenic pathways, signal transducer and activator of transcription 3 (STAT3) is constitutively activated both in tumor cells and tumor-infiltrated immune cells. Activated STAT3 persistently triggers tumor progression through direct regulation of oncogenic gene expression. Apart from its oncogenic role in regulating gene expression in tumor cells, STAT3 also paves the way for human cancer growth through immunosuppression. Activated STAT3 in immune cells results in inhibition of immune mediators and promotion of immunosuppressive factors. Therefore, STAT3 modulates the interaction between tumor cells and host immunity. Accumulating evidence suggests that targeting STAT3 may enhance anti-cancer immune responses and rescue the suppressed immunologic microenvironment in tumors. Taken together, STAT3 has emerged as a promising target in cancer immunotherapy. Highlights STAT3 is constitutively activated in both tumor cells and immune cells. Tumor progression can be triggered by STAT3 through direct regulation of oncogenes. STAT3 also mediates human cancer growth through tumor-induced immunosuppression. STAT3's dual role in both cancer and immunity renders it a promising target for cancer therapy.

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  3. [해외논문]   Diabetes as risk factor for pancreatic cancer: Hyperglycemia promotes epithelial-mesenchymal-transition and stem cell properties in pancreatic ductal epithelial cells   SCI SCIE

    Rahn, Sascha (Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UKSH) Campus Kiel, Kiel, Germany ) , Zimmermann, Vivien (Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UKSH) Campus Kiel, Kiel, Germany ) , Viol, Fabrice (Department of Medicine I, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ) , Knaack, Hendrike (Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UKSH) Campus Kiel, Kiel, Germany ) , Stemmer, Kerstin (Helmholtz Zentrum München, Deutsches Forschungszentrum für Gesundheit und Umwelt (GmbH), Neuherberg, Germany ) , Peters, Lena (Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medical Center Schleswig-Holstein (UKSH) Campus Kiel, Kiel, Germany ) , Lenk, Lennart (Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel (CAU) and University Medi) , Ungefroren, Hendrik , Saur, Dieter , Schä , fer, Heiner , Helm, Ole , Sebens, Susanne
    Cancer letters v.415 ,pp. 129 - 150 , 2018 , 0304-3835 ,

    초록

    Abstract Type 2 diabetes mellitus (T2DM) is associated with hyperglycemia and a risk to develop pancreatic ductal adenocarcinoma (PDAC), one of the most fatal malignancies. Cancer stem cells (CSC) are essential for initiation and maintenance of tumors, and acquisition of CSC-features is linked to epithelial-mesenchymal-transition (EMT). The present study investigated whether hyperglycemia promotes EMT and CSC-features in premalignant and malignant pancreatic ductal epithelial cells (PDEC). Under normoglycemia (5 mM D -glucose), Panc1 PDAC cells but not premalignant H6c7-kras cells exhibited a mesenchymal phenotype along with pronounced colony formation. While hyperglycemia (25 mM D -glucose) did not impact the mesenchymal phenotype of Panc1 cells, CSC-properties were aggravated exemplified by increased Nanog expression and Nanog-dependent formation of holo- and meroclones. In H6c7-kras cells, high glucose increased secretion of Transforming-Growth-Factor-beta1 (TGF-β1) as well as TGF-β1 signaling, and in a TGF-β1-dependent manner reduced E-cadherin expression, increased Nestin expression and number of meroclones. Finally, reduced E-cadherin expression was detected in pancreatic ducts of hyperglycemic but not normoglycemic mice. These data suggest that hyperglycemia promotes the acquisition of mesenchymal and CSC-properties in PDEC by activating TGF-β signaling and might explain how T2DM facilitates pancreatic tumorigenesis. Highlights Elevated glucose levels aggravate cancer stemness in pancreatic cancer cells. Hyperglycemia essentially impacts already on pancreatic ductal epithelial cells. Hyperglycemia-induced mesenchymal and CSC-properties are TGF-β1 dependent. This study gives insight how hyperglycemia contributes to pancreatic tumorigenesis.

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  4. [해외논문]   The atypical protein kinase RIOK3 contributes to glioma cell proliferation/survival, migration/invasion and the AKT/mTOR signaling pathway   SCI SCIE

    Zhang, Tong (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Ji, Daofei (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Wang, Peng (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Liang, Dong (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Jin, Lei (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Shi, Hengliang (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Liu, Xuejiao (Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Meng, Qingming (Brain Hospital, The Affiliated Hospital of Xuzhou Medical University, 99 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China ) , Yu, Rutong (Institute of Nervous System Disease) , Gao, Shangfeng
    Cancer letters v.415 ,pp. 151 - 163 , 2018 , 0304-3835 ,

    초록

    Abstract The RIO (right open reading frame) protein kinases include RIOK1, RIOK2 and RIOK3. Emerging evidence has suggested an important role of RIO kinases in cancer cell proliferation, apoptosis, migration and invasion. However, the expression profile and specific roles of RIOK3 are largely unknown during glioma progression. In the current study, quantitative real-time PCR, Western blot, and immunohistochemical analysis showed that RIOK3 was upregulated in glioma tissues. Available database analysis revealed that higher levels of RIOK3 were associated with poorer survival outcome in glioma patients. Flow cytometry, CCK8 and EdU assays showed that downregulation of RIOK3 arrested cell cycle progression and inhibited glioma cell proliferation. Wound healing, transwell and gelatin zymography assays revealed that silencing RIOK3 decreased glioma cell migration and invasion. Furthermore, the downregulation of RIOK3 significantly decreased the activity of AKT/mTOR signaling and induced apoptosis in glioma cells. Overexpression of RIOK3 showed the opposite effects on glioma cell proliferation, migration, invasion and the AKT/mTOR pathway. These results indicate that high RIOK3 levels in gliomas appear to contribute to the growth and expansion of this cancer, and may thus serve as a novel therapeutic target. Highlights Increased RIOK3-mRNA and -protein levels in glioma tissues. Silencing RIOK3 inhibits glioma cell proliferation, migration and invasion. Overexpressing RIOK3 promotes glioma cell proliferation, migration and invasion. Silencing RIOK3 induces glioma cell apoptosis. RIOK3 positively regulates the activity of the AKT/mTOR pathway in glioma cells.

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  5. [해외논문]   HDAC6 inhibition induces glioma stem cells differentiation and enhances cellular radiation sensitivity through the SHH/Gli1 signaling pathway   SCI SCIE

    Yang, Wei (School of Radiological Medicine and Protection, Medical College of Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, Jiangsu, 215123, China ) , Liu, Yingying (School of Radiological Medicine and Protection, Medical College of Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, Jiangsu, 215123, China ) , Gao, Ruoling (School of Radiological Medicine and Protection, Medical College of Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, Jiangsu, 215123, China ) , Yu, Hongquan (Department of Neurosurgery of the First Affiliated Hospital of Jilin University, Changchun, Jilin, 130021, China ) , Sun, Ting (Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China)
    Cancer letters v.415 ,pp. 164 - 176 , 2018 , 0304-3835 ,

    초록

    Abstract The existence of small numbers of stem-like cells, called glioma stem cells (GSCs), in human glioblastoma multiforme (GBM) is responsible for recurrence due to resistance to radiotherapy and chemotherapy. Inhibition of histone deacetylase 6 (HDAC6) enhanced radiosensitivity of cancer cells. However, the effect of inhibiting HDAC6 on stemness and radioresistance of GSCs and its molecular mechanism are largely unknown. In the present study, we found that HDAC6 was upregulated in GSCs comparing to non-stem tumor cells. Inhibiting HDAC6 downregulated glioma-associated oncogene homolog 1 (Gli1), Patched (Ptch1 and Ptch2) receptors, components of SHH signal, expression and activity in GSCs. Restraining HDAC6 decreased cell proliferation, induces differentiation and increased apoptosis of GSCs via inactivation of SHH/Gli1 signaling pathway. Moreover, HDAC6 inhibition decreased DNA damage repair capacity of GSCs through degradation of checkpoint kinase (CHK) 1 caused by X-linked inhibitor of apoptosis (XIAP) downregulation, leading to elevated radiosensitivity. Taken together, these findings indicate that HDAC6 inhibition decreased stemness of GSCs and enhanced GSCs radiosensitivity through inactivating SHH/Gli1 pathway. This provides a promising novel drug target to overcome GSCs stemness and radioresistance. Highlights HDAC6i decreased stemness of GSCs. HDAC6i enhanced GSCs radiosensitivity via inactivating SHH/Gli1 pathway. HDAC6i decreased DDR of GSCs via CHK1/XIAP pathway.

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  6. [해외논문]   Bad phosphorylation as a target of inhibition in oncology   SCI SCIE

    Bui, Ngoc-Linh-Chi (Cancer Science Institute of Singapore, National University of Singapore, Singapore ) , Pandey, Vijay (Tsinghua Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, Guangdong, PR China ) , Zhu, Tao (Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China ) , Ma, Lan (Tsinghua Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, Guangdong, PR China ) , Basappa, Lan (Laboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore, 570006, India ) , Lobie, Peter E. (Cancer Science Institute of Singapore, National University of Singapore, Singapore)
    Cancer letters v.415 ,pp. 177 - 186 , 2018 , 0304-3835 ,

    초록

    Abstract Bcl-2 agonist of cell death (BAD) is a BH3-only member of the Bcl-2 family which possesses important regulatory function in apoptosis. BAD has also been shown to possess many non-apoptotic functions closely linked to cancer including regulation of glycolysis, autophagy, cell cycle progression and immune system development. Interestingly, BAD can be either pro-apoptotic or pro-survival depending on the phosphorylation state of three specific serine residues (human S75, S99 and S118). Expression of BAD and BAD phosphorylation patterns have been shown to influence tumor initiation and progression and play a predictive role in disease prognosis, drug response and chemosensitivity in various cancers. This review aims to summarize the current evidence on the functional role of BAD phosphorylation in human cancer and evaluate the potential utility of modulating BAD phosphorylation in cancer. Highlights BAD has pro-apoptosis and pro-survival functions involved in cancer development. BAD is phosphorylated by kinases that are linked to cancer cell survival pathways. Phosphorylation of BAD were shown to promote survival and drug resistance in cancer. Abrogating BAD phosphorylation by kinase inhibitors have shown limited success. Novel strategies to target BAD phosphorylation need to be developed.

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  7. [해외논문]   Supersulfated low-molecular weight heparin synergizes with IGF1R/IR inhibitor to suppress synovial sarcoma growth and metastases   SCI SCIE

    Cassinelli, Giuliana (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy ) , Dal Bo, Laura (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy ) , Favini, Enrica (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy ) , Cominetti, Denis (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy ) , Pozzi, Sabina (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy ) , Tortoreto, Monica (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy ) , De Cesare, Michelandrea (Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42,) , Lecis, Daniele , Scanziani, Eugenio , Minoli, Lucia , Naggi, Annamaria , Vlodavsky, Israel , Zaffaroni, Nadia , Lanzi, Cinzia
    Cancer letters v.415 ,pp. 187 - 197 , 2018 , 0304-3835 ,

    초록

    Abstract Synovial sarcoma (SS) is an aggressive tumor with propensity for lung metastases which significantly impact patients' prognosis. New therapeutic approaches are needed to improve treatment outcome. Targeting the heparanase/heparan sulfate proteoglycan system by heparin derivatives which act as heparanase inhibitors/heparan sulfate mimetics is emerging as a therapeutic approach that can sensitize the tumor response to chemotherapy. We investigated the therapeutic potential of a supersulfated low molecular weight heparin (ssLMWH) in preclinical models of SS. ssLMWH showed a potent anti-heparanase activity, dose-dependently inhibited SS colony growth and cell invasion, and downregulated the activation of receptor tyrosine kinases including IGF1R and IR. The combination of ssLMWH and the IGF1R/IR inhibitor BMS754807 synergistically inhibited proliferation of cells exhibiting IGF1R hyperactivation, also abrogating cell motility and promoting apoptosis in association with PI3K/AKT pathway inhibition. The drug combination strongly enhanced the antitumor effect against the CME-1 model, as compared to single agent treatment, abrogating orthotopic tumor growth and significantly repressing spontaneous lung metastatic dissemination in treated mice. These findings provide a strong preclinical rationale for developing drug regimens combining heparanase inhibitors/HS mimetics with IGF1R antagonists for treatment of metastatic SS. Highlights ssLMWH inhibits heparanase and activation of RTKs in synovial sarcoma cells. ssLMWH enhances IGF1R pathway inhibition and apoptosis induced by BMS754807. ssLMWH and BMS754807 synergize inhibiting growth of cells with hyperactive IGF1R. ssLMWH and BMS754807 synergize inhibiting cell migration. ssLMWH/BMS754807 cooperation results in strong antitumor/antimetastatic efficacy.

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  8. [해외논문]   ELL2 regulates DNA non-homologous end joining (NHEJ) repair in prostate cancer cells   SCI SCIE

    Zang, Yachen (Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China ) , Pascal, Laura E. (Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA ) , Zhou, Yibin (Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China ) , Qiu, Xiaonan (Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA ) , Wei, Leizhen (University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 5117 Centre Avenue, Pittsburgh, PA 15213, USA ) , Ai, Junkui (Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA ) , Nelson, Joel B. (Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA ) , Zhong, Mingming (Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA ) , Xue, Boxin (Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China ) , Wang, Shaoxiong (Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China ) , Yang, Dongrong (Department o) , Lan, Li , Shan, Yuxi , Wang, Zhou
    Cancer letters v.415 ,pp. 198 - 207 , 2018 , 0304-3835 ,

    초록

    Abstract ELL2 is an androgen-responsive gene that is expressed by prostate epithelial cells and is frequently down-regulated in prostate cancer. Deletion of Ell2 in the murine prostate induced murine prostatic intraepithelial neoplasia and ELL2 knockdown enhanced proliferation and migration in C4-2 prostate cancer cells. Here, knockdown of ELL2 sensitized prostate cancer cells to DNA damage and overexpression of ELL2 protected prostate cancer cells from DNA damage. Knockdown of ELL2 impaired non-homologous end joining repair but not homologous recombination repair. Transfected ELL2 co-immunoprecipitated with both Ku70 and Ku80 proteins. ELL2 could bind to and co-accumulate with Ku70/Ku80 proteins at sites of DNA damage. Knockdown of ELL2 dramatically inhibited Ku70 and Ku80 recruitment and retention at DNA double-strand break sites in prostate cancer cells. The impaired recruitment of Ku70 and Ku80 proteins to DNA damage sites upon ELL2 knockdown was rescued by re-expression of an ELL2 transgene insensitive to siELL2. This study suggests that ELL2 is required for efficient NHEJ repair via Ku70/Ku80 in prostate cancer cells. Highlights ELL2 knockdown sensitized prostate cancer cells to DNA damage; ELL2 overexpression protected cells. ELL2 knockdown impaired non-homologous end joining repair but not homologous recombination repair. ELL2 could bind to and co-accumulate with Ku70/Ku80 proteins at DNA damage sites. ELL2 knockdown inhibited Ku70/Ku80 recruitment and retention at DNA double-strand break sites. ELL2 is required for efficient NHEJ repair via Ku70/Ku80 in prostate cancer cells.

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  9. [해외논문]   Prohibitin: A new player in immunometabolism and in linking obesity and inflammation with cancer   SCI SCIE

    Zi Xu, Yang Xin (Department of Physiology and Pathophysiology, Canada ) , Ande, Sudharsana Rao (Department of Internal Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada ) , Mishra, Suresh (Department of Physiology and Pathophysiology, Canada)
    Cancer letters v.415 ,pp. 208 - 216 , 2018 , 0304-3835 ,

    초록

    Abstract Immunometabolism, which has important implications in cancer biology, has emerged as a major regulator of different immune cell types. Various factors that integrate metabolic switches within immune cells with signal directed program that promote or inhibit their functions remain largely unidentified. Furthermore, sex differences are known to exist in immune functions and cancer incidences in the body and sex steroid hormones are integral component of these differences. However, factors that mediate such differences, and the potential link between the two fundamental aspects of immune cell biology that contributes to sex differences in health and disease remain unexplored. New evidence derived from novel tissue-specific transgenic mouse models of prohibitin (PHB) has revealed its crucial role in sex differences in adipocyte and macrophage functions and a potential role in endocrine-immune crosstalk. This review provides a point of view on the emerging role of PHB in immune functions with special focus on immunometabolism and on the immunomodulatory effects of sex steroids. We propose that PHB plays a crucial role in integrating cell signaling events with metabolic switches, and may serve as a potential target for cancer immunotherapeutic. Highlights PHB plays a crucial role in sex differences in adipose and immune functions. PHB and sex steroids regulate each other's functions in adipocyte and immune cells. PHB has a role in the immunomodulatory effects of estrogen. PHB integrates cell signaling events with immunometabolism.

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  10. [해외논문]   LB-100, a novel Protein Phosphatase 2A (PP2A) inhibitor, sensitizes malignant meningioma cells to the therapeutic effects of radiation   SCI SCIE

    Ho, Winson S. (Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA ) , Sizdahkhani, Saman (Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA ) , Hao, Shuyu (Neuro-oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA ) , Song, Hua (Neuro-oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA ) , Seldomridge, Ashlee (Neuro-oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA ) , Tandle, Anita (Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA ) , Maric, Dragan (Flow Cytometry Core, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA ) , Kramp, Tamalee (Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA ) , Lu, Rongze (AbbVie Biotherapeutics, Redwood City, CA, USA ) , Heiss, John D. (Surgical Neurology Branch, National Inst) , Camphausen, Kevin , Gilbert, Mark R. , Zhuang, Zhengping , Park, Deric M.
    Cancer letters v.415 ,pp. 217 - 226 , 2018 , 0304-3835 ,

    초록

    Abstract Atypical and anaplastic meningiomas (AAM) represent 20% of all meningiomas. They are associated with poor outcomes due to their tendency to recur. While surgery and radiation (RT) are first line therapy, no effective systemic medical treatment has been identified. Protein phosphatase 2A (PP2A) is a ubiquitously expressed serine/threonine phosphatase involved in cell cycle regulation and DNA repair. Here, we examined radiosensitizing effects of LB-100, a novel inhibitor of PP2A against AAM as a novel treatment strategy. Three human-derived immortalized meningioma cell lines, IOMM-LEE, GAR, and CH-157, were used to investigate the radio-sensitizing potential of LB-100 in AAM. Survival fraction by clonogenic assay, immunofluorescence, cell cycle analysis and protein expression were evaluated in vitro. The antitumor effects of combining LB-100 with RT were verified in vivo by using intracranial orthotopic xenograft mouse model. Pharmacologic PP2A inhibition with LB-100 prior to RT enhanced the radiosensitivity of meningioma cells and reduced survival fraction in clonogenic assays. LB-100 increased DNA double-strand breakage (measured by γ-H2AX), mitotic catastrophe cell death, and G2/M cell cycle arrest in irradiated meningioma cells. Also, LB-100 decreased activation of STAT3 and expression of its downstream proteins. In vivo, LB-100 and RT combined treatment prolonged the survival of mice with xenografts compared to RT alone. Taken together, these results provide convincing preclinical data to support the use of LB-100 as a radiosensitizing agent for treatment of malignant meningioma. Its potential for clinical application deserves further investigation. Highlights Inhibition of Protein Phosphatase 2A Inhibitor (PP2A) enhances the cytotoxic effect of radiation in meningioma cells. PP2A inhibition increases radiation induced DNA double-strand breakage, mitotic catastrophe and G2/M cell cycle arrest. PP2A inhibition decreases activation of STAT3 and expression of its downstream proteins. Combining PP2A inhibition with radiation significant increased survival of mice with meningioma xenograft.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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