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[PMID]: 29524832
[Au] Autor:Jonsson S; Oda H; Lundin E; Olsson J; Idahl A
[Ad] Address:Department of Clinical Science, Obstetrics and Gynecology, Umeå University, SE-901 87 Umeå, Sweden.
[Ti] Title:Chlamydia trachomatis, Chlamydial Heat Shock Protein 60 and Anti-Chlamydial Antibodies in Women with Epithelial Ovarian Tumors.
[So] Source:Transl Oncol;11(2):546-551, 2018 Mar 07.
[Is] ISSN:1936-5233
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Chlamydia trachomatis (C. trachomatis) infection has been suggested to promote epithelial ovarian cancer (EOC) development. This study sought to explore the presence of C. trachomatis DNA and chlamydial heat shock protein 60 (chsp60) in ovarian tissue, as well as anti-chlamydial IgG antibodies in plasma, in relation to subtypes of EOC. METHODS: This cross-sectional cohort consisted of 69 women who underwent surgery due to suspected ovarian pathology. Ovarian tissue and corresponding blood samples were collected at the time of diagnosis. In ovarian tumor tissue, p53, p16, Ki67 and chsp60 were analyzed immunohistochemically, and PCR was used to detect C. trachomatis DNA. Plasma C. trachomatis IgG and cHSP60 IgG were analyzed with a commercial MIF-test and ELISA, respectively. RESULTS: Eight out of 69 women had C. trachomatis DNA in their ovarian tissue, all were invasive ovarian cancer cases (16.7% of invasive EOC). The prevalence of the chsp60 protein, C. trachomatis IgG and cHSP60 IgG in HGSC, compared to other ovarian tumors, was 56.0% vs. 37.2% P = .13, 15.4% vs. 9.3% P = .46 and 63.6% vs. 45.5% P = .33 respectively. None of the markers of C. trachomatis infection were associated with p53, p16 or Ki67. CONCLUSIONS: C. trachomatis was detected in invasive ovarian cancer, supporting a possible role in carcinogenesis of EOC. However, there were no statistically significant associations of chsp60 in ovarian tissue, or plasma anti-chlamydial IgG antibodies, with any of the subtypes of ovarian tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 90446 MEDLINE  
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[PMID]: 29524560
[Au] Autor:Khan AQ; Kuttikrishnan S; Siveen KS; Prabhu KS; Shanmugakonar M; Al Naemi H; Haris M; Dermime S; Uddin S
[Ad] Address:Academic Health System, Translational Research Institute, Hamad Medical Corporation, Doha, Qatar.
[Ti] Title:RAS-mediated oncogenic signaling pathways in human malignancies.
[So] Source:Semin Cancer Biol;, 2018 Mar 07.
[Is] ISSN:1096-3650
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Abnormally activated RAS proteins are the main oncogenic driver that governs the functioning of major signaling pathways involved in the initiation and development of human malignancies. Mutations in RAS genes and or its regulators, most frequent in human cancers, are the main force for incessant RAS activation and associated pathological conditions including cancer. In general, RAS is the main upstream regulator of the highly conserved signaling mechanisms associated with a plethora of important cellular activities vital for normal homeostasis. Mutated or the oncogenic RAS aberrantly activates a web of interconnected signaling pathways including mitogen-activated protein kinases (MAPK), phosphoinositide-3 kinase (PI3K)/AKT pathways, protein kinase C (PKC) and ral guanine nucleotide dissociation stimulator (RalGDS), etc., leading to uncontrolled transcriptional expression and reprogramming in the functioning of a range of nuclear and cytosolic effectors critically associated with the hallmarks of carcinogenesis. This review highlights the recent literature on how oncogenic RAS negatively use its signaling web in deregulating the expression and functioning of various effector molecules in the pathogenesis of human malignancies.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 90446 MEDLINE  
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[PMID]: 29524520
[Au] Autor:Malojirao VH; Vigneshwaran V; Thirusangu P; Mahmood R; Prabhakar BT
[Ad] Address:Molecular Biomedicine Laboratory, Postgraduate Department of Studies and Research in Biotechnology, Sahyadri Science College (Autonomous), Kuvempu University, Shivamogga 577203, Karnataka, India.
[Ti] Title:The tumor antagonistic steroidal alkaloid Solanidine prompts the intrinsic suicidal signal mediated DFF-40 nuclear import and nucleosomal disruption.
[So] Source:Life Sci;, 2018 Mar 07.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Aim Deformity in the cellular homeostatic event associated with cell survival and apoptosis are committing factors for carcinogenesis. Interventions of these events by pharmacologically active agent gain predominance in cancer treatment. In current investigation Solanidine, a steroidal alkaloid was evaluated on tumorigenesis by targeting death signal using multiple tumor cells and model systems. MAIN METHODS: Anti-proliferative effect was evaluated using cytotoxic studies. Prolonged cytotoxic effect of Solanidine was examined by colony formation assay. Exhibition of apoptotic hallmark induced by Solanidine was examined using FACS analysis, Annexin-V staining, Acridine orange staining, TUNEL assay. Altered gene expression was evaluated using Immunoblot, Immunofluorescence and Immunohistochemistry technique. In-vitro results were revalidated in EAC solid tumor and CAM xenograft model. KEY FINDINGS: Solanidine exerts its potential effect in a target specific manner. The cytotoxic/anticlonogenic activity was due to induction of typical cellular apoptotic hallmarks and cell cycle blockage at S-G2/M phase. The molecular events underlying this effect is through activation of intrinsic pathway via Bax, Bad and Cytochrome c activation by neutralizing Bcl-2 expression, along with downregulated PI3K/Akt survival signal. As a consequence, downstream pro apoptogenic gene, active Caspase-3 was over expressed by Solanidine to cleave its substrate PARP and promotes nuclear import of DFF-40. Anti-carcinogenic aptitude was further confirmed by murine solid tumors and in-vivo CAM xenograft studies. SIGNIFICANCE: Solanidine emerged as active molecule against tomorigenesis by activating nuclear import of DFF-40 mediated nucleosomal disruption and cell demise. It can be developed as a potential apoptogenic small molecule for cancer therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 90446 MEDLINE  
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[PMID]: 29524472
[Au] Autor:van der Toorn M; Sewer A; Marescotti D; Johne S; Baumer K; Bornand D; Dulize R; Merg C; Corciulo M; Scotti E; Pak C; Leroy P; Guedj E; Ivanov N; Martin F; Peitsch M; Hoeng J; Luettich K
[Ad] Address:PMI R&D, Philip Morris Products S.A. (Part of Philip Morris International group of companies), Quai Jeanrenaud 5, CH-2000 Neuchâtel, Switzerland. Electronic address: Marco.vanderToorn@pmi.com.
[Ti] Title:The biological effects of long-term exposure of human bronchial epithelial cells to total particulate matter from a candidate modified-risk tobacco product.
[So] Source:Toxicol In Vitro;, 2018 Mar 07.
[Is] ISSN:1879-3177
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cigarette smoking is the leading cause of preventable lung cancer (LC). Reduction of harmful constituents by heating rather than combusting tobacco may have the potential to reduce the risk of LC. We evaluated functional and molecular changes in human bronchial epithelial BEAS-2B cells following a 12-week exposure to total particulate matter (TPM) from the aerosol of a candidate modified-risk tobacco product (cMRTP) in comparison with those following exposure to TPM from the 3R4F reference cigarette. Endpoints linked to lung carcinogenesis were assessed. Four-week 3R4F TPM exposure resulted in crisis and epithelial to mesenchymal transition (EMT) accompanied by decreased barrier function and disrupted cell-to-cell contacts. By week eight, cells regained E-cadherin expression, suggesting that EMT was reversible. Increased levels of inflammatory mediators were noted in cells treated to 3R4F TPM but not in cells treated to the same or a five-fold higher concentration of cMRTP TPM. A 20-fold higher concentration of cMRTP TPM increased oxidative stress and DNA damage and caused reversible EMT. Anchorage-independent growth was observed in cells treated to 3R4F or a high concentration of cMRTP TPM. 3R4F TPM-derived clones were invasive, while cMRTP TPM-derived clones were not. Long-term exposure to TPM from the cMRTP had a lower biological impact on BEAS-2B cells compared with that of exposure to TPM from 3R4F.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 90446 MEDLINE  
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[PMID]: 29511364
[Au] Autor:Huang SF; Chu SC; Hsieh YH; Chen PN; Hsieh YS
[Ad] Address:Division of Chest Medicine, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung City, Taiwan, ROC.
[Ti] Title:Viola Yedoensis Suppresses Cell Invasion by Targeting the Protease and NF-κB Activities in A549 and Lewis Lung Carcinoma Cells.
[So] Source:Int J Med Sci;15(4):280-290, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:Cancer metastasis is a vital trait in malignancies with complicated early diagnosis and therapeutic management. Therefore, the development of new remedies and the utilization of natural medicines that target metastasis are of great interest and have been studied extensively. Chinese medicinal herbs have various anti-carcinogenesis properties; however, the in vitro effect and mechanism of on cancer cell metastasis remains poorly understood. extracts (VYE) can suppress the invasion of a highly metastatic human lung cancer cell line, A549 cells. According to gelatin zymography and casein zymography assays, VYE inhibited the activities of matrix metalloproteinases (MMPs) and urokinase-type plasminogen activator (u-PA). The results of reverse transcription-polymerase chain reaction and Western blotting revealed that VYE can alter the expression of proteinase inhibitor. VYE also suppressed the DNA binding activity of nuclear factor-kappa B. We concluded that VYE may inhibit tumor invasion by suppressing the activities of MMP and u-PA in lung cancer cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22793

  6 / 90446 MEDLINE  
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[PMID]: 29501572
[Au] Autor:Lu L; Xu H; Yang P; Xue J; Chen C; Sun Q; Yang Q; Lu J; Shi A; Liu Q
[Ad] Address:The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 211166, Jiangsu, People's Republic of China; Key Laboratory of the Model Animal, Animal Core Facility, Jiangsu Animal Experimental Center for Medical and Pharmaceutical Resear
[Ti] Title:Involvement of HIF-1α-regulated miR-21, acting via the Akt/NF-κB pathway, in malignant transformation of HBE cells induced by cigarette smoke extract.
[So] Source:Toxicol Lett;289:14-21, 2018 Mar 06.
[Is] ISSN:1879-3169
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Although the relationship between cigarette smoke and lung cancer has been widely studied, the molecular mechanism for cigarette smoke-induced lung cancer remains largely unclear. The present study investigated the roles of hypoxia-inducible factor (HIF)-1α and miR-21 in the malignant transformation of human bronchial epithelial (HBE) cells induced by cigarette smoke extract (CSE). In case of acute and chronic treatment of HBE cells, CSE increased the levels of HIF-1α, p-Akt, p-NF-κB, and miR-21 and decreased PTEN levels. The increased miR-21 levels induced by CSE were prevented by down-regulation of HIF-1α. Further, elevated miR-21 suppressed PTEN levels, which decreased the levels of p-Akt and p-NF-κB. However, those changes were attenuated in cells co-transfected with HIF-1α siRNA and an miR-21 mimic. Silencing of HIF-1α or NF-κB decreased colony formation and the invasion and migration capacities of CSE-transformed HBE cells; however, up-regulation of miR-21 reversed these effects. These results indicate that the oncogenic capacity of HIF-1α in regulation of miR-21-inhibited PTEN in a manner dependent on the Akt/NF-κB pathway, a process that is involved in the CSE-induced malignant transformation of HBE cells. Thus, the present research has established a new mechanism for cigarette smoke-induced lung carcinogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 90446 MEDLINE  
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[PMID]: 29477046
[Au] Autor:Hegedus C; Kovács K; Polgár Z; Regdon Z; Szabó É; Robaszkiewicz A; Forman HJ; Martner A; Virág L
[Ad] Address:Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
[Ti] Title:Redox control of cancer cell destruction.
[So] Source:Redox Biol;16:59-74, 2018 Feb 03.
[Is] ISSN:2213-2317
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Redox regulation has been proposed to control various aspects of carcinogenesis, cancer cell growth, metabolism, migration, invasion, metastasis and cancer vascularization. As cancer has many faces, the role of redox control in different cancers and in the numerous cancer-related processes often point in different directions. In this review, we focus on the redox control mechanisms of tumor cell destruction. The review covers the tumor-intrinsic role of oxidants derived from the reduction of oxygen and nitrogen in the control of tumor cell proliferation as well as the roles of oxidants and antioxidant systems in cancer cell death caused by traditional anticancer weapons (chemotherapeutic agents, radiotherapy, photodynamic therapy). Emphasis is also put on the role of oxidants and redox status in the outcome following interactions between cancer cells, cytotoxic lymphocytes and tumor infiltrating macrophages.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  8 / 90446 MEDLINE  
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[PMID]: 29471110
[Au] Autor:Pushparajah DS; Ioannides C
[Ad] Address:Molecular Toxicology Group, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK.
[Ti] Title:Antagonistic and synergistic interactions during the binding of binary mixtures of polycyclic aromatic hydrocarbons to the aryl hydrocarbon receptor.
[So] Source:Toxicol In Vitro;50:54-61, 2018 Feb 19.
[Is] ISSN:1879-3177
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In order to assess the potential of polycyclic aromatic hydrocarbons (PAHs) to interact with each other, benzo(a)pyrene (B(a)P) was incubated either alone or in combination with other isomeric 5-ring PAHs in precision-cut rat liver slices. At the end of the incubation, the slices were removed and the O-deethylation of ethoxyresorufin (EROD) was determined in microsomal preparations. The BP-mediated rise in EROD activity was suppressed in the presence of dibenzo(a,j)anthracene, dibenzo(a,c)anthracene and picene, whereas it was increased in the presence of pentacene. In the case of benzo(b)chrysene, benzo(c)chrysene and benzo(g)chrysene the effect was concentration-dependent with both antagonism and synergism being observed. The binding of B(a)P to the aryl hydrocarbon (Ah) receptor was similarly modulated by other PAHs. No correlation was evident between binding avidity of the PAH to the Ah receptor and either its potential for interaction or nature of interaction, e.g. synergism or antagonism. These interactions were also independent of the molecular shape (ring arrangement) of the 5-ring isomeric PAHs. Bearing in mind the role of the Ah receptor in chemical carcinogenesis, it may be concluded that interactions at the Ah receptor site may contribute to the well-established modulation of the carcinogenicity of one PAH in the presence of another.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 90446 MEDLINE  
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[PMID]: 29454075
[Au] Autor:Placet M; Arguin G; Molle CM; Babeu JP; Jones C; Carrier JC; Robaye B; Geha S; Boudreau F; Gendron FP
[Ad] Address:Department of Anatomy and Cell Biology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
[Ti] Title:The G protein-coupled P2Y receptor promotes colorectal cancer tumorigenesis by inhibiting apoptosis.
[So] Source:Biochim Biophys Acta;1864(5 Pt A):1539-1551, 2018 Feb 14.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Colorectal tumors are immersed in an array of tumor-promoting factors including extracellular nucleotides such as uridine 5'­diphosphate (UDP). UDP is the endogenous agonist of the G protein-coupled P2Y receptor (P2Y R), which may contribute to the formation of a tumor-promoting microenvironment by coordinating resistance to apoptosis. Colorectal cancer (CRC) was chemically induced in P2ry6 knockout (P2ry6 ) mice using azoxymethane and dextran sulfate sodium challenges. Mice were euthanatized and their tumor load determined. Fixed tissues were stained for histological and immunohistochemistry analysis. Tumoroids were also prepared from CRC tumors resected from P2ry6 mice to determine the role of P2Y R in resistance to apoptosis, whereas HT29 carcinoma cells were used to elucidate the signaling mechanism involved in P2Y R anti-apoptotic effect. P2ry6 mice developed a reduced number of colorectal tumors with apparent tumors having smaller volumes. Overall dysplastic score was significantly lower in P2ry6 animals. Stimulation of P2Y R with the selective agonist MRS2693 protected HT-29 cells from TNFα-induced apoptosis. This protective effect was mediated by the stabilizing phosphorylation of the X-linked inhibitor of apoptosis protein (XIAP) by AKT. Using CRC-derived tumoroids, P2Y R activation was found to contribute to chemoresistance since addition of the P2Y R agonist MRS2693 significantly prevented the cytotoxic effect of 5-fluorouracil. The present study shows that sustained activation of P2Y R may contribute to intestinal tumorigenesis by blocking the apoptotic process and by contributing to chemoresistance, a substantial concern in the treatment of patients with CRC. These results suggest that P2Y R may represent a prime target for reducing colorectal carcinogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 90446 MEDLINE  
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[PMID]: 29448044
[Au] Autor:Hashimoto Y; Hata T; Tada M; Iida M; Watari A; Okada Y; Doi T; Kuniyasu H; Yagi K; Kondoh M
[Ad] Address:Graduate School of Pharmaceutical Sciences, Osaka University, Osaka 565-0871, Japan.
[Ti] Title:Safety evaluation of a human chimeric monoclonal antibody that recognizes the extracellular loop domain of claudin-2.
[So] Source:Eur J Pharm Sci;117:161-167, 2018 Feb 13.
[Is] ISSN:1879-0720
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Claudin-2 (CLDN-2), a pore-forming tight junction protein with a tetra-transmembrane domain, is involved in carcinogenesis and the metastasis of some cancers. Although CLDN-2 is highly expressed in the tight junctions of the liver and kidney, whether CLDN-2 is a safe target for cancer therapy remains unknown. We recently generated a rat monoclonal antibody (mAb, clone 1A2) that recognizes the extracellular domains of human and mouse CLDN-2. Here, we investigated the safety of CLDN-2-targeted cancer therapy by using 1A2 as a model therapeutic antibody. Because most human therapeutic mAbs are IgG1 subtype that can induce antibody-dependent cellular cytotoxicity, we generated a human-rat chimeric IgG1 form of 1A2 (xi-1A2). xi-1A2 activated Fcγ receptor IIIa in the presence of CLDN-2-expressing cells, indicating that xi-1A2 likely exerts antibody-dependent cellular cytotoxicity. At 24 h after its intravenous injection, xi-1A2 was distributed into the liver, kidney, and tumor tissues of mice bearing CLDN-2-expressing fibrosarcoma cells. Treatment of the xenografted mice with xi-1A2 attenuated tumor growth without apparent adverse effects, such as changes in body weight and biochemical markers of liver and kidney injury. These results support xi-1A2 as the lead candidate mAb for safe CLDN-2-targeted cancer therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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