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In vitro and in vivo effect of artesunate against prostate cancer:Targetting STAT3 pathway to combat disease progression

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中国药理学与毒理学杂志 2015年第S1期29卷 81-82页

作者： NachiyappanALAMELU KwangSeokAHN KodappullySivaramanSIVEEN alanpremkumar GautamSETHI Department of Pharmacology Yong Loo Lin School of Medicine National University of Singapore Singapore 117597 College of Oriental Medicine Kyung Hee University Seoul 130-701 Republic of Korea Cancer Science Institute of Singapore Centre for Translational Medicine Singapore 117599 School of Biomedical Sciences Faculty of Health Sciences Curtin University Western Australia 6009 Australia Department of Biological Sciences University of North Texas Denton TX 76203 USA

OBJECTIVE In prostate cancer(PCa),signal transducer and activator of transcription factor3(STAT3)has been strongly associated with tumor progression,through numerous *** this allows STAT3 to be an important target for therapeutic ***(ART),a well know antimalarial agentis making its way as an anticancer *** the present study,we investigated whether ART can control aberrant STAT3 signaling,and thereby take a toll on PCa *** Various PCa cell lines(DU145,PC3,LNCaP)and in vivo xenograft mouse model are *** effects of ART against various PCa cell lines were evaluated by MTT *** cytometry cell cycle analysis and DNA fragmentation assay was done to detect the apoptotic effect of *** of STAT3 and its regulated gene in the presence and absence of ART were measured by WB,IHC and RT ***3 DNA binding activities was analyzed by *** ART was found to dephosphorylate STAT3 at Tyr 405,thereby reducing its nuclear translocation and DNA binding efficiency in DU145 PCa *** proclaim that ART can prevent the PCa development,as it can inhibit proliferation,bring about cell cycle arrest at G0/G1 phase,AnnexinⅤ positive staining,DNA fragmentation,caspase 3activation and PARP cleavage in PCa cell ***,inhibition of constitutive STAT3 expression was associated with the ability of ART to suppress its upstream kinases such as Janus kinase 1and 2(JAK1and JAK2).SHP-1,protein tyrosine phosphatases which are considered to be one of the major regulators of STAT3 phosphorylation was upregulated in the presence of *** observed reversal in ART mediated inhibition of STAT3 in the presence of pervanadate,tyrosine phosphates inhibitor and during SHP-1 knock *** was able to inactivate STAT3 in DU145 cells exposed to conditioned media(CM)rich in *** the presence of ART we observed the down regulation of various STAT3 regulated gene products which are involved in proliferation,survival,and

关键词： antitumor DU145 JAK SHP-1

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Ascochlorin overcomes chemoresistance and regulates the plasticity of doxorubicin induced EMT via modulation of the NF-кB pathway in hepatocellular carcinoma

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中国药理学与毒理学杂志 2015年第S1期29卷 79-80页

作者： Xiao-yunDAI KwangSeokAHN ChulwonKIM MuthuKSHANMUGAM FengLI Ji-zhongSHI alanpremkumar Ling-zhiWANG BoonCherGOH JunjiMAGAE TinaHONG KamMHUI GautamSETHI Department of Pharmacology Yong Loo Lin School of Medicine National University of Singapore Singapore 117597 College of Oriental Medicine Kyung Hee University Seoul 130-701 Republic of Korea Cancer Science Institute of Singapore Cancer Science Singapore 117599 Department of Haematology-Oncology National University Health System Singapore 117599 Magae Bioscience Institute 49-4 Fujimidai Tsukuba 300-1263 Japan Division of Cellular and Molecular Research Humphrey Oei Institute of Cancer Research National Cancer Centre Singapore 169610

OBJECTIVE Doxorubicin-based therapy has been found to be not significantly effective for the treatment of advanced stage hepatocellular carcinomas(HCCs),which often undergo epithelial-mesenchymal transition(EMT)during tumor *** evidence suggest(s)that epithelial cell transformation to mesenchymal state canenhance the ability to self-renew and confer greater resistance to the conventional chemotherapeutic *** aim of this study was to examine the potential efficacyof ascochlorin,an isoprenoid antibiotic to overcome drug resistance induced by doxorubicin in HCC cell lines and to elucidate its underlying mechanism(s)of *** The effect of doxorubicin and ascochlorin on HCC cell lines was determined by MTT,Western blotting,immunofluorescence and NF-кB DNA binding *** Our results indicate that HCC cells that show a mesenchymal-like phenotype,are resistance to the doxorubicin therapy which directly correlated with an increased slug *** also observed that activation of NF-кB pathway plays an essential role in doxorubicin induced-chemoresistance and pharmacological inhibition of this pathway with ascochlorin can significantly reverse drug-induced invasion/migration and resistance in HCC *** Our results indicate that combination treatment of doxorubicin with ascochlorin has the potential to inhibit HCC growth and metastasis.

关键词： doxorubicin ascochlorin chemoresistance EMT NF-кB

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RNA helicase DDX20 as a surrogate marker of statin activity in invasive breast cancer

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中国药理学与毒理学杂志 2015年第S1期29卷 84-84页

作者： ChaoWANG BeiyingQIU JeanPaulTHIERY GautamSETHI PatrickJ.CASEY CelestialT.YAP SooChinLEE VinayTERGAONKAR alanpremkumar Cancer Science Institute of Singapore National University of Singapore Department of Pharmacology Yong Loo Lin School of Medicine National University of Singapore Institute of Molecular and Cell Biology ASTAR Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore National University Cancer Institute of Singapore Duke-NUS Graduate Medical School Department of Physiology Yong Loo Lin School of Medicine National University of Singapore Department of Haematology-Oncology National University Hospital Singapore Department of Biological Sciences University of North Texas

OBJECTIVE To evaluate if RNA helicase DDX20,highly expressed in triple negative breast cancer(TNBC)cells,could serve as a surrogate marker for simvastatin treatment *** We first assessed correlation between 17 mevalonate pathway-related genes and expression of DDX20 in a cohort of 1325 breast cancer *** cells,MDA-MB-231,were then treated with simvastatin and mevalonate pathway intermediates to assess the alteration in DDX20 *** the mouse model,MDA-MB-231 cells were injected to tail veins of mice,groups of 8mice each were injected intraperioneally with vehicle or simvastatin 25mg·kg-1 3times a week for *** number of metastatic colonies formed was quantified and immunohistochemical(IHC)staining of DDX20 was carried out in the lung *** Among the 17 genes evaluated,positive correlation with DDX20 expression was observed in eight of them,with HMGCR having the highest *** in vitro experiments show exposure of breast cancer cells to simvastatin lead to a Rho-dependent decrease in gene expression of DDX20,leading to decreased tumor proliferation in a mevalonate pathway-dependent ***,ectopic overexpression of DDX20 significantly abrogated the anti-metastatic activity of simvastatin.A similar observation is seen in the mouse model,where simvastatin-injected mice show significantly fewer visible lung metastases compared to placebo-fed *** staining on these lung tissues showed decreased DDX20 expression in simvastatin-injected group,corroborating our observations in *** DDX20 is a potential surrogate marker for simvastatin treatment response in breast cancer and a long term implication of our findings is the possibility of an effective combinatorial therapeutic intervention using statins(to suppress DDX20 gene expression)and a suitable firstline agent″for the kill″of invasive breast cancer.

关键词： RNA helicase DDX20 surrogate marker simvastatin br

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