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姜黄素对肝细胞生长因子诱导的前列腺癌细胞上皮细胞间质化的逆转作用 被引量:11

Effect of Curcumin on epithelial-mesenchymal transition of prostate cancer cell induced by HGF
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摘要 目的:探讨姜黄素对肝细胞生长因子诱导前列腺癌DU145细胞上皮细胞间质化的影响及可能机制。方法:将DU145细胞分为3组:正常对照组、HGF组、HGF联合姜黄素组。分组干预48小时后,显微镜观察细胞形态变化,划痕试验及Transwell试验检测细胞迁移、侵袭能力,Western blot检测上皮细胞表面标志E-Cadherin和间质细胞表面标志Vimentin的变化,以及HGF/c-Met信号通路分子的表达情况。Real time RT-PCR检测c-Met mRNA的表达变化。结果:分组处理48h,HGF处理组细胞较正常对照组细胞迁移能力显著增强,HGF联合姜黄素处理组细胞迁移能力与HGF处理组相比明显下降;Western blot结果发现,相对于正常对照组,HGF处理组E-cadherin表达水平下降而Vimentin表达水平上升,而姜黄素能明显逆转HGF诱导的EMT相关蛋白表达的改变。进一步研究发现姜黄素能显著下调c-Met mRNA和蛋白水平,进而抑制HGF/c-Met信号下游p-AKT和p-ERK信号以及Snail的表达。结论:姜黄素可逆转HGF诱导的前列腺癌细胞DU145迁移能力,可能与其抑制c-Met的表达和上皮细胞间质化有关。 Objective:To investigate the effect of Curcumin on epithelial-mesenchymal transition in prostate cancer cell line DU145 induced by HGF.Methods:DU145 cells were divided to 3 groups: normal control group,HGF treated group,and HGF + Curcumin treated group.After 48h of treatment,migration of DU145 cells were detected by wound healing and transwell assay.The protein expression of E-cadherin,Vimentin,Snail,c-Met,p-AKT,and p-ERK were determined by Western blot.The mRNA expression of c-Met was determined by Real-time RT-PCR.Results:The migration of DU145 cells induced by HGF was significantly inhibited by Curcumin.Western blot showed that E-cadherin was decreased,whereas Vimentin was increased in HGF treated cells.And these effects were abolished by Curcumin.Meanwhile,Curcumin significantly inhibited c-Met expression,and then inhibited AKT and ERK signaling.Conclusion:Curcumin revised the migration of DU145 cells induced by HGF through inhibiting c-Met expression,and then inhibited the epithelial-mesenchymal transition of DU145 cell.
出处 《现代肿瘤医学》 CAS 2013年第7期1425-1429,共5页 Journal of Modern Oncology
基金 国家自然科学基金资助项目(No.81272311 No.81071712)
关键词 前列腺癌 姜黄素 肝细胞生长因子 上皮细胞间质化 prostate cancer Curcumin HGF epithelial-mesenchymal transition
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参考文献15

  • 1Sturge J,Caley MP,Waxman J.Bone metastasis in prostate cancer: emerging therapeutic strategies [J].Nat Rev Clin Oncol,2011,8(6):357-368.
  • 2Varkaris A,Corn PG,Gaur S,et al.The role of HGF/c-Met signaling in prostate cancer progression and c-Met inhibitors in clinical trials [J].Expert Opin Investig Drugs,2011,20(12):1677-1684.
  • 3Naughton M,Picus J,Zhu X,et al.Scatter factor-hepatocyte growth factor elevation in the serum of patients with prostate cancer [J].J Urol,2001,165:1325-1328.
  • 4Maheshwari RK,Singh AK,Gaddipati J,et al.Multiple biological activities of curcumin: a short review [J].Life Sci,2006,78(18):2081-2087.
  • 5Ksiazkiewicz M,Markiewicz A,Zaczek AJ.Epithelial-mesenchymal transition: a hallmark in metastasis formation linking circulating tumor cells and cancer stem cells [J].Pathobiology,2012,79(4):195-208.
  • 6Elliott BE,Hung WL,Boag AH,et al.The role of hepatocyte growth factor (scatter factor) in epithelial-mesenchymal transition and breast cancer [J].Can J Physiol Pharmacol,2002,80(2):91-102.
  • 7Nagai T,Arao T,Furuta K,et al.Sorafenib inhibits the hepatocyte growth factor-mediated epithelial mesenchymal transition in hepatocellular carcinoma[J].Mol Cancer Ther,2011,10(1):169-177.
  • 8van Leenders G,van Balken B,Aalders T,et al.Intermediate cells in normal and malignant prostate epithelium express c-Met: implications for prostate cancer invasion [J].Prostate,2002,51(2):98-107.
  • 9Nishimura K,Kitamura M,Takada S,et al.Regulation of invasive potential of human prostate cancer cell lines by hepatocyte growth factor[J].Int J Urol,1998,5(3):276-281.
  • 10Davies G,Watkins G,Mason MD,et al.Targeting the HGF/SF receptor c-Met using a hammerhead ribozyme transgene reduces in vitro invasion and migration in prostate cancer cells[J].Prostate,2004,60(4):317-324.

二级参考文献11

  • 1Iwatsuki M, Mimori K, Yokobori T, et al. Epithelial - mesenchymal transition in cancer development and its clinical significance [ J ]. Cancer Sci ,2010,101 (2) :293 - 299.
  • 2Yan W,Fu Y,Tian D,et al. PI3 kinase/Akt signaling mediates epi- thelial- mesenchymal transition in hypoxic hepatocellular carcino- ma cells [ J]. Biochem Biophys Res Commun, 2009,382 ( 3 ) :631 - 636.
  • 3Darvesh AS, Aggarwal BB, Bishayee A. Curcumin and liver cancer: A review [ J]. Curr Pharm Biotechnol. 2011,23 : 15.
  • 4Singh A,Settleman J. EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer [ J ]. Oncogene ,2010, 29(34) :4741 -4751.
  • 5Hanahan D, Weinberg RA. Hallmarks of cancer:the next generation [J]. Cell,2011,144(5) :646 -674.
  • 6Liu L, Zhu XD, Wang WQ, et al. Activation of beta - eatenin by hy-poxia in hepatocellular carcinoma contributes to enhanced metastat- ic potential and poor prognosis [ J ]. Clin Cancer Res, 2010, 16 (10) :2740 -2750.
  • 7Krishnamachary B, Zagzag D, Nagasawa H, et al. Hypoxia - induc- ible factor - 1 - dependent repression of E - cadherin in von Hippel - Lindau tumor suppressor - null renal cell carcinoma mediated by TCF3, ZFHX1 A, and ZFHX1B [ J ]. Cancer Res, 2006,65 ( 5 ) : 2725 - 2731.
  • 8Paraskeva PA, Ridgway PF, Olsen S, et al. A surgically induced hy- poxic environment causes changes in the metastatic behaviour of tumours in vitro [ J ]. Clin Exp Metastasis, 2006,23 (2) : 149 - 157.
  • 9Ciafrs SA NF, Giorda E FMG, Caporossi D. CoC1 ( 2 ) - stimulated hypoxia in skeletal muscle cell lines: Role of free radicals in gene up - regulation and induction of apoptosis [ J ]. Free Radic Res, 2007,41 (4) :391 -401.
  • 10Cheng CY,Lin YH,Su CC. Curcumin inhibits the proliferation of human hepatocellular carcinoma J5 cells by inducing endoplasmie reticulum stress and mitochondrial dysfunction [ J ]. Int J Mol Med. 2010.26 ( 5 ) : 673 - 678.

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