期刊文献+

乳腺癌上皮间质转化与耐药关系的研究进展 被引量:7

Research progress on relationship between epithelial-mesenchymal transitions and drug resistance in breast cancer
原文传递
导出
摘要 肿瘤上皮-间质转化(epithelial-mesenchymal transitions,EMT)是指肿瘤在各种因素作用下上皮细胞转变为具有高侵袭、转移能力间质表型的过程。EMT与细胞上皮表型标志物E-钙黏蛋白表达下调、间质表型标志物上调和相关基因表达改变有关。EMT的发生能够促进乳腺癌侵袭、转移和干细胞特性获得,诱导乳腺癌细胞对化疗、内分泌治疗和靶向药物治疗产生获得性耐药。同时研究发现,乳腺癌耐药细胞能够发生EMT,并获得干细胞表型。因此,针对乳腺癌细胞EMT的相关研究可以帮助人们在肿瘤抗耐药治疗中找到新的策略。本文旨在对EMT与乳腺癌发生获得性耐药之间关系的最新研究进展作一综述。 EMT (epithelial-mesenchymal transitions) refers to the progression in which tumor epithelial cells acquire mesenchymal features with high abilities of invasiveness and metastasis under various factors. EMT is characterized by downregulation of epithelial marker E-cadherin, upregulation of mesenchymal markers and regulation of expressions of related genes. EMT can promote the metastasis and invasiveness of breast cancer which acquiring a stem cell-like cell phenotype, and induce the acquired resistance of breast cancer to chemotherapy, endocrine therapy and target therapy. It is also shown that the breast cancer cells, which display drug resistance, exhibit stem cell-like characteristics and EMT. The studies focusing on EMT may be helpful to find new strategies to reverse drug resistance in breast cancer. This article reviews the research progress on the relationship between EMT and acquired drug-resistance in breast cancer.
出处 《肿瘤》 CAS CSCD 北大核心 2012年第11期945-948,共4页 Tumor
基金 国家自然科学基金资助项目(编号:81172520) 上海市教育委员会重点学科建设项目(编号:J50208)
关键词 乳腺肿瘤 细胞转化 肿瘤 抗药性 肿瘤 上皮间质转化 Breast neoplasms Cell transformation, neoplastic Drug resistance, neoplasm Epithelial-mesenchymal transitions
  • 相关文献

参考文献28

  • 1FORONI C, BROGGINI M, GENERALI D, et al. Epithelial- mesenchymal transition and breast cancer: role, molecular mechanisms and clinical impact[J]. Cancer Treat Rev, 2012, 38(6):689-697.
  • 2VINCENT-SALOMON A, THIERY J P. Host microenvironment in breast cancer development: epithelial-mesenchymal transition in breast cancer development[J]. Breast Cancer Res, 2003, 5(2):101-106.
  • 3VALCOURT U, KOWANETZ M, NIIMI H, et al. TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transition[J]. Mol Biol Cell, 2005, 16(4):1987-2002.
  • 4NAWSHAD A, LAGAMBA D, POLAD A, et al. Transforming growth factor-β signaling during epithelial-mesenchymal transformation: implications for embryogenesis and tumor metastasis[J]. Cells Tissues Organs, 2005,1 79(1-2):11-23.
  • 5黄学德,熊吕平,叶小群.低氧对人肺腺癌A549多细胞球体上皮-间质转化促转移的影响[J].肿瘤,2012,32(3):182-188. 被引量:4
  • 6DIMEO T A, ANDERSON K, PHADKE P, et al. A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer[J]. Cancer Res, 2009, 69(13):5364-5373.
  • 7HUBER M A, BEUG H, WlRTH T. Epithelial-mesenchymal transition: NF-kappaB takes center stageD]. Cell Cycle, 2004, 3(12):1477-1480.
  • 8GREGORY P A, BERT A G, PATERSON E L, et al. The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1 [J]. Nat Cell Biol, 2008, 10(5):593-601.
  • 9GEE H E, CAMPS C, BUFFA F M, et al. MicroRNA-lOb and breast cancer metastasis[J]. Nature, 2008, 455(7216): E8-E9.
  • 10GEBESHUBER C A, ZATLOUKAL K, MARTINEZ J. MiR- 29a suppresses tristetraprolin, which is a regulator of epithelial polarity and metastasis[J]. EMBO Rep, 2009, 10(4):400-405.

二级参考文献6

共引文献17

同被引文献89

  • 1姚婵,来茂德.上皮间质转化(EMT)及其分子机制[J].国际遗传学杂志,2006,29(4):290-294. 被引量:25
  • 2Zaczek A,Brandt B,Bielawski KP. The diverse signaling network of EGFR,HER2,HER3 and HER4 tyrosine kinase receptors and the consequences for therapeutic approaches[J].{H}Histology and Histopathology,2005.1005-1015.
  • 3Cobleigh MA,Vogel CL,Tripathy D. Multinational study of the efficacy and safety of humanized anti-HER2 monoclonal antibody in women who have HER2-overexpressing metastatic breast cancer that has progressed after chemotherapy for metastatic disease[J].{H}Journal of Clinical Oncology,1999.2639-2648.
  • 4Sáez R,Molina MA,Ramsey EE. p95HER-2 predicts worse outcome in patients with HER-2-positive breast cancer[J].{H}Clinical Cancer Research,2006.424-431.
  • 5Carraway KL,Theodoropoulos G,Kozloski GA. Muc4/MUCA functions and regulation in cancer[J].{H}FUTURE ONCOLOGY,2009.1631-1640.
  • 6Sikov WM,Dizon DS,Strenger R. Frequent pathologic complete responses in aggressive stages II to III breast cancers with every-4-week carboplatin and weekly paclitaxel with or without trastuzumab:a Brown University Oncology Group study[J].{H}Journal of Clinical Oncology,2009.4693-4700.
  • 7Liu L,Greger J,Shi H. Novel mechanism of lapatinib resistance in HER2-positive breast tumor cells:activation of AXL[J].{H}CANCER RESEARCH,2009.6871-6878.
  • 8Zhuang G,Brantley-Sieders DM,Vaught D. Elevation of receptor tyrosine kinase EphA2 mediates resistance to trastuzumab therapy[J].{H}CANCER RESEARCH,2010.299-308.
  • 9Nahta R,Takahashi T,Ueno NT. P27(kip1) down-regulation is associated with trastuzumab resistance in breast cancer cells[J].{H}CANCER RESEARCH,2008.10005.
  • 10Wang Z,Fukushima H,Inuzuka H. Skp2 is a promising therapeutic target in breast cancer[J].Front Oncol,2012.57.

引证文献7

二级引证文献48

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部