| [1] 葛世丽，楼铁柱，项晓琼，等. α粒子照射诱发BEP2D恶性转化模型的建立[J]. 癌症，2001，20 (9)：901-905. [2] Burk U， Schubert J， Wellner U， et al. A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells[J]. EMBO Rep， 2008， 9 (6)：582-589. [3] Park SM， Gaur AB， Lengyel E， et al. The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2[J]. Genes Dev， 2008， 22 (7)：894-907. [4] Gregory PA， Bert AG， Paterson EL， 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. [5] Gibbons DL， Lin W， Creighton CJ， et al. Contextual extracellular cues promote tumor cell EMT and metastasis by regulating miR-200 family expression[J]. Genes Dev， 2009， 15 (18)：2140-2151. [6] Mani SA， Guo WJ， Liao MJ， et al. The epithelial-mesenchymal transition generates cells with properties of stem cells[J]. Cell， 2008， 133 (4)：704-715. [7] Comijn J， Berx G， Vermassen P， et al. The two-handed E box binding zinc finger protein SIP1 downregulates E-cadherin and induces invasion[J]. Mol Cell， 2001， 7 (6)：1267-1278. [8] Eger A， Aigner K， Sonderegger S， et al. Delta EF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells[J]. Oncogene， 2005， 24 (14)：2375-2385. [9] Schliekelman MJ， Gibbons DL， Faca VM， et al. Targets of the tumor suppressor miR-200 in regulation of the epithelial-mesenchymal transition in cancer[J]. Cancer Res， 2011， 71 (24)：7670-7682. [10] Tsukamoto H， Shibata K， Kajiyama H， et al. Irradiation-induced epithelial–mesenchymal transition (EMT) related to invasive potential in endometrial carcinoma cells[J]. Gynecol Oncol，2007， 107 (3)：500-504. [11] Andarawewa KL， Erickson AC， Chou WS， et al. Ionizing radiation predisposes nonmalignant human mammary epithelial cells to undergo transforming growth factor B–induced epithelial to mesenchymal transition[J]. Cancer Res， 2007， 67 (18)： 8662-8670. |
