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10.1111/cas.12668

http://scihub22266oqcxt.onion/10.1111/cas.12668
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suck abstract from ncbi


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pmid25854938
      Cancer+Sci 2015 ; 106 (6 ): 718-725
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  • Persistent activation of STAT3 by PIM2-driven positive feedback loop for epithelial-mesenchymal transition in breast cancer #MMPMID25854938
  • Uddin N ; Kim RK ; Yoo KC ; Kim YH ; Cui YH ; Kim IG ; Suh Y ; Lee SJ
  • Cancer Sci 2015[Jun]; 106 (6 ): 718-725 PMID25854938 show ga
  • Metastasis of breast cancer is promoted by epithelial-mesenchymal transition (EMT). Emerging evidence suggests that STAT3 is a critical signaling node in EMT and is constitutively activated in many carcinomas, including breast cancer. However, its signaling mechanisms underlying persistent activation of STAT3 associated with EMT remain obscure. Here, we report that PIM2 promotes activation of STAT3 through induction of cytokines. Activation of STAT3 caused an increase in PIM2 expression, implicating a positive feedback loop between PIM2 and STAT3. In agreement, targeting of either PIM2, STAT3 or PIM2-dependent cytokines suppressed EMT-associated migratory and invasive properties through inhibition of ZEB1. Taken together, our findings identify the signaling mechanisms underlying the persistent activation of STAT3 and the oncogenic role of PIM2 in EMT in breast cancer.
  • |*Epithelial-Mesenchymal Transition [MESH]
  • |Breast Neoplasms/metabolism/*pathology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Movement [MESH]
  • |Female [MESH]
  • |Homeodomain Proteins/physiology [MESH]
  • |Humans [MESH]
  • |Interleukin-1alpha/metabolism [MESH]
  • |Interleukin-8/metabolism [MESH]
  • |Neoplasm Invasiveness [MESH]
  • |Protein Serine-Threonine Kinases/*physiology [MESH]
  • |Proto-Oncogene Proteins/*physiology [MESH]
  • |STAT3 Transcription Factor/*physiology [MESH]
  • |Signal Transduction [MESH]
  • |Transcription Factors/physiology [MESH]


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