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10.1002/1878-0261.12162

http://scihub22266oqcxt.onion/10.1002/1878-0261.12162
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suck abstract from ncbi


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pmid29215776
      Mol+Oncol 2018 ; 12 (3 ): 305-321
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  • TGF-? transactivates EGFR and facilitates breast cancer migration and invasion through canonical Smad3 and ERK/Sp1 signaling pathways #MMPMID29215776
  • Zhao Y ; Ma J ; Fan Y ; Wang Z ; Tian R ; Ji W ; Zhang F ; Niu R
  • Mol Oncol 2018[Mar]; 12 (3 ): 305-321 PMID29215776 show ga
  • Transforming growth factor-beta (TGF-?) functions as a potent proliferation inhibitor and apoptosis inducer in the early stages of breast cancer, yet promotes cancer aggressiveness in the advanced stages. The dual effect of TGF-? on cancer development is known as TGF-? paradox, and the remarkable functional conversion of TGF-? is a pivotal and controversial phenomenon that has been widely investigated for decades. This phenomenon may be attributed to the cross talk between TGF-? signaling and other pathways, including EGF receptor (EGFR) signaling during cancer progression. However, the underlying mechanism by which TGF-? shifts its role from a tumor suppressor to a cancer promoter remains elusive. In this study, TGF-? is positively correlated with EGFR expression in breast cancer tissues, and a functional linkage is observed between TGF-? signaling and EGFR transactivation in breast cancer cell lines. TGF-? promotes the migration and invasion abilities of breast cancer cells, along with the increase in EGFR expression. EGFR is also essential for TGF-?-induced enhancement of these abilities of breast cancer cells. Canonical Smad3 signaling and ERK/Sp1 signaling pathways mediate TGF-?-induced EGFR upregulation. Hence, our study provided insights into a novel mechanism by which TGF-? supports breast cancer progression.
  • |Breast Neoplasms/metabolism/*pathology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Movement/drug effects [MESH]
  • |ErbB Receptors/genetics/metabolism [MESH]
  • |Female [MESH]
  • |Gene Knockdown Techniques [MESH]
  • |Humans [MESH]
  • |MAP Kinase Signaling System/drug effects/physiology [MESH]
  • |Neoplasm Invasiveness [MESH]
  • |Smad3 Protein/genetics/*metabolism [MESH]
  • |Sp1 Transcription Factor/genetics/*metabolism [MESH]


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