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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Lethal EMTによるTGF-β腫瘍抑制

Charles J David1, Yun-Han Huang1, Mo Chen2

  • 1Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

Cell
|February 23, 2016
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まとめ

変形成長因子β (TGF-β) のシグナル伝達は,がんにおいて二重の役割を果たします. 臓がんでは,TGF-βは重要な転写ネットワークを破壊し,アポトーシスを促進することにより,致命的な上皮膜-メゼンキーマ移行 (EMT) を誘導する.

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関連する実験動画

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科学分野:

  • 分子生物学
  • 癌の研究
  • セル・シグナル

背景:

  • 変形成長因子β (TGF-β) のシグナル伝達は,腫瘍発生における二重の役割を示し,プロ腫瘍原性または腫瘍抑制性として作用する.
  • 管腺がん (PDA) と他の胃腸がんでは,TGF-βシグナル伝達の主な媒介体であるSmad4の不活性化が頻繁に現れます.
  • エピテリア・メゼンキマ移行 (EMT) は通常,がんの進行を促進します.

研究 の 目的:

  • 管腺がん (PDA) のTGF-βシグナル伝達における二重の役割を調査する.
  • PDAにおけるTGF-βシグナル伝達が腫瘍形成と細胞運命を影響するメカニズムを解明する.
  • PDAにおけるSmad4,EMT,および転写因子の相互作用を理解する.

主な方法:

  • PDA細胞におけるTGF-βシグナル伝達経路を調査した.
  • TGF-βによる上皮-メゼンキマ移行 (EMT) の誘導を分析した.
  • PDA細胞の行動におけるSmad4,Sox4,Klf5の役割を調べました.
  • EMTが転写因子に与える影響を研究した.

主要な成果:

  • TGF-βはPDA細胞でEMTを誘導し,逆説的にSox4を腫瘍発生促進からアポトーシス促進に変換することによってアポトーシスを促進します.
  • EMTは,腫瘍形成において通常Sox4と協力する胃腸の主調節体Klf5を抑制して,転写のパターンを破壊する.
  • Smad4はEMTには不可欠ですが,TGF-β誘発のSox4アップレギュレーションには不可欠ではありません.

結論:

  • TGF-βは,EMT媒介による重要な系統特有の転写ネットワークの破壊を通じて,PDAにおける腫瘍抑制機能を発揮する.
  • EMTと Sox4やKlf5のような転写因子の相互作用が PDAの細胞運命を決定する.
  • これらの複雑なシグナル相互作用を理解することは 臓がんの標的治療の開発に不可欠です