Jove
Visualize
お問い合わせ
このページは機械翻訳されています。他のページは英語で表示される場合があります。View in English
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 腫瘍学とがん発生
  9. 分子標的
  11. Trop2の細胞外領域の放出は,前立腺がんの転移を誘導するegfrシグナリングを活性化します.
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 腫瘍学とがん発生
  9. 分子標的
  11. Trop2の細胞外領域の放出は,前立腺がんの転移を誘導するegfrシグナリングを活性化します.

関連する実験動画

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.3K

TROP2の細胞外領域の放出は,前立腺がんの転移を誘導するEGFRシグナリングを活性化します.

Shiqin Liu1, En-Chi Hsu2, Merve Aslan3

  • 1University of California, Los Angeles, Los Angeles, United States.

Cancer research
|September 5, 2025

PubMed で要約を見る

まとめ
この要約は機械生成です。

TROP2 (TROP2- EC) の細胞外ドメインは,細胞の移動と侵入を強め,前立腺がんの転移を促進する. TROP2- ECはEGFR経路を活性化し,がんの進行を促し,潜在的な治療目標を提供します.

科学分野:

  • 腫瘍学
  • 分子生物学
  • 癌の転移に関する研究

背景:

  • 前立腺がんの転移は死亡の主な原因であり,その背後にあるメカニズムの研究が必要である.
  • TROP2 (TACSTD2) は腫瘍性タンパク質で,転移性前立腺がんでは高発現している.
  • TROP2の分裂により,前立腺がん細胞と患者の血清に含まれる細胞外ドメイン (TROP2- EC) が放出されます.

研究 の 目的:

  • 前立腺がんの進行における脱皮TROP2細胞外領域 (TROP2-EC) の機能的役割を調査する.
  • TROP2-ECが前立腺がんの転移に影響を与える分子メカニズムを解明する.
  • TROP2-EC,EGFRシグナル伝達と前立腺がんの侵襲性の関係を調査する.

主な方法:

  • 前立腺がん細胞媒介と患者の血清におけるTROP2- ECの検出
  • 細胞の移転と侵入を in vitro で測定し,転移による植民を in vivo で測定する.
  • TROP2-EC結合パートナーと下流経路を特定するためのインタラクトームとプロテオミック分析.
  • EGFRのリン酸化と経路の活性化 (EGFR-PI3K-AKT-mTOR) の評価
  • TECD過剰発現する前立腺がん細胞におけるEGFR阻害剤の有効性の評価

さらに関連する動画

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

35.3K
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

14.1K

関連する実験動画

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.3K
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

35.3K
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

14.1K

関連する概念動画

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.6K
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...
6.6K
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

79.9K
Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
79.9K
Receptor Tyrosine Kinases01:26

Receptor Tyrosine Kinases

13.9K
Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
13.9K
Metastasis02:30

Metastasis

5.7K
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.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.7K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

2.1K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.1K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

7.6K
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...
7.6K
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

主要な成果:

  • TROP2- ECの放出は,前立腺がん細胞の移動と侵入を in vitro で著しく増加させた.
  • TROP2- ECは,体内での転移と自発転移を促した.
  • TROP2- ECはEGFRと相互作用し,侵入,移動,mTORシグナル伝達,および上皮からメゼンキマへの移行に関与するタンパク質を調節する.
  • EGFR- PI3K- AKT- mTOR経路のリン酸化と活性化が増加した.
  • EGFR阻害剤は,前立腺がん細胞におけるTECD過剰発現の侵入的効果を相殺した.

結論:

  • シェードTROP2- ECは前立腺がんの進行と転移を促す上で重要な役割を果たします.
  • TROP2- ECはEGFR経路の活性化によって侵入性と転移を促進する.
  • TECD-EGFR軸をターゲットにすることで,転移性前立腺がんの治療戦略が実現できます.