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akaturk Akademik ölçüm

Makale detayı · 2008

Loss of E-cadherin promotes metastasis via multiple downstream transcriptional pathways

Dergi

Cancer Research

ISSN 0008-5472

YÖKSİS OpenAlex Açık erişim · bronze SJR Q1 JCR Q1 Atıf 1527 Üst %1 Yüzdelik 99.8% FWCI 27.88
Yıl
2008
Tür
article

Veri kaynağı ayrımı

  • YÖKSİS YÖKSİS makale kaydı
  • YÖKSİS dergi adı CANCER RESEARCH
  • Katalog eşleşmesi (ISSN) Cancer Research
  • OpenAlex OpenAlex zenginleştirmesi (özet, atıf, konular)

Özet

OpenAlex · İngilizce

Loss of the epithelial adhesion molecule E-cadherin is thought to enable metastasis by disrupting intercellular contacts-an early step in metastatic dissemination. To further investigate the molecular basis of this notion, we use two methods to inhibit E-cadherin function that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. Whereas the disruption of cell-cell contacts alone does not enable metastasis, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition, invasiveness, and anoikis resistance. We find the E-cadherin binding partner beta-catenin to be necessary, but not sufficient, for induction of these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes.

Konular

Atıflar

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Yazarlar

  1. TEVFİK TAMER ÖNDER KOÇ ÜNİVERSİTESİ