Related Experiment Video
Updated: Apr 12, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Targeting epithelial-mesenchymal transition phenotype for gastro-intestinal cancer
Hueng-Chuen Fan, Shinn-Zong Lin, Horng-Jyh Harn1
1Department of Pathology, China Medical University and Hospital, Taichung, Taiwan, R.O.C. duke_harn@yahoo.com.tw.
Abstract:
Gastrointestinal (G-I) cancers are one of the most common malignant tumors worldwide. Symptoms relate to the organ affected in the G-I tract are non-specific, making early detection and effective treatment difficult to achieve. Epithelial-mesenchymal transition (EMT), a reversible and dynamical process, can disperse cells in embryos, form mesenchymal cells in injured tissues, and regulate embryonic stem cell differentiation. A variety of signaling molecules and distinct pathways are involved in the initiation and progression of EMT. Recent evidence has established that EMT may endow G-I cancer cells with the capacity to invade surrounding tissues, resist apoptosis, migrate to distant organs, and develop chemoresistance. Targeting these signaling molecules and pathways associated with EMT may provide clinicians with a new approach to the treatment of G-I malignancy.
Related Concept Videos
Metastasis
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...
Cadherins in Tissue Organization
Cell Sorting During Development
Cell sorting plays an...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Renewal of Intestinal Stem Cells
The Tumor Microenvironment
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

