Epithelial-Mesenchymal Transition Induced in Cancer Cells by Adhesion to Type I Collagen

被引:7
|
作者
Fujisaki, Hitomi [1 ]
Futaki, Sugiko [2 ]
机构
[1] Nippi Res Inst Biomatrix, Ibaraki 3020017, Japan
[2] Osaka Med & Pharmaceut Univ, Fac Med, Anat & Cell Biol, Osaka 5698686, Japan
关键词
type I collagen; gel formation; epithelial-mesenchymal transition; tumor microenvironment; cancer cells; EXTRACELLULAR-MATRIX; GENE-EXPRESSION; E-CADHERIN; GROWTH; PROGRESSION; FIBRONECTIN; METASTASIS; INTEGRINS; INVOLVEMENT; MIGRATION;
D O I
10.3390/ijms24010198
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The epithelial-mesenchymal transition (EMT) is an important biological process that is physiologically observed during development, wound healing, and cancer invasion. During EMT induction, cancer cells lose their epithelial properties owing to various tumor microenvironmental factors and begin to exhibit mesenchymal properties, such as loss of apical-basal polarity, weakened intercellular adhesion, and promotion of single cell migration. Several factors, including growth factor stimulation and adhesion to type I collagen (Col-I), induce EMT in cancer cells. Cells adhere to Col-I via specific receptors and induce EMT by activating outside-in signals. In vivo, Col-I molecules often form fibrils, which then assemble into supramolecular structures (gel form). Col-I also self-assembles in vitro under physiological conditions. Notably, Col-I can be used as a culture substrate in both gel and non-gel forms, and the gel formation state of Col-I affects cell fate. Although EMT can be induced in both forms of Col-I, the effects of gel formation on EMT induction remain unclear and somewhat inconsistent. Therefore, this study reviews the relationship between Col-I gel-forming states and EMT induction in cancer cells.
引用
收藏
页数:14
相关论文
empty
未找到相关数据