» Articles » PMID: 36613638

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

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2023 Jan 8
PMID 36613638
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Proteomic profiling reveals biological processes and biomarkers involved in the pathogenesis of occult breast cancer.

Zhang J, Wang Y, Liu Y, Chen H, Chai N, Zhao Y BMC Cancer. 2025; 25(1):231.

PMID: 39930421 PMC: 11812265. DOI: 10.1186/s12885-025-13657-4.


Post-Translational Modifications of Proteins Orchestrate All Hallmarks of Cancer.

Bruno P, Arshad A, Gogu M, Waterman N, Flack R, Dunn K Life (Basel). 2025; 15(1).

PMID: 39860065 PMC: 11766951. DOI: 10.3390/life15010126.


gene expression in melanoma tissues and its effects on the malignant biological functions of melanoma cells.

Qu J, Cheng X, Liu M, Zhang Q Transl Cancer Res. 2024; 13(11):6347-6363.

PMID: 39697757 PMC: 11651744. DOI: 10.21037/tcr-24-2159.


Hypoxia inducible factor-1ɑ as a potential therapeutic target for osteosarcoma metastasis.

Zhou J, Lan F, Liu M, Wang F, Ning X, Yang H Front Pharmacol. 2024; 15:1350187.

PMID: 38327979 PMC: 10847273. DOI: 10.3389/fphar.2024.1350187.

References
1.
Cukierman E, Pankov R, Stevens D, Yamada K . Taking cell-matrix adhesions to the third dimension. Science. 2001; 294(5547):1708-12. DOI: 10.1126/science.1064829. View

2.
Aumailley M . The laminin family. Cell Adh Migr. 2012; 7(1):48-55. PMC: 3544786. DOI: 10.4161/cam.22826. View

3.
Kolahi K, Donjacour A, Liu X, Lin W, Simbulan R, Bloise E . Effect of substrate stiffness on early mouse embryo development. PLoS One. 2012; 7(7):e41717. PMC: 3409240. DOI: 10.1371/journal.pone.0041717. View

4.
LaGamba D, Nawshad A, Hay E . Microarray analysis of gene expression during epithelial-mesenchymal transformation. Dev Dyn. 2005; 234(1):132-42. DOI: 10.1002/dvdy.20489. View

5.
Shukla V, Higuita-Castro N, Nana-Sinkam P, Ghadiali S . Substrate stiffness modulates lung cancer cell migration but not epithelial to mesenchymal transition. J Biomed Mater Res A. 2016; 104(5):1182-93. DOI: 10.1002/jbm.a.35655. View