» Articles » PMID: 22528876

Lysyl Oxidase, Extracellular Matrix Remodeling and Cancer Metastasis

Overview
Publisher Springer
Specialty Oncology
Date 2012 Apr 25
PMID 22528876
Citations 115
Authors
Affiliations
Soon will be listed here.
Abstract

Lysyl oxidase (LOX) family oxidases, LOX and LOXL1-4, oxidize lysine residues in collagens and elastin, resulting in the covalent crosslinking and stabilization of these extracellular matrix (ECM) structural components, thus provide collagen and elastic fibers much of their tensile strength and structural integrity. Abnormality in LOX expression and/or activity results in connective tissue disorders and fibrotic diseases. Despite LOX family oxidases have been reported to function as tumor suppressors, recent studies have highlighted the roles of LOX family oxidases in promoting cancer metastasis. LOX family oxidases are highly expressed in invasive tumors, and are closely associated with metastasis and poor patient outcome. Consistent to their roles in connective tissue homeostasis, LOX family oxidases expedite tumorigenesis and metastasis through active remodeling of tumor microenvironment. LOX family oxidases are also actively involved in the process of epithelial-mesenchymal transition (EMT), an event critical in cancer cell invasion and metastasis. In this review, we will summarize the recent progress on LOX family oxidases, with much of the focus on the roles and mechanism of LOX in tumor progression and metastasis.

Citing Articles

The matrix stiffness is increased in the eutopic endometrium of adenomyosis patients: a study based on atomic force microscopy and histochemistry.

Wang X, Cai W, Liang T, Li H, Gu Y, Wei X Eur J Histochem. 2024; 68(4).

PMID: 39629520 PMC: 11694501. DOI: 10.4081/ejh.2024.4131.


Actuating Extracellular Matrices Decouple the Mechanical and Biochemical Effects of Muscle Contraction on Motor Neurons.

Bu A, Afghah F, Castro N, Bawa M, Kohli S, Shah K Adv Healthc Mater. 2024; 14(6):e2403712.

PMID: 39523700 PMC: 11874633. DOI: 10.1002/adhm.202403712.


Copper-Based Nanomedicines for Cuproptosis-Mediated Effective Cancer Treatment.

Noh D, Lee H, Lee S, Sun I, Yoon H Biomater Res. 2024; 28:0094.

PMID: 39430913 PMC: 11486892. DOI: 10.34133/bmr.0094.


Copper homeostasis and cuproptosis in gynecological cancers.

Huang X, Lian M, Li C Front Cell Dev Biol. 2024; 12:1459183.

PMID: 39386020 PMC: 11461353. DOI: 10.3389/fcell.2024.1459183.


Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer.

Kozbor D, Winkler M, Malhotra N, Mistarz A, Wang S, Hutson A Res Sq. 2024; .

PMID: 39372930 PMC: 11451647. DOI: 10.21203/rs.3.rs-4940287/v1.


References
1.
Araya J, Nishimura S . Fibrogenic reactions in lung disease. Annu Rev Pathol. 2010; 5:77-98. DOI: 10.1146/annurev.pathol.4.110807.092217. View

2.
Moreno-Bueno G, Salvador F, Martin A, Floristan A, Cuevas E, Santos V . Lysyl oxidase-like 2 (LOXL2), a new regulator of cell polarity required for metastatic dissemination of basal-like breast carcinomas. EMBO Mol Med. 2011; 3(9):528-44. PMC: 3377095. DOI: 10.1002/emmm.201100156. View

3.
In Yook J, Li X, Ota I, Fearon E, Weiss S . Wnt-dependent regulation of the E-cadherin repressor snail. J Biol Chem. 2005; 280(12):11740-8. DOI: 10.1074/jbc.M413878200. View

4.
Levental K, Yu H, Kass L, Lakins J, Egeblad M, Erler J . Matrix crosslinking forces tumor progression by enhancing integrin signaling. Cell. 2009; 139(5):891-906. PMC: 2788004. DOI: 10.1016/j.cell.2009.10.027. View

5.
Larue L, Bellacosa A . Epithelial-mesenchymal transition in development and cancer: role of phosphatidylinositol 3' kinase/AKT pathways. Oncogene. 2005; 24(50):7443-54. DOI: 10.1038/sj.onc.1209091. View