Oncotarget

Reviews:

Lysyl oxidase family members in urological tumorigenesis and fibrosis

Tao Li, Changjing Wu, Liang Gao, Feng Qin, Qiang Wei and Jiuhong Yuan _

PDF  |  HTML  |  How to cite

Oncotarget. 2018; 9:20156-20164. https://doi.org/10.18632/oncotarget.24948

Metrics: PDF 2054 views  |   HTML 2787 views  |   ?  


Abstract

Tao Li1,2, Changjing Wu1, Liang Gao3, Feng Qin1, Qiang Wei2 and Jiuhong Yuan1,2

1The Andrology Laboratory, West China Hospital, Sichuan University, Chengdu, Sichuan, China

2Department of Urology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

3Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China

Correspondence to:

Jiuhong Yuan, email: [email protected]

Keywords: lysyl oxidase; tumorigenesis; fibrosis; urological cancer; collagen

Received: September 29, 2017     Accepted: March 11, 2018     Published: April 13, 2018

ABSTRACT

Lysyl oxidase (LOX) is an extracellular copper-dependent monoamine oxidase that catalyzes crosslinking of soluble collagen and elastin into insoluble, mature fibers. Lysyl oxidase-like proteins (LOXL), LOX isozymes with partial structural homology, exhibit similar catalytic activities. This review summarizes recent findings describing the roles of LOX family members in urological cancers and fibrosis. LOX/LOXL play key roles in extracellular matrix stability and integrity, which is essential for normal female pelvic floor function. LOX/LOXL inhibition may reverse kidney fibrosis and ischemic priapism. LOX and LOXL2 reportedly promote kidney carcinoma tumorigenesis, while LOX, LOXL1 and LOXL4 suppress bladder cancer growth. Multiple studies agree that the LOX propeptide may suppress tumor growth, but the role of LOX in prostate cancer remains controversial. Further studies are needed to clarify the exact effects and mechanism of LOX/LOXL on urological malignancies.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 24948