. higher expression in non-cancerous than in cancerous samples
. upregulated in the breast malignant compared to the benign tumors, and patients with positive KLK12sv1/2 levels presented a significantly longer disease-free survival
2018
29807016
-
splicing
-
-
-
. higher expression in non-cancerous than in cancerous samples
. downregulated in the malignant breast compared to the benign tumors, and patients with positive KLK12sv3 levels presented a significantly longer disease-free survival
2018
29807016
EXPRESSION
Type
widely
expressed in
(based on citations)
organ(s)
System
Organ level 1
Organ level 2
Organ level 3
Organ level 4
Level
Pubmed
Species
Stage
Rna symbol
Digestive
intestine
large intestine
colon
salivary gland
highly
Homo sapiens
stomach
highly
Homo sapiens
Reproductive
male system
prostate
highly
Homo sapiens
Respiratory
lung
highly
Homo sapiens
respiratory tract
trachea
highly
Homo sapiens
tissue
System
Tissue
Tissue level 1
Tissue level 2
Level
Pubmed
Species
Stage
Rna symbol
Blood / hematopoietic
bone marrow
highly
Homo sapiens
Connective
bone
highly
Homo sapiens
Epithelial
secretory
glandular
endocrine
cell lineage
cell lines
fluid/secretion
salivary gland
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
isoforms
Precursor
secreted as an inactive pro-enzyme, which is able to autoactivate to gain enzymatic activity
involved in pathogenesis and/or progression of certain cancer types
possesses trypsin-like activity, cleaving peptide bonds after both arginine and lysine
may participate in enzymatic cascades involving other kallikreins
may indirectly regulate the bioavailability and activity of several growth factors through processing of their CCN binding partners
involvement of KLK12 in different homeostatic and disease pathways through modulation of growth factor availability and/or activity
play a critical role in controlling normal angiogenesis
KLK12-mediated proteolysis of CYR61 and WISP3 can reduce or abolish the binding of VEGFA, BMP2, and TGFB1
KLK12-mediated hydrolysis of CCNs may be involved in the modulation of the bioavailability and/or activity of several growth factors including VEGFA, BMP2, TGFB1, and FGF2
may play an important role in angiogenesis modulating proangiogenic factor bioavailability and activating the kinin receptor B2 pathway
proangiogenic activity of KLK12 in lung endothelial cells was not related to a kinin release
KLK5, KLK12 are involved in the cleavage activation of human-adapted influenza virus subtypes
KLK12 proangiogenic effect is mediated through several molecular mechanisms
plays likely a tumor-supporting role in Triple-negative breast cancer (TNBC)
CELLULAR PROCESS
protein, degradation
PHYSIOLOGICAL PROCESS
PATHWAY
metabolism
signaling
a component
INTERACTION
DNA
RNA
small molecule
protein
might be responsible for the shedding of CYR61 from the cell surface
can target all six members of the CCN family at different proteolytic sites (WISP1, WISP2, WISP3, CYR61, CTGF, NOV)
interacting with CYR61 and WISP3 (fragmentation of CYR61 and WISP3 by KLK12 on cells of the tumor microenvironment, including neoplastic and endothelial cells)
angiogenesis is stimulated by KLK12 acting via a PDGFB-dependent paracrine pathway
efficiently cleaved the extracellular matrix proteins fibronectin and tenascin, both of which are involved in the regulation of endothelial cell adhesion and migration
cell & other
REGULATION
induced by
steroid hormone
ASSOCIATED DISORDERS
corresponding disease(s)
Other morbid association(s)
Type
Gene Modification
Chromosome rearrangement
Protein expression
Protein Function
tumoral
--low
in breast cancer
tumoral
--over
in prostate cancer
tumoral
--over
in Gastric cancer tissue
Susceptibility
Variant & Polymorphism
Candidate gene
Marker
may have potential use as a cancer biomarker
KLK12 might serve as a novel diagnosis and prognosis biomarker in gastric cancer
