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FLASH GENE
Symbol KLK10 contributors: mct - updated : 08-04-2020
HGNC name kallikrein-related peptidase 10
HGNC id 6358
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
6 splicing 3123 30.1 276 - 2017 2841983
6 splicing 2985 30.1 276 - 2017 2841983
6 - 3024 - 276 - 2017 2841983
EXPRESSION
Type widely
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Lymphoid/Immunetonsils   highly Homo sapiens
Reproductivefemale systembreast  highly
 female systemovary  highly
 male systemprostate  highly
Respiratoryrespiratory tractlarynx  highly
Urinarykidneytubule  highly
cells
SystemCellPubmedSpeciesStageRna symbol
Lymphoid/ImmuneB cell Homo sapiens
cell lineage
cell lines
fluid/secretion secreted
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
HOMOLOGY
interspecies homolog to C.elegans T27E9.4b
Homologene
FAMILY
  • kallikrein family
  • peptidase S1 family
  • CATEGORY enzyme , tumor suppressor
    SUBCELLULAR LOCALIZATION extracellular
        intracellular
    intracellular,cytoplasm,cytosolic,granule
    basic FUNCTION
  • tumor suppressor role in breast and prostate cancer
  • KLK9 and KLK10, once activated, are unlikely to participate in further pro-KLK activation pathways, although similar to KLK1 they may activate other bioactive peptides
  • estrogen-sensitive kallikreins with KLK14, and KLK11, all synergistically enhanced and upregulated by androgens in breast cancer cells via a membrane bound androgen receptor
  • having the ability to inhibit anchorage-independent growth in hepatoma cells
  • lower KLK10 levels in salivary gland pleomorphic adenoma, suggesting aberrant expression in a tumour that develops primarily from myoepithelial cells
  • may function as a tumour suppressor by repressing proliferation, enhancing apoptosis and decreasing glucose metabolism in PC3 prostate cancer cells
  • CELLULAR PROCESS protein, degradation
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • kinin B1 receptor agonist induces secretion of KLK1, KLK6, KLK10, KLK13 and KLK14 into the medium nof neutrophils
  • LMNA and EMD modulate KLK10, SMAD2 and BCL2L12 expression levels as well as the spatial positions of gene loci in the interphase nucleus
  • cell & other
    REGULATION
    Other differentially regulated through distinct epigenetic mechanisms in HBV- and HCV-related hepatocellular carcinoma
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in ovarian, colorectal and gastric cancer and higher expression of KLK10 closely correlates with advanced disease stage, which predicts a poorer prognosis
    tumoral     --low  
    in breast cancer (in progression), and in testicular cancer, in cervical cancer, prostate cancer and acute lymphocytic leukemia
    tumoral     --over  
    in oral squamous cell carcinoma and may be implicated in malignant progression
    tumoral     --low  
    in hepatocellular carcinoma by hypermethylation, significantly associated with cirrhosis and HCV infection as well as inversely associated with HBV infection
    constitutional     --over  
    significantly increased in Alzheimer disease
    tumoral     --over  
    increased KLK10 and KLK11 protein expression is associated with favorable prognosis in advanced high-grade serous ovarian cancer
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
  • potential biomarker in colon adenocarcinoma
  • promising biomarker for diagnosis in Pancreatic Ductal Adenocarcinoma (PADC)
  • KLK6 and KLK10 may be useful markers in gastroesophageal junction tumors
  • Therapy target
    SystemTypeDisorderPubmed
    cancerendocrinepancreas
    potential target for therapy in Pancreatic Ductal Adenocarcinoma (PADC)
    cancerdigestiveoesophagus
    potential therapeutic targets in gastroesophageal junction tumors
    ANIMAL & CELL MODELS