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FLASH GENE

Symbol

TFF3

contributors: mct - updated : 25-10-2010

HGNC name	trefoil factor 3 (intestinal)
HGNC id	11757

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

DNA

TYPE	functioning gene
SPECIAL FEATURE	component of a cluster
text	trefoil family member genes are found in a cluster on chromosome 21
STRUCTURE	3.54 kb     3 Exon(s)

10 Kb 5' upstream gene genomic sequence study

MAPPING

cloned

Y

linked

N

status

confirmed

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_003226 3 - 1054 NP_003217 12 94 - 1996 8833157

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 Cardiovascular heart       highly Digestive intestine small intestine         intestine large intestine colon   highly Endocrine thyroid       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Epithelial secretory glandular exocrine

cells

System Cell Pubmed Species Stage Rna symbol Digestive epithelial cell Digestive goblet

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	three intrachain disulfide bonds, forming the three leaf structure (P domain, trefoil motif)
	at least one copy of the trefoil motif, a 40-amino acid domain that contains three conserved disulfides

HOMOLOGY

Homologene

FAMILY

trefoil family

CATEGORY

regulatory , secretory

SUBCELLULAR LOCALIZATION

extracellular

basic FUNCTION	maybe involved in mitogenic processes
	cell adhesion migration by controling the expression of APC and E-cadherin-catenin complexes
	may have a role in promoting cell migration
	regulating mucosal regeneration and repair
	may enhance mucosal healing by modulating motogenic activity, inhibiting apoptosis, and promoting angiogenesis
	likely to contribute to oral wound healing
	could play a role in neurosensory signaling
	contributes to the malignant behavior of colon cancer cells
	playing a pivotal role in corneal wound healing mechanism
	may have a role in normal thyroid tissue function
	plays a major part in regeneration and restitution processes in urinary tract epithelia

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

TFF3-mediated pathway for stimulation of beta-cell replication that could ultimately be exploited for expansion or preservation of islet beta-cell mass

a component

INTERACTION

DNA

RNA

small molecule

protein

TWIST1 is an important potential downstream effector, playing a key role in TFF3-modulated metastasis in gastric cancer

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral     --over   in gastric cancer tumoral     --over   during inflammatory processes and cancer progression tumoral     --over   overexpression in hepatocellular carcinogenesis, and the specific promoter CpG hypomethylation may be one of the regulation mechanisms of TFF3 overexpression tumoral     --over   by hypomethylation of the promoter/enhancer region, significantly lower in prostate carcinoma compared to benign prostatic hyperplasia tumoral     --low   in follicular neoplastic lesions compared with that in normal thyroid tissue samples

Susceptibility

Variant & Polymorphism

Candidate gene
Marker	overexpression and promoter hypomethylation of trefoil factors may serve as biomarkers in prostate carcinoma
	novel serum marker for early detection and/or monitoring of poorly differentiated endometrioid endometrial carcinomas (G3-EEC) patients
	TFF2 and probably also TFF3 are candidate biomarkers for nephrolithiasis and possibly other inflammatory conditions of the urinary tract
Therapy target	having broad implications for developing novel therapeutic strategies for treating nonhealing wounds
	System Type Disorder Pubmed immunology autoimmune digestive may have therapeutic potential in the treatment of inflammatory bowel disease, and one of the mechanisms may related to inhibit the TLR4/NF-kappaB signaling pathways

ANIMAL & CELL MODELS

	Tff3-deficient (Tff3(-)(/)(-)) mice (Paulsen, 2008)
	Tff3 knock-out animals show an accelerated presbyacusis and a hearing loss of about 15 dB at low frequencies increasing to 25 dB loss at higher frequencies