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KANGAI 1; KAI1 OKDB#: 1574
 Symbols: KANGAI 1; KAI1 Species: human
 Synonyms: PROSTATE CANCER ANTIMETASTASIS GENE KAI1| LEUKOCYTE SURFACE ANTIGEN R2, SAR2| ANTIGEN CD82, CD82| SUPPRESSOR OF TUMORIGENICITY 6, ST6| R2 LEUKOCYTE ANTIGEN|  Locus: 11p11.2 in Homo sapiens


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General Comment KAI1 is capable of inhibiting the metastatic process in experimental animals. The expression of the KAI1 gene is also downregulated during tumor progression of prostate, breast, lung, bladder, and pancreatic cancers in humans, and this downregulation appears to be at the level of transcription or posttranscription. Dong et al. (1995) isolated the metastasis suppressor gene on 11p11.2 by PCR methods and designated it KAI1 for 'kang ai' (Chinese for anticancer). Expression of this gene was reduced in human cell lines derived from metastatic prostate tumors. KAI1 specifies a protein of 267 amino acids, with 4 hydrophobic and presumably transmembrane domains and 1 large extracellular hydrophilic domain with 3 potential N-glycosylation sites. KAI1 is evolutionarily conserved, is expressed in many human tissues, and encodes a member of a structurally distinct family of leukocyte surface glycoproteins. Decreased expression of this gene may be involved in the malignant progression of prostate and other cancers. The gene has also been referred to as ST6.

NCBI Summary: This metastasis suppressor gene product is a membrane glycoprotein that is a member of the transmembrane 4 superfamily. Expression of this gene has been shown to be downregulated in tumor progression of human cancers and can be activated by p53 through a consensus binding sequence in the promoter. Its expression and that of p53 are strongly correlated, and the loss of expression of these two proteins is associated with poor survival for prostate cancer patients.
General function Cell adhesion molecule
Comment
Cellular localization Plasma membrane
Comment
Ovarian function
Comment
Expression regulated by
Comment
Ovarian localization Luteal cells
Comment Houle CD,et al 2002 reported that loss of expression and altered localization of KAI1 and CD9 protein are associated with epithelial ovarian cancer progression. Impairment of cell adhesion plays a vital role in tumor progression. E- and N-cadherin, CD9, and KAI1 are all adhesion molecules that have been implicated in the progression of several different tumor types. To help explain the potential role these adhesion molecules have in ovarian cancer, comparisons were made between expression patterns in normal ovary and various grades of primary and metastatic epithelial ovarian cancers. Thirty-two primary and 8 metastatic human ovarian epithelial carcinomas and 18 samples of normal ovarian tissue were examined for adhesion molecule expression using immunohistochemistry. KAI1 and CD9 revealed an inverse relationship between tumor grade and expression levels, characterized by high expression in low-grade tumors and low expression in high-grade tumors and metastases. KAI1 and CD9 also demonstrated a shift in cellular localization from the membrane in grade 1 tumors to the cytoplasm in grade 3 tumors. N-cadherin expression showed a positive trend between expression levels and tumor grade. E-cadherin expression varied little between different tumor grades and metastases. Inclusion cysts (n = 6) and surface invaginations often strongly expressed KAI1, CD9, and E-cadherin. KAI1 expression was variable in ovarian follicles and corpora lutea depending on their stage of development. Although sample size is limited, these findings suggest that progression of ovarian epithelial carcinomas is associated with down-regulation and altered cellular localization of KAI1 and CD9. In addition, variable KAI1 expression during follicular and luteal development suggests that it has a physiological function in the ovary. Further investigation will be needed to see if it is also regulated this way during progression of ovarian cancers.
Follicle stages Antral, Corpus luteum
Comment
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Mutations 0 mutations
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created: Aug. 13, 2002, 12:31 p.m. by: hsueh   email:
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last update: Aug. 13, 2002, 12:31 p.m. by: system    email:



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