P120-catenin expression in human colorectal cancer

✍ Scribed by Anouchka Skoudy; Silvia Gomez; Myriam Fabre; Antonio Garcia de Herreros

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: French
• Weight: 913 KB
• Volume: 68
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/(sici)1097-0215(19960927)68:1<14::aid-ijc3>3.0.co;2-#

✦ Synopsis

Recent data suggest that pl2O-catenin plays a role in the regulation of functionality of E-cadherin, a protein essential for the establishment and maintenance of cell-cell contacts. Since dysfunction of intercellular adhesiveness is an alteration frequently observed in colon cancer we have studied the expression and distribution of p 120-catenin in human colorectal tumors. In normal colon, pl20-catenin was observed in the crypt and surface epithelium; the cells showed reactivity both in the membrane and in the cytosol. Thirteen primary tumors were examined for p 120-catenin expression: they were graded as uniformly positives (+) (4); heterogeneous (k) (6), with a diminished ex ression, detected mainly in the cytosol; and negatives (-) 6). Although the number of tumors was low, the reduction in pl20-catenin correlated with a larger size of the tumors (p = 0.038). Association of p 120-catenin to the cytoskeleton was also determined in 5 tumors by detergent extraction and Western blot; this analysis shows that lack of reactivity in the membrane was accompanied by absence of p 120-catenin in the cytoskeleton-associated fraction. Analysis of E-cadherin was performed in order to compare the distribution of this protein and p 120-catenin. Although no complete correlation was found between the expression of both proteins (p = 0.077), our results showed that alterations in the level or distribution of p 120-catenin were accompanied by lack of E-cadherin reactivity in the membrane, whereas absence of pl20-catenin in the cytoskeleton fraction was associated with important decreases in the amount of E-cadherin in this same fraction. These results show that alterations in pl20-catenin levels are a common event in colorectal tumors, and suggest that the distribution of this protein and E-cadhenn is coordinately regulated.