Familial adenomatous polyposis (FAP), which includes familial polyposis coli (FPC) and the Gardner syndrome (GS), is a genetically determined premalignant disease of the colon inherited by a locus (APC) mapping within 5q15-q22. To elucidate the role of 5q loss in FAP tumorigenesis, we analysed 51 co
Enhanced phosphoinositide metabolism in colorectal carcinoma cells derived from familial adenomatous polyposis patients
✍ Scribed by Miwako K. Homma; Yoshimi Homma; Masayoshi Namba; Yasuhito Yuasa
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 870 KB
- Volume
- 55
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The production of the second messenger molecules diacylglycerol and inositol 1,4,5‐trisphosphate is mediated by activated phosphatidylinositol‐specific phospholipase C (PLC) enzymes. We report the enhancement of the phosphoinositide metabolism pathway in KMS‐4 and KMS‐8 cells, both of which are human colorectal carcinoma cell lines derived from familial adenomatous polyposis patients. In these cells, the cellular contents of diacylglycerol and inositol 1,4,5‐trisphosphate were constitutively increased and the PLC activity in vitro was significantly high, as compared with those in normal colon cells or in other sporadic colorectal carcinoma cells. Northern and Western analyses showed the high expression levels of both PLC‐γ1 and PLC‐δ1 in KMS‐4 and KMS‐8 cells. Moreover, we detected the enhancement of protein–tyrosine kinase activity and tyrosine phosphorylation of PLC‐γ1 in these KMS cells. These results suggest the involvement of activated phosphoinositide signaling pathways in the colorectal tumorigenesis of familial adenomatous polyposis. © 1994 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
Endocrine neoplasms have been reported occasionally in patients with familial adenomatous polyposis (FAP). An adrenocorotical carcinoma was studied in a patient with a family history of FAP. Loss of heterozygosity (LOH) in the region close to the adenomatous polyposis coli (APC) gene was detected in
## Abstract Accumulation of genetic alterations in oncogenes and tumor suppressor genes causes the transformation of a normal cell into a malignant cell. Recently, Fearon and Vogelstein (Cell 61:759‐767, 1990) reported on a model for the genetic pathway in development of colorectal neoplasia. To in
## Abstract Sera from eight of 15 patients with colonic carcinoma exhibited demonstrable cytotoxicity against an established cell strain derived from adenocarcinoma of the ileocecum, HCT‐8. Sera from 12 of 16 patients with rectal carcinoma were cytotoxic for an established cell strain derived from