ABSTRACT
OBJECTIVE: We studied the relationship between the occurrence of laterally spreading tumors (LSTs) and the activation of Wnt/ß-catenin/c-myc pathway. PATIENTS AND METHODS: 20 cases of colorectal polypoid adenomas (PAs) tissue sample, 20 cases of LSTs tissue sample and 20 cases of colorectal cancer tissue sample were acquired, and positive expression of Wnt/ß-catenin/c-myc proteins were detected by immunohistochemical staining. In addition, relative expression levels of mRNA and protein were measured using RT-PCR and Western blotting method. RESULTS: The positive expression levels of Wnt/ß-catenin/c-myc protein in the colorectal cancer group were higher than that in LST group, and the value of the PAs group was the lowest; differences were statistically significant (p < 0.05). The relative expression levels of Wnt/ß-catenin/c-myc mRNA and protein in colorectal cancer group were higher than that in LST group, and the value of PAs group was the lowest; differences were statistically significant (p < 0.05). CONCLUSIONS: The activation level of the Wnt/ß-catenin/c-myc pathway has a close relation to the occurrence and deterioration of LSTs.
Subject(s)
Colorectal Neoplasms/metabolism , Proto-Oncogene Proteins c-myc/metabolism , Wnt Proteins/metabolism , Wnt Signaling Pathway , beta Catenin/metabolism , Adult , Aged , Female , Humans , Male , Middle AgedABSTRACT
The effect of angiotensin II on adrenal cortisol secretion was studied using incubated adrenal tissues of cells preparation of guinea pig and dog. The results showed that: the cortisol secretion in guinea pigs was increased by the addition of angiotensin II in both dose-dependent and time-dependent manner at concentration > or = 10(-9) mol/L (P < 0.01). When ACTH was further added to the angiotensin primed preparation, the output of cortisol was further increased. Deprivation of free calcium largely suppressed the production of cortisol induced by angiotensin II (P < 0.05). These results suggested that angiotensin II exerts a direct effect on the secretion of adrenal cortisol, which required the presence of Ca2+ and is promoted by ACTH.
