Real-time PCR and western blotting showed that the expression levels of p15, p21 and E-cadherin significantly decreased, and levels of cyclinD1 and MMP-2 increased in endometrial cancer cells.
Collectively, our data indicated that SPOCK2 contributed to the progression of EC by regulating the biological behavior of cancer cells, which is achieved partly through regulating protein expression of MT1-MMP and MMP2 and activation of MMP2.
Immunohistochemical expression of hormone receptors, Ki-67, endoglin (CD105), claudins 3 and 4, MMP-2 and -9 in endometrial polyps and endometrial cancer type I.
Compared with those with endometriosis or normal endometria, the positive rate of MMP-2 expression is significantly higher in patients with endometrial cancer (RR = 2.31, 95% CI: 1.78-3.00, P < .01).
We observed statistically significant differences in mean serum levels of HE4 and MMP2 between the group of endometrial cancer patients and the group of patients with no changes in the endometrium (<i>P</i>=0.002/0.003).
In conclusion, STMN1 is an oncogene and it enhances the growth and invasion of EC possibly by mediating the secretion and activation of MMP2 and MMP9 protein.
Moreover, we identified signal transducer and activator of transcription 3 (STAT3) as a direct target of miR-124, and over expression of miR-124 not only induced changes in STAT3 expression but also altered expression of its target genes, cyclin D2 and matrix metalloproteinase 2, in the human endometrial carcinoma cell line HEC-1B.
A positive correlation was also observed between KAI1 and MMP-2 expression, and a borderline one between KAI1 and MMP-9 expression in endometrial cancer.
MicroRNA-200b is overexpressed in endometrial adenocarcinomas and enhances MMP2 activity by downregulating TIMP2 in human endometrial cancer cell line HEC-1A cells.
Twenty-nine endometrial carcinoma biopsies were investigated immunohistochemically to determine the tissue localization of MMP-2 (gelatinase A), MMP-9 (gelatinase B), MT1-MMP, and TIMPs 1-3.
Tissues from 64 biopsies of endometrial carcinoma (EC) and 15 biopsies of normal (control) endometrium were investigated immunohistochemically to determine their microvessel number, and by in situ hybridisation to determine the expression of mRNA of the matrix metalloproteinase-2 (MMP-2, gelatinase A) and metalloproteinase-9 (MMP-9 gelatinase B).