Expression of Id1 and Id3 in endometrial carcinoma and their roles in regulating biological behaviors of endometrial carcinoma cells in vitro.
- Author:
Lili SUN
1
;
Xuenong LI
;
Guobing LIU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Adhesion; Cell Line, Tumor; Cell Movement; Cell Proliferation; Endometrial Neoplasms; metabolism; pathology; Female; Humans; Inhibitor of Differentiation Protein 1; metabolism; Inhibitor of Differentiation Proteins; metabolism; Matrix Metalloproteinase 2; metabolism; Neoplasm Proteins; metabolism; Proto-Oncogene Proteins p21(ras); metabolism; RNA Interference; Receptors, CXCR4; metabolism
- From: Journal of Southern Medical University 2013;33(6):812-818
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expression of inhibitor of DNA differentiation/DNA binding 1 (Id1) and Id3 in endometrial carcinoma and explore their roles in regulating the proliferation, invasion, migration and adhesion of endometrial carcinoma cells in vitro.
METHODSId1 and Id3 expression in 4 fresh endometrial cancer tissue specimens and matched adjacent tissues were detected using Western blotting. Two endometrial cancer cell lines, HEC-1-B and RL-952, were both divided into 4 groups, namely the untreated group, blank virus group, promoter group and Id1/Id3 double-knockdown group, and their expressions of MMP2, CXCR4 and P21 were detected by qRT-PCR and Western blotting. The proliferation, invasion, migration and adhesion of the cells were evaluated with MTT, Transwell, wound-healing, and adhesion assays.
RESULTSEndometrial carcinoma tissues showed significantly higher Id1 and Id3 expression than the adjacent tissues (P<0.05). In the two endometrial carcinoma cell lines, Id1/Id3 double-knockdown significantly decreased MMP2 and CXCR4 expression and increased P21 expression at both mRNA and protein levels (P<0.05), and resulted in suppressed cell proliferation, invasion, migration and adhesion.
CONCLUSIONId1 and Id3 expressions are up-regulated in endometrial carcinoma to promote the proliferation, invasion, migration and adhesion of the tumor cells by increasing MMP2 and CXCR4 expression and reducing P21 expression. Therapies targeting Id1/Id3 can be a novel strategy for treatment of endometrial carcinoma.