CTHRC1 overexpression promotes ectopic endometrial stromal cell proliferation, migration and invasion via activation of the Wnt/β-catenin pathway
| Autor: | Liqi Zhang, Yifei Lv, Junyan Ma, Kaihong Xu, Jun Lin, Xiangwei Fei |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Adult Small interfering RNA Stromal cell Biology 03 medical and health sciences Endometrium 0302 clinical medicine Western blot Cell Movement medicine Humans Wnt Signaling Pathway beta Catenin Endometrial Stromal Cell Cell Proliferation Gene knockdown Extracellular Matrix Proteins 030219 obstetrics & reproductive medicine medicine.diagnostic_test Wnt signaling pathway Obstetrics and Gynecology Cell migration 030104 developmental biology Reproductive Medicine Catenin Cancer research Female Stromal Cells Developmental Biology |
| Zdroj: | Reproductive biomedicine online. 40(1) |
| ISSN: | 1472-6491 |
| Popis: | Research question Endometriosis is characterized by the occurrence of endometrial-like tissue outside the uterus. Collagen triple helix repeat containing-1 (CTHRC1) is known as a tumour-promoting factor in several neoplasms. This study aimed to examine the roles of CTHRC1 in the development and progression of endometriosis, and to unravel the underlying mechanisms. Design Quantitative real-time PCR, western blot analyses and enzyme-linked immunosorbent assay were performed to determine the expression levels of CTHRC1 in tissues and serum. In addition, CTHRC1 expression levels were knocked down by small-interfering RNA in ectopic endometrial stromal cells (EESC). Cell Counting Kit-8, fluorescence-activated cell sorting, Transwell and wound scratch assays were carried out to assess the underlying biological behaviours, and western blot analyses were performed to reveal the molecular mechanisms. Results mRNA and protein expression levels of CTHRC1 were markedly higher in ectopic endometrial tissues than in eutopic and control endometrial tissues. In addition, the serum concentration of CTHRC1 was apparently higher in the endometriosis group than the control group. Small interfering RNA knockdown of CTHRC1 suppressed the proliferation, migration, invasion and healing abilities of EESC. Furthermore, the protein expressions of key molecules in the Wnt/β-catenin pathway showed an obvious down-regulated expression after siRNA transfection. Conclusions These findings suggest that CTHRC1 may be partly responsible for the development and progression of endometriosis by increasing EESC proliferation, migration and invasion via the Wnt/β-catenin pathway. CTHRC1 may thus serve as a diagnostic and therapeutic target for endometriosis. |
| Databáze: | OpenAIRE |
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