Cold-shock domain family member YB-1 expression in endometrium and endometriosis
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⤵ 4 in-corpus citations
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YB-1 expression was higher in endometriosis tissues and macrophages, and its knockdown reduced cell proliferation, invasion, and apoptosis in an endometriosis cell line.
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Abstract
BACKGROUND: The Y-box-binding protein (YB-1) is described as a potential oncogene highly expressed in tumors and associated with increased cell survival, proliferation, migration and anti-apoptotic signaling. The aim of our study was to examine the expression and role of YB-1 in human endometriosis (Eo) and its association with cell survival, proliferation and invasion.
METHODS: We analyzed the gene and protein expression levels of YB-1 by quantitative real-time RT-PCR and immunoassays, respectively, in peritoneal macrophages, ovarian endometrioma and eutopic endometrial tissues/cells derived from women with (n= 120) and without (n= 91) Eo. We also evaluated the functional consequences of YB-1 knockdown in the Z12 Eo cell line by measuring cell proliferation [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromid cell proliferation assay], invasion (Matrigel invasion assay) and spontaneous and tumour necrosis factor (TNFα)-induced RANTES (regulated upon activation, normal T-cell expressed and secreted chemokine) expression and apoptosis (ELISA-based assay).
RESULTS: YB-1 gene and protein expression was statistically significantly higher in ovarian lesions, eutopic endometrium and peritoneal macrophages of patients with Eo in comparison with the control group. Interestingly, the strongest YB-1 expression was observed in the epithelial compartment of endometrial tissues. In the Z12 cell line, YB-1 knockdown resulted in significant cell growth inhibitory effects including reduced cell proliferation and increased rates of spontaneous and TNFα-induced apoptosis. Significantly, higher RANTES expression and decreased cell invasion in vitro were also associated with YB-1 inactivation.
CONCLUSION: High YB-1 expression could have an impact on the development and progression of Eo. This study suggests the role of YB-1 as a potential therapeutic target for Eo patients.
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References (59)
- Behaviour of cytokine levels in serum and peritoneal fluid of women with endometriosis via openalex
- Chemokine bioactivity of RANTES in endometriotic and normal endometrial stromal cells and peritoneal fluid via openalex
- Endometriosis and the risk of cancer with special emphasis on ovarian cancer via openalex
- Epidemiology of endometriosis via openalex
- Gene expression profiles and functional characterization of human immortalized endometriotic epithelial and stromal cells via openalex
- Identification of an invasive, N-cadherin-expressing epithelial cell type in endometriosis using a new cell culture model via openalex
- Immunolocalization and regulation of the chemokine RANTES in human endometrial and endometriosis tissues and cells via openalex
- Immunolocalization and Regulation of the Chemokine RANTES in Human Endometrial and Endometriosis Tissues and Cells via openalex
- Induction of peritoneal endometriosis in nude mice with use of human immortalized endometriosis epithelial and stromal cells: a potential experimental tool to study molecular pathogenesis of endometriosis in humans via openalex
- Is endometriosis associated with systemic subclinical inflammation? via openalex
- Pathogenesis of endometriosis--current research via openalex
- Peritoneal cellular immunity and endometriosis via openalex
- Prevalence of endometriosis in malignant epithelial ovary tumours via openalex
- The peritoneal environment in endometriosis via openalex
- Tumor Necrosis Factor- Promotes Proliferation of Endometriotic Stromal Cells by Inducing Interleukin-8 Gene and Protein Expression via openalex
- W2030902700 via openalex
- W2036638105 via openalex
- W2041615411 via openalex
- W2042642675 via openalex
- W2043865646 via openalex
- W2063845207 via openalex
- W2066289540 via openalex
- W2071334751 via openalex
- W2080309793 via openalex
- W2083430665 via openalex
- W2087602949 via openalex
- W2088245792 via openalex
- W2092388342 via openalex
- W2104790898 via openalex
- W2118526748 via openalex
- W2122472408 via openalex
- W2127564111 via openalex
- W2130336313 via openalex
- W2134812217 via openalex
- W2134885709 via openalex
- W2142657147 via openalex
- W2149775431 via openalex
- W2156898973 via openalex
- W2159228424 via openalex
- W2161320035 via openalex
- W2167100625 via openalex
- W2168704602 via openalex
- W2404450017 via openalex
- W1753924780 via openalex
- W4294216491 via openalex
- W1881031803 via openalex
- W1915377938 via openalex
- W1965232244 via openalex
- W1965587103 via openalex
- W1971538947 via openalex
- W1995333503 via openalex
- W2002143651 via openalex
- W2003060940 via openalex
- W2007951687 via openalex
- W2011813310 via openalex
- W2012688912 via openalex
- W2016431132 via openalex
- W2027509505 via openalex
- W2029102082 via openalex
Cited by (4)
- Ping-Chong-Jiang-Ni Formula Induces Apoptosis and Inhibits Proliferation of Human Ectopic Endometrial Stromal Cells in Endometriosis via the Activation of JNK Signaling Pathway 2017
- Endometrial biomarkers for the non-invasive diagnosis of endometriosis 2016
- Evaluation of YB-1 levels in patients with endometriosis 2015
- Altered Biological Characteristics of Eutopic and Ectopic Endometrium 2014
Source provenance
- europepmc
- last seen: 2026-10-11T09:27:45.537177+00:00
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00
- pubmed
- last seen: 2026-10-08T21:09:44.076416+00:00
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