Survivin Gene Expression in Endometriosis
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This study found survivin and MMP gene expression is higher in aggressive endometriosis lesions than normal endometrium and correlates with reduced apoptosis and increased invasion.
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Abstract
Survivin is a novel inhibitor of apoptosis and is expressed during fetal development and in cancer tissues, but its expression has not been reported in normal adult tissues or benign diseases. We investigated survivin gene and protein expression in a tumor-like benign disease, endometriosis, and correlated them with apoptosis and invasive phenotype of endometriotic tissues. Gene expression levels of survivin, matrix metalloproteinase (MMP)-2, MMP-9, and membrane type 1 (MT1)-MMP in 63 pigmented or nonpigmented endometriotic tissues surgically obtained from 35 women with endometriosis were compared with those in normal eutopic endometrium obtained from 12 women without endometriosis. Survivin, MMP-2, MMP-9, and MT1-MMP mRNA expression levels in clinically aggressive pigmented lesions were significantly higher than those in normal eutopic endometrium, and survivin gene expression in pigmented lesions was also higher than that in nonpigmented lesions (P < 0.05). There was a close correlation between survivin and MMP-2, MMP-9, or MT1-MMP gene expression levels in 63 endometriotic tissues examined (P < 0.01). Apoptotic cells detected by the dUTP nick-end labeling were rare in 11 ovarian endometriotic tissues, which showed positive immunohistochemical expression for survivin and MMPs. Our findings suggest that up-regulation of survivin and MMPs may cooperatively contribute to survival and invasion of endometriosis.
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Cited by (21)
- Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis 2018
- CD33<sup>+</sup>CD14<sup>+</sup>CD11b<sup>+</sup>HLA‐DR<sup>−</sup> monocytic myeloid‐derived suppressor cells recruited and activated by CCR9/CCL25 are crucial for the pathogenic progression of endometriosis 2018
- Matrix metalloproteinase-2 (MMP-2), MMP-9, tissue inhibitor of matrix metalloproteinases (TIMP-1) and transforming growth factor-β2 (TGF-β2) expression in eutopic endometrium of women with peritoneal endometriosis 2016
- Macrophages promote the growth and invasion of endometrial stromal cells by downregulating IL-24 in endometriosis 2016
- Effects of Danchi decoction on P450AROM, survivin of eutopic endometrium of patients with endometriosis after conservative surgery 2015
- EFFECTS OF DANCHI DECOCTION ON P450AROM, SURVIVIN OF EUTOPIC ENDOMETRIUM OF PATIENTSWITH ENDOMETRIOSIS AFTER CONSERVATIVE SURGERY 2015
- The molecular connections between the cannabinoid system and endometriosis 2012
- CXCL8 enhances proliferation and growth and reduces apoptosis in endometrial stromal cells in an autocrine manner via a CXCR1-triggered PTEN/AKT signal pathway 2012
- Survivin, MMP-2, MT1-MMP, and TIMP-2: their impact on survival, implantation, and proliferation of endometriotic tissues 2012
- Biology of Eutopic and Ectopic Endometrium in Women with Endometriosis 2011
- Apoptosis and endometriosis 2010
- Faculty Opinions recommendation of A conditionally replicative adenovirus, CRAd-S-pK7, can target endometriosis with a cell-killing effect. 2010
- A conditionally replicative adenovirus, CRAd-S-pK7, can target endometriosis with a cell-killing effect 2010
- Endometriotic stromal cells lose the ability to regulate cell-survival signaling in endometrial epithelial cells in vitro 2009
- The role of survivin in the resistance of endometriotic stromal cells to drug-induced apoptosis 2009
- Vascular endothelial growth factor A and C gene expression in endometriosis 2004
- Endometriosis and the neoplastic process 2004
- Immunology of endometriosis 2004
- Ubiquitin is associated with the survival of ectopic stromal cells in endometriosis. 2004
- Pathogenesis of endometriosis 2004
- Biological Implications of Survivin Gene Expression in the Development of Endometriosis and Endometrial Carcinoma 2003
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- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
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- last seen: 2026-06-04T02:00:05.705006+00:00
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