Endometrial expression of the estrogen-sensitive genes MMP-26 and TIMP-4 is altered by a substitution protocol without down-regulation in IVF patients

Pilka, R; Oborná, I; Lichnovský, V; Havelka, P; Fingerová, H; Eriksson, Per; Hansson, Stefan R.; Casslén, Bertil

doi:10.1093/humrep/del180

Cited by 14 publications

(8 citation statements)

References 70 publications

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“…Interestingly, it lacks AP1 or AP2 sites, which are involved in the inducible and basal expression of TIMP-1, -2 and -3 genes [ 45 ]. Additionally, the TIMP-4 promoter contains an estrogen response element (ERE), in accordance with the observed regulation by estrogen during endometrial normal cycle and preimplantation period [ 46 , 47 ]. Similar to TIMP-3, TIMP-4 expression is regulated by promoter methylation in cancer cell lines and tumor samples [ 48 ].…”

Section: Introductionsupporting

confidence: 55%

Tissue Inhibitor of Metalloproteinases-4. The road less traveled

et al. 2008

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Tissue inhibitors of metalloproteinases (TIMPs) regulate diverse processes, including extracellular matrix (ECM) remodeling, and growth factors and their receptors' activities through the inhibition of matrix metalloproteinases (MMPs). Recent evidence has shown that this family of four members (TIMP-1 to TIMP-4) can also control other important processes, such as proliferation and apoptosis, by a mechanism independent of their MMP inhibitory actions. Of these inhibitors, the most recently identified and least studied is TIMP-4. Initially cloned in human and, later, in mouse, TIMP-4 expression is restricted to heart, kidney, pancreas, colon, testes, brain and adipose tissue. This restricted expression suggests specific and different physiological functions. The present review summarizes the information available for this protein and also provides a putative structural model in order to propose potential relevant directions toward solving its function and role in diseases such as cancer.

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Section: Introductionsupporting

confidence: 55%

Tissue Inhibitor of Metalloproteinases-4. The road less traveled

et al. 2008

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“…In agreement with the presence of the estrogen response element in the MMP-26 gene promoter, E2, via its interactions with the ERs, regulated the MMP-26 gene expression in Ishikawa cells. These results explain the association of the MMP-26 expression with hormone-regulated malignancies and MMP-26 cycling in the course of a menstrual period (6,9,19,20,37,38).…”

Section: Mmp-26 Cleaves Estrogen Receptor Bmentioning

confidence: 58%

Matrix Metalloproteinase 26 Proteolysis of the NH2-Terminal Domain of the Estrogen Receptor β Correlates with the Survival of Breast Cancer Patients

et al. 2006

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Estrogens have many cellular functions, including their interactions with estrogen receptors A and B (ERA and ERB). Earlier, we determined that the estrogen-ER complex stimulates the transcriptional activity of the matrix metalloproteinase 26 (MMP-26) gene promoter. We then determined that ERB is susceptible to MMP-26 proteolysis whereas ERA is resistant to the protease. MMP-26 targets the NH 2 -terminal region of ERB coding for the divergent NH 2 -terminal A/B domain that is responsible for the ligand-independent transactivation function. As a result, MMP-26 proteolysis generates the COOH-terminal fragments of ERB. Immunohistochemical analysis of tissue microarrays derived from 121 cancer patients corroborated these data and revealed an inverse correlation between the ERA-dependent expression of MMP-26 and the levels of the intact ERB in breast carcinomas. MMP-26 is not expressed in normal mammary epithelium. The levels of MMP-26 are strongly up-regulated in ductal carcinoma in situ (DCIS). In the course of further disease progression through stages I to III, the expression of MMP-26 decreases. In contrast to many tumor-promoting MMPs, the expression of MMP-26 in DCIS correlated with a longer patient survival. Our data suggest the existence of an MMP-26-mediated intracellular pathway that targets ERB and that MMP-26, a novel and valuable cancer marker, contributes favorably to the survival of the ERA/B-positive cohort of breast cancer patients. (Cancer Res 2006; 66(5): 2716-24)

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“…MMP26 is different from most MMP family members because it lacks a conserved C-terminal protein domain. MMP26 is an estrogen-sensitive gene and is co-expressed with estrogen receptor alpha in normal and pathological endometrium; an elevated progesterone level can exaggerate a decrease in MMP26 expression 39 40 . The expression of MMP26 in the endometrium in natural cycles is highest in the early secretory phase and decreased in the late secretory phase 41 .…”

Section: Discussionmentioning

confidence: 99%

MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day

Chen

Zhao

et al. 2016

Sci Rep

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On the women undergoing IVF-ET with elevated progesterone on human chorionic gonadotrophin priming, the assisted reproductive technology outcome is poor. But, due to the unknown mechanism of this process, no effective method has been found to overcome this difficulty. Here, we investigated the roles of miR-125b and its target gene, MMP26, in endometrial receptivity (ER) in these women. The expression of miR-125b was significantly up-regulated in EECs in women with elevated progesterone during the window of implantation, and it showed a progesterone-dependent effect in vitro. Similarly, the expression of miR-125b was significantly up-regulated in the preimplantation period, and was down-regulated in the implantation period and the post-implantation period in mouse EECs. In addition, miR-125b showed a greater decrease at implantation sites than it did at interimplantation sites. The luciferase report assay demonstrated that MMP26 is a target gene of miR-125b. And the expression profile of MMP26 showed an inverse relationship with miR-125b in vivo and in vitro. Overexpression of miR-125b in human EECs inhibited cell migration and invasion. Gain-of-function of miR-125b induced a significant decrease in the number of implantation sites. In conclusion, these data shed new light on how miR-125b triggers ER decline through the regulation of MMP26 function.

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Endometrial expression of the estrogen-sensitive genes MMP-26 and TIMP-4 is altered by a substitution protocol without down-regulation in IVF patients

Cited by 14 publications

References 70 publications

Tissue Inhibitor of Metalloproteinases-4. The road less traveled

Tissue Inhibitor of Metalloproteinases-4. The road less traveled

Matrix Metalloproteinase 26 Proteolysis of the NH2-Terminal Domain of the Estrogen Receptor β Correlates with the Survival of Breast Cancer Patients

MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day

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