The Wnt/β-catenin signaling in endometriosis, the expression of total and active forms of β-catenin, total and inactive forms of glycogen synthase kinase-3β, WNT7a and DICKKOPF-1

Pazhohan, Azar; Amidi, Fardin; Akbari-Asbagh, Firoozeh; Seyedrezazadeh, Ensiyeh; Farzadi, Laya; Khodarahmin, Mahshad; Mehdinejadiani, Shayesteh; Sobhani, Aligholi

doi:10.1016/j.ejogrb.2017.10.025

Cited by 31 publications

(26 citation statements)

References 40 publications

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“…A previous study demonstrated that such a pathway serves a vital role in the genesis, metastasis and invasion of multiple tumors (6). In addition, it may be involved in the adhesion, invasion and angiogenesis of the ectopic endometrium (7). Wnt/β-catenin signaling pathway serves a decisive role in endometrial gland formation and mesenchymal development (7).…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of miR‑33b promotes endometriosis via inhibition of Wnt/β‑catenin signaling and ZEB1 expression

Zhang

Sheng

et al. 2019

Mol Med Report

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The present study aimed to investigate the role and mechanisms of microRNA (miR)-33b in endometriosis (Ems). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), MTT assays, flow cytometry, caspase-3/9 activity assays and western blotting were performed in the present study. Initially, miR-33b expression in an Ems rat model was investigated by RT-qPCR and was demonstrated to be upregulated in Ems tissue samples of rats compared with the control group. In addition, miR-33b upregulation inhibited cell growth and enhanced apoptosis in an Ems model (primary cell cultures) compared with the control group. In addition, miR-33b up-regulation reduced Wnt/β-catenin signaling pathway and suppressed zinc finger E-box-binding homeobox 1 (ZEB1) protein expression in the in vitro Ems model (primary cell cultures) compared with the control group. Furthermore, small interfering-ZEB1 ameliorated the effects of miR-33b downregulation on Ems cell growth in the in vitro Ems model. Additionally, a Wnt agonist reduced the effects of miR-33b upregulation on Ems cell growth in the in vitro Ems model. In conclusion, the present study demonstrated that upregulation of miR-33b may promote Ems through Wnt/β-catenin by ZEB1 expression.

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Section: Introductionmentioning

confidence: 99%

“…In addition, it may be involved in the adhesion, invasion and angiogenesis of the ectopic endometrium (7). Wnt/β-catenin signaling pathway serves a decisive role in endometrial gland formation and mesenchymal development (7).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miR‑33b promotes endometriosis via inhibition of Wnt/β‑catenin signaling and ZEB1 expression

Zhang

Sheng

et al. 2019

Mol Med Report

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“…The loss of ARID1A in 10/25 (40%) uterine endometrioid carcinoma cases along with 15/58 (26%) loss of ARID1A immunoexpression led Guan et al [135] to suggest that the molecular basis of pathogenesis of low-grade uterine endometrioid carcinoma is comparable to that of lowgrade OCs. Additionally, aberrant activation of CTNNB1 due to its mutation affect the expressions/activities of c-MYC, PTEN/PI3K, and this appears to be a crucial step in the progression of several cancers including OCs and ECs and this functional network has been implicated in endometriosis as well [145][146][147][148][149][150][151][152].…”

Section: Oncogenes and Tumor Suppressor Genesmentioning

confidence: 99%

How Benign is Endometriosis: Multi-Scale Interrogation of Documented Evidence

Ghosh

Anupa

et al. 2019

COGO

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Endometriosis is an inflammatory disease characterized by the presence of endometrium-like tissue outside the uterus primarily on pelvic organs and tissues. It affects up to 15% of women in the reproductive age group and is often associated with pelvic pain and subfertility. Different theories explain how retrograde menstruation gives rise to endometrial deposits at ectopic sites, and how several other factors are involved in the progression of the disease. Its final diagnosis is established through direct visualization at laparoscopy or surgery followed by histological confirmation. Available epidemiological reports along with histopathological observations and molecular studies shed interesting light on the pathogenetic basis of different variants of the disease like deep infiltrating endometriosis and ovarian endometriosis. Evidence also suggests that endometriosis is a neoplastic condition which serves as a precursor of ovarian and endometrial cancers. In the present review, we have attempted to take a stock of the current epidemiological and molecular knowledge regarding endometriosis associated cancers and develop a model of functional network with interactions among critical genomic factors regulating cellular processes leading to fibrotic reaction. It is being conjectured that cyclic bleeding associated with inflammatory and oxidative stress followed by repeated tissue injury and repair along with recurrent estrogenic stimulation and ovulatory events in the pelvic environment bring about the complex phenotype of atypical endometriosis and associated neoplasm with a trade-off malignant transformation in high risk population. Finally, we have presented an algorithm for pre-emptive monitoring and management of endometriosis-associated cancers.

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“…A previous research using immunohistochemical methods to compare the different expressions of tissues of endometriosis and EAOC indicated that the expression of PR and ER in EAOC was statistical significantly lower than that in endometriosis [ 50 ]. In addition, estrogen and progesterone regulated normal endometrial cells in proliferation and differentiation via mediating Wnt/ β -catenin signaling whose main components include WNT7a, DKK-1, β -catenin, and GSK-3 β [ 51 ]. However, abnormal activation the WNT/ β -catenin signaling pathway via multiple regulators is reputed to be associated with ovarian cancer with epigenetic modification [ 52 – 56 ].…”

Section: Dna Methylationmentioning

confidence: 99%

Endometriosis Malignant Transformation: Epigenetics as a Probable Mechanism in Ovarian Tumorigenesis

Chang

Feng

et al. 2018

International Journal of Genomics

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Endometriosis, defined as the presence of ectopic endometrial glands and stroma outside the uterine cavity, is a chronic, hormone-dependent gynecologic disease affecting millions of women across the world, with symptoms including chronic pelvic pain, dysmenorrhea, dyspareunia, dysuria, and subfertility. In addition, there is well-established evidence that, although endometriosis is considered benign, it is associated with an increased risk of malignant transformation, with the involvement of various mechanisms of development. More and more evidence reveals an important contribution of epigenetic modification not only in endometriosis but also in mechanisms of endometriosis malignant transformation, including DNA methylation and demethylation, histone modifications, and miRNA aberrant expressions. In this present review, we mainly summarize the research progress about the current knowledge regarding the epigenetic modifications of the relations between endometriosis malignant transformation and ovarian cancer in an effort to identify some risk factors probably associated with ectopic endometrium transformation.

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The Wnt/β-catenin signaling in endometriosis, the expression of total and active forms of β-catenin, total and inactive forms of glycogen synthase kinase-3β, WNT7a and DICKKOPF-1

Cited by 31 publications

References 40 publications

Upregulation of miR‑33b promotes endometriosis via inhibition of Wnt/β‑catenin signaling and ZEB1 expression

Upregulation of miR‑33b promotes endometriosis via inhibition of Wnt/β‑catenin signaling and ZEB1 expression

How Benign is Endometriosis: Multi-Scale Interrogation of Documented Evidence

Endometriosis Malignant Transformation: Epigenetics as a Probable Mechanism in Ovarian Tumorigenesis

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