Serial analysis of gene expression reveals differential expression between endometriosis and normal endometrium. Possible roles for AXL and SHC1 in the pathogenesis of endometriosis

Honda, Hiroshi; Barrueto, Fermin; Gogusev, Jean; Im, Dwight D.; Morin, Patrice J.

doi:10.1186/1477-7827-6-59

Cited by 69 publications

(57 citation statements)

References 47 publications

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“…It has been reported that NUCB2 protein and its binding sites are expressed in mouse uterus, and play pivotal roles in the collapse and recovery of endometrium [26]. Honda et al also found out that NUCB2 expression was differentially detected in endometriosis by Serial Analysis of Gene Expression (SAGE) methods [27]. These findings all suggest the importance of NUCB2 in endometrial disorders as well as normal endometrium.…”

Section: Discussionmentioning

confidence: 58%

Nucleobindin 2 (NUCB2) in human endometrial carcinoma: a potent prognostic factor associated with cell proliferation and migration

et al. 2016

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Section: Discussionmentioning

confidence: 58%

Nucleobindin 2 (NUCB2) in human endometrial carcinoma: a potent prognostic factor associated with cell proliferation and migration

et al. 2016

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“…Studies on the differences in gene expression between the ectopic and eutopic endometrium (17)(18)(19)(20)(21)(22) have found that many genes related to cell adhesion, cell migration, cell proliferation, immune regulation and inflammation are differentially expressed in ectopic vs. eutopic endometrial tissue. In the study by Ohlsson Teague et al (12), it was suggested that c-Jun mRNA expression was significantly increased in endometriosis.…”

Section: Discussionmentioning

confidence: 99%

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Long

Wan

et al. 2015

International Journal of Molecular Medicine

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Abstract. Endometriosis is a prevalent and complex gynecological disease which affects 10% of women of reproductive age. Certain studies have suggested that a substantial number of microRNAs (miRNAs or miRs) are aberrantly or differentially expressed in the ectopic endometrium. To date, to the best of our knowlewdge, there is no report available on the role of miR-29 in the endometrium. In this study, we investigated the expression of the miR-29 family in the endometrium samples from women without endometriosis, as well as in paired ectopic and eutopic endometrium samples by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results revealed that miR-29c was differentially expressed in the paired eutopic and ectopic endometrium samples. In addition, c-Jun was differentially expressed in the ectopic and eutopic endometrial tissues as determined by western blot analysis. Furthermore, the role of miR-29c in endometrial cell proliferation, invasion and apoptosis was examined in vitro. The results revealed that miR-29c exerted its effects on endometrial cells by suppressing cell proliferation and invasion, as well as promoting cell apoptosis. Furthermore, it was found that c-Jun was a novel target of miR-29c, and c-Jun reversed the effects of miR-29c on the proliferation, invasion and apoptosis of endometrial cells. To the best of our knowledge, this study is the first to identify miR-29c as a suppressor of endometriosis. Taken together, our results suggest that miR-29c exerts its effects on endometrial cell proliferation, apoptosis and invasion by inhibiting the expression of c-Jun. Our data may provide a novel potential therapeutic target for the treatment of endometriosis.

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“…It has been shown before that the PI3K/Akt signaling pathway is abnormally activated during endometriosis and that this activation was partly responsible for the endometriotic cells' reduced decidual response (Matsuzaki et al 2005, Cinar et al 2009); serial analysis of gene expression revealed an increased level of both PI3K and phosphorylated AKT (S473) in endometriotic tissues, probably through the enhanced expression of GAS6, AXL, and ACTN4, responsible for enhanced proliferation and motility (Honda et al 2008). On the other hand, AKT was not involved in endometriotic cells' expression of EMT markers in response to TNFa, a crucial component of inflammation in this disease (Berkkanoglu & Arici 2003, Grund et al 2008.…”

Section: Endometriosismentioning

confidence: 99%

“…Increased and decreased expression of phosphorylated AKT (S473) is usually concomitant with similar changes in the activity of mTORc1, leading us to think that one of the primary effect of AKT in endometriosis is the activation of the mTOR pathway (Lucidi et al 2005, Honda et al 2008, Zhang et al 2009). The NFkB pathway also seems to be entwined in the hormonal response as well as survival mechanisms in which AKT is involved (Grund et al 2008, Zhang et al 2010, Capp et al 2011.…”

Section: Endometriosismentioning

confidence: 99%

Expression, activation, and role of AKT isoforms in the uterus

Fabi¹,

Asselin²

2014

Reproduction

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The three isoforms of AKT: AKT1, AKT2, and AKT3, are crucial regulators of both normal and pathological cellular processes. Each of these isoforms exhibits a high level of homology and functional redundancy with each other. However, while being highly similar and structurally homologous, a rising amount of evidence is showing that each isoform possesses specific targets as well as preferential subcellular localization. The role of AKT has been studied extensively in reproductive processes, but isoform-specific roles are yet to be fully understood. This review will focus on the role of AKT in the uterus and its function in processes related to cell death and proliferation such as embryo implantation, decidualization, endometriosis, and endometrial cancer in an isoform-centric manner. In this review, we will cover the activation of AKT in various settings, localization of isoforms in subcellular compartments, and the effect of isoform expression on cellular processes. To fully understand the dynamic molecular processes taking place in the uterus, it is crucial that we better understand the physiological role of AKT isoforms as well as their function in the emergence of diseases.Reproduction (2014) 148 R85-R95

show abstract

Serial analysis of gene expression reveals differential expression between endometriosis and normal endometrium. Possible roles for AXL and SHC1 in the pathogenesis of endometriosis

Cited by 69 publications

References 47 publications

Nucleobindin 2 (NUCB2) in human endometrial carcinoma: a potent prognostic factor associated with cell proliferation and migration

Nucleobindin 2 (NUCB2) in human endometrial carcinoma: a potent prognostic factor associated with cell proliferation and migration

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Expression, activation, and role of AKT isoforms in the uterus

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