ArticleReproductive sciences (Thousand Oaks, Calif.)2020
Aberrant Overexpression of RNA-Editing Enzyme ADAR1 Promotes the Progression of Endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Adenosine Deaminase Family Acting on RNA 1 (In vivo (Athens, Greece)Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Considerable efforts have been invested to elucidate the potential mechanisms involved in the physiopathology of endometriosis. However, to date, prior research has not been conclusive. This research has examined one particular mechanism, i.e., the effect of ADAR1 on endometriosis lesions. Eutopic endometrium was collected from women with (n = 25) and without endometriosis (n = 25), respectively. The expression of ADAR1 mRNA was measured based on quantitative real-time polymerase chain reactions (RT-qPCR). Both Western blot and immunohistochemistry were performed to establish ADAR1 protein expression levels. The results indicated that ADAR1 mRNA and proteins were significantly greater in the eutopic endometrium of the women with endometriosis, compared to the women without (P < 0.05). The Cell Counting Kit-8 (CCK-8) and EdU method were conducted to examine the effect of ADAR1 on cell viability and proliferation in eutopic endometriosis cells. A transwell assay was also used to detect the role of ADAR1 in the invasion of endometrial cells. The results obtained showed that ADAR1 promoted endometrial cell viability, proliferation, and invasion (P < 0.05). This informed our conclusion that the ADAR1 gene is upregulated in endometriosis, potentially paying a pivotal role in the physiopathology of endometriosis.
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