ArticleCell cycle (Georgetown, Tex.)2020
MicroRNA-572/hMOF/Sirt6 regulates the progression of ovarian cancer.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Functions and mechanisms of non-histone post-translational modifications in cancer progression.Cell death discovery · 2025Review
- SIRT6 promotes ferroptosis and attenuates glycolysis in pancreatic cancer through regulation of the NF-κB pathway.Experimental and therapeutic medicine · 2022Article
- SIRT6 Promotes the Progression of Prostate Cancer via Regulating the Wnt/Journal of oncology · 2022Article
- The Histone Acetyltransferase MOF Regulates SIRT1 Expression to Suppress Renal Cell Carcinoma Progression.Frontiers in oncology · 2022Article
Corrections and comments
- Retraction · 2022-06-21Concerns/Issues about Data · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human males absent on the first (hMOF) is a histone acetyltransferase (HAT) and is involved in the pathogenesis of various cancers. This article aimed to reveal the potential mechanism of the miR-572/hMOF/Sirt6 axis in ovarian cancer (OC). In this study, we found that the mRNA and protein levels of hMOF and Sirt6 were abnormally down-regulated in OC tissues and cells. Further study indicated that the overexpression of hMOF increased the level of H4 histone acetylation in the Sirt6 promoter region and enhanced the ability of hMOF to bind to the Sirt6 promoter in OC cells, and repressed the proliferation of SKOV3 cells and promoted the apoptosis of SKOV3 cells via up-regulating Sirt6. Moreover, it was found that miR-572 negatively regulated hMOF luciferase activity. After the transfection of miR-572 inhibitor into SKOV3 cells, the cell proliferation was significantly repressed, while this repression was reversed after the transfection of shRNA-hMOF. Besides, the overexpression of hMOF could significantly inhibit the growth of tumors. Overall, our findings uncovered a novel regulatory pattern of hMOF in OC progression and provided new insights for relieving OC.
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Registered trials
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