ArticleOncoTargets and therapy2019
MLL3 promotes the senescence of esophageal squamous cell carcinoma.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- The modification role and tumor association with a methyltransferase: KMT2C.Frontiers in immunology · 2024Review
- miR-181a, delivered by hypoxic PTC-secreted exosomes, inhibits DACT2 by downregulating MLL3, leading to YAP-VEGF-mediated angiogenesis.Molecular therapy. Nucleic acids · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSenescence has been recognized as a mechanism for the suppression of tumorigenesis. However, how the senescence is regulated is not fully understood.
aimsThe present study aims to elucidate MLL3-mediated regulation of senescence. MATERIALS AND
methodsMLL3 protein levels in esophageal squamous cell carcinoma (ESCC) tissues were examined by Western blotting and immunohistochemistry. The effects of MLL3 on the growth and senescence of ESCC cells were examined using MTT assay, soft agar assay, and β-gal staining. The interaction between MLL3 and P16 was evaluated by immunoprecipitation and GST pull-down assay.
resultsIn this study, we found that MLL3 promoted the senescence of ESCC cells. MLL3 was downregulated in ESCC. MLL3 inhibited the growth and colony formation of ESCC cells. Mechanistically, MLL3 interacted with P16 and impaired the interaction between P16 and UHRF1 (the E3 ligase for P16), thus upregulating the protein levels of several senescence regulators.
conclusionCollectively, this study demonstrated the regulation of senescence by MLL3.
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