ArticleJournal of cell communication and signaling2022
Lysine demethylase 5A promotes prostate adenocarcinoma progression by suppressing microRNA-330-3p expression and activating the COPB2/PI3K/AKT axis in an ETS1-dependent manner.
Article in Journal of cell communication and signaling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The RBP2-BECN1-VEGFA axis orchestrates a self-amplifying circuit to drive malignant progression in gastric carcinoma.Frontiers in oncology · 2026Article
- Review
- Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023Review
- Modulation of AKT Pathway-Targeting miRNAs for Cancer Cell Treatment with Natural Products.International journal of molecular sciences · 2023Review
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Lysine demethylase 5A (KDM5A) is a histone demethylase frequently involved in cancer progression. This research aimed to explore the function of KDM5A in prostate adenocarcinoma (PRAD) and the molecular mechanism. KDM5A was highly expressed in collected PRAD tissues and acquired PRAD cells. High KDM5A expression was correlated with reduced survival and poor prognosis of patients with PRAD. Knockdown of KDM5A suppressed the proliferation, colony formation, migration, and invasiveness of PRAD cells and reduced angiogenesis ability of endothelial cells. Downstream molecules implicated in KDM5A mediation were predicted using integrated bioinformatic analyses. KDM5A enhanced ETS proto-oncogene 1 (ETS1) expression through demethylation of H3K4me2 at its promoter. ETS1 suppressed the transcription activity of miR-330-3p, and either further ETS1 overexpression or miR-330-3p inhibition blocked the functions of KDM5A knockdown in PRAD. miR-330-3p targeted coatomer protein complex subunit β2 (COPB2) mRNA. Downregulation of miR-330-3p restored the expression of COPB2 and activated the PI3K/AKT pathway in PRAD. The results in vitro were reproduced in vivo where KDM5A downregulation suppressed the growth and metastasis of xenograft tumors in nude mice. In conclusion, this study demonstrated that KDM5A promoted PRAD by suppressing miR-330-3p and activating the COPB2/PI3K/AKT axis in an ETS1-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.