ArticleJournal of cancer research and clinical oncology2023
CACYBP knockdown inhibits progression of prostate cancer via p53.
Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Silencing CACYBP suppresses lung adenocarcinoma growth via CDK1 inhibition.Biomolecules & biomedicine · 2025Article
- Integrative bioinformatics and experimental analyses identify U2SURP as a novel lactylation-related prognostic signature in esophageal carcinoma.Immunologic research · 2025Article
- From actinic keratosis to cutaneous squamous cell carcinoma: the key pathogenesis and treatments.Frontiers in immunology · 2025Review
- Pan-analysis reveals CACYBP to be a novel prognostic and predictive marker for multiple cancers.American journal of translational research · 2024Article
- Blockage of CacyBP inhibits macrophage recruitment and improves anti-PD-1 therapy in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeProstate cancer (PC) is one of the most common malignant tumors of genitourinary system in men. CACYCLIN binding protein (CACYBP) is involved in the progression of a variety of cancers. The aim of this study was to explore the expression and functional role of CACYBP in PC.
methodsThe expression of CACYBP in PC was evaluated by immunohistochemical (IHC) staining and qRT-PCR. Subsequently, we established lentivirus-mediated CACYBP knockdown in PC cell lines. The biological roles of CACYBP on proliferation, apoptosis, cycle distribution, migration and tumor formation of PC were investigated by Celigo cell counting assay, flow cytometry, transwell assay, wound-healing assay and mice xenograft models, respectively.
resultsCACYBP was highly expressed in PC and was positively correlated with the pathological grade of PC patients. Knockdown of CACYBP inhibited proliferation, enhanced apoptosis, arrested cell cycle in G2 and suppressed migration of PC cell lines in vitro. In addition, CACYBP knockdown weakened the tumor growth of PC in vivo. Moreover, addition of p53 inhibitor could effectively alleviate the inhibitory effect of CACYBP knockdown on cell activity.
conclusionThis study revealed that knockdown of CACYBP inhibited the proliferation, migration and tumorigenicity of PC, which may serve as a potential therapeutic target for the treatment of PC.
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