ArticleCell death & disease2023
Inhibition of CDKL3 downregulates STAT1 thus suppressing prostate cancer development.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Identification of STAT1 as a biomarker for lymph node metastasis in esophageal squamous cell carcinoma.Journal of molecular histology · 2026Article
- Integrative Bioinformatics and Machine Learning Analysis Identifies Novel Molecular Biomarkers in Prostate Adenocarcinoma.International journal of molecular sciences · 2026Article
- Macrophage PRMT9 Ameliorates Acute Myocardial Infarction by Promoting Symmetric Dimethylation and Degradation of STAT1.Circulation · 2026Article
- A feedback mechanism from prostate cancer cells to macrophages, reinforced by STAT1, regulates tumor progression and resistance to radiotherapy.Cell death & disease · 2026Article
- Article
- Fibroblast growth factor pathway promotes glycolysis by activating LDHA and suppressing LDHB in a STAT1-dependent manner in prostate cancer.Journal of translational medicine · 2024Article
- The role of CBL family ubiquitin ligases in cancer progression and therapeutic strategies.Frontiers in pharmacology · 2024Review
- CDKL3 shapes immunosuppressive tumor microenvironment and initiates autophagy in esophageal cancer.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer poses a great threat to men's health worldwide, yet its treatment is still limited by the unclear understanding of its molecular mechanisms. CDKL3 is a molecule with a recently discovered regulatory role in human tumors, and its relationship with prostate cancer is unknown. The outcomes of this work showed that CDKL3 was significantly upregulated in prostate cancer tissues compared with adjacent normal tissues, and was significantly positively correlated with tumor malignancy. Knockdown of CDKL3 levels in prostate cancer cells significantly inhibited cell growth and migration and enhanced apoptosis and G2 arrest of the cell cycle. Cells with lower CDKL3 expression also had relatively weaker in vivo tumorigenic capacity as well as growth capacity. Exploration of downstream mechanisms of CDKL3 may regulate STAT1, which has co-expression characteristics with CDKL3, by inhibiting CBL-mediated ubiquitination of STAT1. Functionally, STAT1 is aberrantly overexpressed in prostate cancer and has a tumor-promoting effect similar to that of CDKL3. More importantly, the phenotypic changes of prostate cancer cells induced by CDKL3 were dependent on ERK pathway and STAT1. In summary, this work identifies CDKL3 as a new prostate cancer-promoting factor, which also has the potential to be a therapeutic target for prostate cancer.
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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 OpenQuestion graph.