ReviewActa pharmacologica Sinica2025
PRL-3: unveiling a new horizon in cancer therapy.
Review in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Phosphatase of Regenerating Liver-3 Expression Correlates With PTENP1/miR-21 and miR-17/PTEN Dysregulation in Endometrial Adenocarcinoma Progression.World journal of oncology · 2026Article
- A Potential miR-1246-5p-H3K27ac-NOL12 Regulatory Axis and Its Putative Tumour-Promoting Function in Hepatocellular Carcinoma.IET systems biologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PRL-3, a protein tyrosine phosphatase (PTP), has a significant influence on the pathogenesis of various cancers with its overexpression significantly correlating with tumor invasion, metastasis and poor prognosis. It significantly affects tumor cell behavior through its involvement in cell proliferation, migration and metabolic processes. Furthermore, the interaction between PRL-3 and the tumor microenvironment characterized by its adaptability to stress and its role in metabolic reprogramming enhances tumor cell survival and dissemination. Targeted therapies against PRL-3, encompassing small molecule inhibitors and the monoclonal antibody PRL-3-zumab, have shown promise in clinical and preclinical studies, presenting new avenues for cancer treatment. In addition, innovative approaches such as CAAX motif-targeting agents and PRL-3 degradation strategies hold promise for developing more precise and effective interventions. This review explores PRL-3's multifaceted roles across different tumor types and microenvironments, while discussing current and emerging therapeutic strategies aimed at exploiting its oncogenic potential.
Indexed as
Identifiers
What OpenQuestion holds
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.