ReviewACS omega2026
The Role of PDE3A in Cancer.
Review in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Article
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
objectivePDE3A is a key member of the cyclic nucleotide phosphodiesterase family. By modulating intracellular cAMP and cGMP levels, it participates in diverse physiological processes such as platelet activation, cardiac function, oocyte maturation, and vascular smooth muscle cell proliferation. Recent studies have revealed that PDE3A also plays critical roles in multiple malignant tumors. This study aims to investigate the regulation of PDE3A expression, its role in cancer, and its potential as a therapeutic target, with a particular focus on its impact on tumor cell proliferation, metastasis, and resistance to chemotherapy.
methodsA systematic review of 221 PubMed-indexed articles published through April 2, 2025, was conducted to examine the expression and functional mechanisms of PDE3A in various cancer types. This study explored the regulation of PDE3A expression in cancer cells, its role in cell signal transduction, and its involvement in tumor initiation, progression, metastasis, and chemotherapy resistance. Additionally, it explored the inhibition of PDE3A and its potential as a therapeutic target for cancer treatment.
resultsPDE3A is aberrantly overexpressed in various cancers, particularly in gastrointestinal stromal tumors, hepatocellular carcinoma, and breast cancer. Its expression is regulated at multiple levels, including DNA mutations (e.g., Y497C), DNA methylation, transcription factors (SFPQ, MYBL2), epigenetic modifications (such as FSCN1-mediated alternative splicing, m6A modification by METTL3, microRNAs targeting PDE3A), and post-translational modification (14-3-3 protein). PDE3A contributes to cancer stem cell characteristics, metastasis, and chemotherapy resistance through both cAMP/PKA-dependent and cAMP/PKA-independent pathways, including the NF-κB, YAP/TEAD, and β-catenin/ID3 signaling axes. Notably, PDE3A can form a molecular gel-dependent complex with SLFN12 to induce apoptosis, a mechanism targeted by novel drugs such as OPB-171775 and BAY 2666605. Furthermore, combining PDE3A inhibitors (e.g., cilostazol) with existing chemotherapy agents (e.g., imatinib) significantly enhances antitumor efficacy, particularly in refractory tumors like gastrointestinal stromal tumors, demonstrating a strong synergistic effect.
conclusionPDE3A plays a pivotal role in tumorigenesis and cancer progression, with aberrant expression strongly associated with tumor proliferation, metastasis, and resistance to chemotherapy. As a therapeutic target, PDE3A holds significant potential. The development of PDE3A inhibitors or molecular adhesive agents may offer novel treatment strategies, particularly for chemotherapy-resistant tumor types.
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.