ArticleCancer science2026
Trichostatin A Sensitizes Tumor Cells to Apoptosis Induced by Soluble Trimeric TRAIL-Expressing Human Mesenchymal Stromal Cells.
Article in Cancer science, 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
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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
1 citing paper in PubMed.
- Helping Apo2L/TRAIL in the Battle: Synergistic Therapeutic Approaches for Cancer Therapies.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Mesenchymal stromal cells (MSCs) are promising vehicles for delivering therapeutic agents to tumors, as a result of their tumor-homing ability. This study aimed to develop MSCs expressing a trimeric soluble form of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which was enhanced by incorporating an isoleucine zipper (SCZT), to improve apoptosis-inducing efficacy. Because some cancer cells are resistant to TRAIL, we also investigated the effects of combining SCZT-expressing MSCs with trichostatin A (TSA), a histone deacetylase inhibitor that enhances the expression of TRAIL death receptors (DR4/DR5) in tumor cells. TSA increased TRAIL sensitivity in resistant tumor cells in vitro by upregulating DR5, leading to enhanced caspase-8 activation and tumor cell death. MSCs accumulated at tumor sites in vivo, and the combination of SCZT-MSCs and TSA significantly suppressed tumor growth in both TRAIL-sensitive and TRAIL-resistant mouse models. Notably, this combination led to complete tumor regression in some TRAIL-resistant tumors. These in vivo findings indicate that efficient tumor targeting by MSCs is crucial for achieving therapeutic efficacy, especially in TRAIL-resistant tumors. Overall, our results demonstrate that co-treatment with TSA enhances the antitumor effect of TRAIL-expressing MSCs, offering a potential strategy to overcome TRAIL resistance and improve MSC-based cancer therapies.
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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.