ArticleScientific reports2025
Taletrectinib promotes pyroptosis in colorectal carcinoma via SRC/AKT/mTOR axis inhibition.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Gasdermin-Mediated Pyroptosis: Novel Strategies Against Colorectal Cancer.Cancer science · 2026Review
- Pyroptosis as a double-edged sword in colorectal cancer: Molecular mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- An evaluation of taletrectinib for the treatment of ROS1+ non-small cell lung cancer.Expert review of anticancer therapy · 2026Review
- Autophagy regulation of pyroptosis and ferroptosis: a new strategy for colorectal cancer treatment.Apoptosis : an international journal on programmed cell death · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Drug resistance develops frequently after colorectal carcinoma (CRC) surgery, indicating the urgent need for new therapeutic strategies. Taletrectinib (DS-6051b/AB-106), a synthetic ROS1/NTRK inhibitor which has shown meaningful antitumor activity, is currently undergoing clinical trials aimed at addressing targeted resistance. However, the anti-cancer effect of taletrectinib on CRC remains unclear. In this study, our purpose was to evaluate taletrectinib-related cytotoxicity in vitro using two CRC cell lines, as well as in vivo in a mouse tumor model. The mechanism underlying the cytotoxicity of taletrectinib was evaluated using light microscopy, scanning electron microscopy, immunofluorescence assays, an annexin V-FITC/propidium iodide detection, lactate dehydrogenase (LDH) release assays, and western blotting. We found that the viability of CRC cells decreased with increasing concentrations of taletrectinib. In addition, transcriptome sequencing indicated that HCT116 and LOVO cell lines did not carry ROS1- or NTRK-related gene fusions and that the cytotoxic effect of taletrectinib was exerted via caspase-3/gasdermin E (GSDME)-dependent pyroptosis. Moreover, the effect of taletrectinib in promoting pyroptosis was reversed by treatment with the SRC agonist, tolimidone, both in vitro and in vivo. Overall, our findings suggest that taletrectinib suppresses tumor growth by inducing GSDME-mediated pyroptosis via the SRC/AKT/mTOR signaling pathway, indicating that taletrectinib shows potential as a promising therapeutic agent against CRC.
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