ArticleJournal of translational medicine2026
In vitro evidence and integrative bioinformatics identify the SGLT2-PPARγ axis as a target against polyethylene microplastic-driven metabolic reprogramming in colorectal cancer cells.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07580326 (Plastic Accumulation in Residual Brain Tissues From Hemorrhagic Events), which is not on this 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.
Plastic Accumulation in Residual Brain Tissues From Hemorrhagic Events: Neurological Outcomes and Pathogenetic Evidence (PARTENOPE Study)
Who cites it
1 citing paper in PubMed.
- Microplastics in food production systems: Sources, exposure pathways, and gastrointestinal health effects.Current research in food science · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundMicroplastics have emerged as a growing burden to human health, with increasing evidence linking chronic exposure to adverse outcomes including inflammation, metabolic disruption, and carcinogenesis. Microplastics can be internalized by colorectal cancer (CRC) cells and influence cancer-related processes including metastasis, chemoresistance, oxidative stress, and cellular metabolism. However, the molecular mechanism underlying microplastic effects on CRC progression and metabolism remain poorly understood.
methodsHT-29 and HCT 116 CRC cells were exposed to polyethylene (PE) microplastics (10 µg/mL) up to 72 h. Cell viability was assessed using the CCK-8 assay, and metabolic and tumorigenic features were evaluated through enzyme-linked immunosorbent (ELISA) assays and XF HS Seahorse Bioanalyzer. The modulatory effects of SGLT2 inhibitor canagliflozin (iSGLT2), γ-butyrobetaine (γBB) and L-carnitine (Cnt) on PE-induced alterations was investigated with immunoblotting, flow cytometric and bioinformatic analyses.
resultsPE exposure enhanced proliferation (p < 0.001), inflammation, angiogenesis and invasive potential. PE also increased cellular bioenergetics, marked by heightened glycolysis and mitochondrial respiration (p < 0.05). At molecular level, upregulation of SIRT1 (p < 0.05), and SGLT2 protein expression (p < 0.05) were observed. iSGLT2 counteracted the effects of PE, by reducing cell proliferation, inflammation, mitochondrial respiration, and glycolysis (p < 0.001), while promoting lipid peroxidation and ferroptotic cell death (p < 0.001), highlighting the potential to target metabolic vulnerability of CRC cells. Similarly, PE, γBB and Cnt (PE + γBB + Cnt) ameliorated the onco-metabolic changes induced by PE and triggered ferroptotic cell death. Bioinformatic analysis identified PPARγ as a common target of CRC and iSGLT2 and was modulated by both canagliflozin and γBB + Cnt, suggesting a shared molecular mechanism.
conclusionResults unveil the adverse effects of PE on CRC progression underscoring a dynamic interplay between environmental pollutants, metabolic regulators and dietary bioactive modulators. This evidence lay the groundwork for future studies on integrative approaches aimed at mitigating the effects of microplastic pollution on CRC.
Indexed as
Identifiers
41629945What Socratic 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 Socratic graph.