ArticleFrontiers in pharmacology2026
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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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Authors and funding
11 authors.
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Abstract
Purpose: Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide. Methods: The anti-tumor effects of acRoots were evaluated in human Colorectal cancer cell lines (HCT-15, CW-2) using Cell Counting Kit-8 (CCK-8), colony formation, wound healing, and Transwell assays. Cell death was analyzed by Annexin V-FITC/PI flow cytometry. Mechanisms were probed by measuring reactive oxygen species (ROS), glutathione (GSH) levels, malondialdehyde (MDA) levels, and performing qRT-PCR and Western blot for ferroptosis-related markers (SLC7A11, GPX4, p53). The ferroptosis inhibitor Ferrostatin-1 (Fer-1) was used in rescue experiments. The Results: The acRoots significantly and dose-dependently inhibits the viability, proliferation, migration, and invasion of colorectal cancer cells. Concurrently, acRoots effectively induces ferroptosis in these cells, characterized by intracellular reactive oxygen species (ROS) accumulation, glutathione (GSH) depletion, and a significant increase in the lipid peroxidation product malondialdehyde (MDA). These ferroptosis-related phenotypes can be reversed by the ferroptosis-specific inhibitor Ferrostatin-1 (Fer-1). Mechanistically, acRoots upregulates the expression of the tumor suppressor gene p53, subsequently downregulating the expression levels of key ferroptosis regulators SLC7A11 and GPX4. Furthermore, pretreatment with Fer-1 effectively reverses acRoots-induced cytotoxicity and ROS accumulation. In an HCT-15 xenograft mouse model, oral administration of acRoots (150 mg/kg/day) significantly inhibited tumor growth, reduced intratumoral GSH levels, and no obvious toxicity was observed. Conclusion: Our findings demonstrate that acRoots exerts potent anti-Colorectal cancer effects by inhibiting malignant phenotypes and inducing ferroptosis. This ferroptosis is mediated, at least in part, through the p53-dependent downregulation of the SLC7A11/GPX4 axis. These results position acRoots as a promising therapeutic candidate and a novel natural ferroptosis inducer for Colorectal cancer treatment, warranting further clinical investigation.
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