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Cancer, Lipids, and Metabolism / Immune Cells in Cancer / Ferroptosis and Cancer Prognosis · Journal article
Discover Oncology · September 10, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a preclinical mechanistic study demonstrating that l-rhamnose inhibits triple-negative breast cancer cell proliferation and tumor growth in mouse xenografts through GSTM5-mediated ferroptosis. The findings are consistent with a candidate mechanism but lack human data, formal comparators, and clinical endpoints; the work is suitable for hypothesis generation and must be confirmed in human trials before any clinical application.
Preclinical in vitro and in vivo study. TNBC cell lines (MDA-MB-231, Hs578T) and nude mice bearing MDA-MB-231 xenografts. Intervention: l-rhamnose (5 g/kg intraperitoneal administration in vivo).
l-rhamnose dose- and time-dependently inhibited TNBC proliferation and colony formation in cell lines Intraperitoneal administration at 5 g/kg significantly suppressed tumor growth without affecting mouse body weight Ferroptosis inhibitor Ferrostatin-1 attenuated l-rhamnose-mediated tumor suppression both in vitro and in vivo
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
These findings do not yet support clinical use. l-rhamnose warrants mechanistic investigation in human TNBC models and early-phase trials, but the current evidence is limited to cell and animal systems without efficacy or safety assessment in patients.
Mechanistic study in cell lines and mouse xenografts with a single candidate agent; no human data, no comparator arm, and no clinical endpoints reported.
As stated by the source record.
Quoted from the source exactly as published.
These findings do not yet support clinical use. l-rhamnose warrants mechanistic investigation in human TNBC models and early-phase trials, but the current evidence is limited to cell and animal systems without efficacy or safety assessment in patients.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Triple-negative breast cancer lacks effective targeted therapies, necessitating novel treatment approaches.To evaluate the antitumor efficacy and molecular mechanisms of l -rhamnose in TNBC. We employed an integrated approach combining in vitro cell-based assays and in vivo xenograft models. TNBC cell lines (MDA-MB-231, Hs578T) were treated with l -rhamnose to assess proliferation and colony formation. Molecular docking predicted the binding between l -rhamnose and GSTM5. GSTM5 gain- and loss-of-function experiments were performed to confirm its functional role. The in vivo efficacy was evaluated using MDA-MB-231 nude mouse xenografts. Ferroptosis dependency was confirmed using Ferrostatin-1. l -rhamnose dose- and time-dependently inhibited TNBC proliferation and colony formation. Intraperitoneal administration (5 g/kg) significantly suppressed tumor growth without affecting mouse body weight. Fer-1 attenuated l -rhamnose-mediated tumor suppression both in vitro and in vivo. Mechanistically, l -rhamnose downregulated GSTM5 protein levels, concomitant with GPX4 reduction and lipid peroxide accumulation. GSTM5 overexpression rescued l -rhamnose-induced cell death and restored GPX4, whereas GSTM5 knockdown sensitized cells to ferroptosis. Molecular docking predicted a potential interaction between l -rhamnose and the GSTM5 protein, with a calculated binding energy of -5.341 kcal/mol, which guided our subsequent functional investigations. l -rhamnose suppresses TNBC growth by inducing ferroptosis, a process associated with the downregulation of GSTM5. Our findings reveal that GSTM5 is a key mediator modulating ferroptosis sensitivity in TNBC. These results position l -rhamnose as a candidate for further investigation in TNBC therapy.
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