Journal of ethnopharmacology · 2025
The central role of ferroptosis-induced therapy mediated by tenacissoside H in anaplastic thyroid cancer.
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He Wanwan, Hu Xiaotian, Ge Minghua, Meng Kexin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Tenacissoside H(TDH), a natural compound extracted from the dried vine stems of Marsdenia tenacissima (Roxb.) Wight et Arn., is considered to have anti-tumor effects. However, the anti-tumor activity of TDH against ATC remains unknown.
AIM OF THE STUDY: Ferroptosis, a novel form of programmed cell death, presents a promising target for therapeutic intervention, particularly in overcoming drug resistance in anaplastic thyroid carcinoma (ATC). We investigated the inhibitory effects of TDH on ATC cells, elucidating its ferroptosis-inducing mechanism, which to our knowledge has not been explored before.
RESULTS: Our findings indicate that TDH exerts an effect on the survival, proliferation, and migration of ATC cells. The strength of effect is dependent on dosage. Notably, ferroptosis marker proteins (GPX4, xCT, HO-1, TFR) were significantly downregulated following TDH treatment, whereas GPX4 and xCT expressions were partially restored post treatment with ferrostatin-1. Furthermore, in vivo studies confirmed that TDH effectively inhibited tumor growth in xenografted 8505C cells.
CONCLUSIONS: TDH could be considered a potential agent against ATC via inducing ferroptosis, providing a novel pharmacological basis for treating ATC.
AIM OF THE STUDY: Ferroptosis, a novel form of programmed cell death, presents a promising target for therapeutic intervention, particularly in overcoming drug resistance in anaplastic thyroid carcinoma (ATC). We investigated the inhibitory effects of TDH on ATC cells, elucidating its ferroptosis-inducing mechanism, which to our knowledge has not been explored before.
RESULTS: Our findings indicate that TDH exerts an effect on the survival, proliferation, and migration of ATC cells. The strength of effect is dependent on dosage. Notably, ferroptosis marker proteins (GPX4, xCT, HO-1, TFR) were significantly downregulated following TDH treatment, whereas GPX4 and xCT expressions were partially restored post treatment with ferrostatin-1. Furthermore, in vivo studies confirmed that TDH effectively inhibited tumor growth in xenografted 8505C cells.
CONCLUSIONS: TDH could be considered a potential agent against ATC via inducing ferroptosis, providing a novel pharmacological basis for treating ATC.