ArticleActa pharmacologica Sinica2026
Long non-coding RNA STMN1P2 promotes breast cancer doxorubicin resistance by inhibiting pyroptosis through the hnRNPU-EZH2-TARF6-MALT1-caspase-1 pathway.
Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Targeting lncRNAs to Overcome Cancer Therapy Resistance: Advances in RNA Therapeutics and Delivery Strategies.Cancers · 2026Review
- Targeting non-coding RNAs in the ferroptosis system: Molecular mechanisms and clinical translation for reversing doxorubicin resistance in breast cancer.Non-coding RNA research · 2026Review
- HSP90AA1-VDAC1 interaction contributes to breast cancer progression and doxorubicin resistance through PI3K/AKT signaling.Breast cancer research : BCR · 2026Article
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14 authors.
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Abstract
Chemotherapeutic resistance is a significant issue in the treatment of breast cancer, which is related to pyroptosis inhibition. Increasing evidence suggests that long non-coding RNAs (lncRNAs) contribute to tumorigenesis and drug resistance. In this study we investigated the role of the lncRNA STMN1P2 in doxorubicin resistance in breast cancer, as well as its correlation with pyroptosis inhibition. Our results showed that the expression levels of lncRNA STMN1P2 were significantly elevated in doxorubicin-resistant breast cancer tissues and cells. We demonstrated that knockdown of STMN1P2 reduced doxorubicin resistance in breast cancer cells; overexpression of STMN1P2 inhibited doxorubicin-induced pyroptosis by reducing the expression of NLRP3, ASC, caspase-1 and GSDMD. Furthermore, STMN1P2 directly bound to and positively regulated heterogeneous nuclear ribonucleoprotein U (hnRNPU), and knockdown of hnRNPU reversed the inhibitory effect of STMN1P2 on pyroptosis and its ability to promote chemoresistance. In doxorubicin-resistant cells, hnRNPU directly bound to enhancer of zeste homologue 2 (EZH2), and STMN1P2 enhanced hnRNPU recruitment of EZH2 and increased EZH2 protein stability. EZH2 acted as a transcription factor to inactivate TNF receptor-associated factor 6 (TRAF6), thereby repressing the binding of TRAF6 with MALT1 and caspase-1, attenuating the canonical pathways of pyroptosis. In MCF7/DOX cells xenograft nude mouse model, we demonstrated that knockdown of STMN1P2 significantly enhanced the suppression of doxorubicin on the tumour growth. This study provides new clues and approaches for the prevention and treatment of breast cancer chemoresistance.
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