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Regulatory roles of pyroptosis-associated lncRnas in breast cancer progression and immune microenvironment.

Created on 06 Sep 2026

Authors

Chou-Yi Hsu, Bilal AbdulMajeed Mukhlif, Ozodbek Nematov, Ibrokhim Sapaev, Mirza R Baig, Safa Alkhayyat, Aseel Smerat

Published in

Cell cycle (Georgetown, Tex.). Volume 25. Issue 1. Pages 1-26. Epub Sep 06, 2026.

Abstract

Breast cancer progression and therapeutic response are profoundly influenced by tumor immune interactions, yet the molecular regulators linking cell death pathways with immune modulation remain incompletely understood. Pyroptosis, a gasdermin-mediated inflammatory form of programmed cell death, has emerged as a key determinant of tumor immunity, while long non-coding RNAs are increasingly recognized as critical upstream regulators of cancer signaling. Recent transcriptomic analyses have identified numerous pyroptosis-associated lncRNAs and generated prognostic signatures that stratify patients into distinct risk groups with significantly different survival outcomes. These signatures are closely associated with the tumor immune microenvironment: low-risk tumors exhibit increased infiltration of CD8+ T cells, NK cells, and B cells, together with elevated immune checkpoint expression, whereas high-risk tumors display immunosuppressive features, including M2 macrophage enrichment and higher tumor mutation burden. Mechanistic studies demonstrate that lncRNAs regulate pyroptosis through inflammasome activation, gasdermin-mediated signaling, and epigenetic modulation, thereby influencing tumor growth, metastasis, and therapeutic resistance. Despite these advances, clinical translation remains limited by dependence on retrospective transcriptomic datasets, insufficient mechanistic validation, lack of standardized assays, and scarce prospective clinical evidence. pyroptosis-associated lncRNAs represent a promising link between tumor progression and immune regulation, with considerable potential as prognostic biomarkers and therapeutic targets in breast cancer.

PMID:
42701903
Bibliographic data and abstract were imported from PubMed on 06 Sep 2026.

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