ReviewCell communication and signaling : CCS2025
GAS5 as a therapeutic target in breast cancer through apoptosis induction.
Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Inverse GAS5-SFXN1 Correlation in Triple-Negative Breast Cancer: Insights from Bioinformatics and Tissue Expression Analysis.Iranian biomedical journal · 2026Article
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Authors and funding
3 authors.
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Abstract
The ongoing discovery of long noncoding RNA (lncRNA) involvement in carcinogenesis prevention and development has made significant strides in breast cancer therapeutics. lncRNA growth arrest-specific 5 (GAS5) is downregulated in breast cancer, and its downregulation is linked to advanced clinical staging and grading as well as poor survival outcomes. The apoptosis modality is the most sought-after cell death modality in cancer therapeutics and a major challenge to the current treatment paradigm is drug resistance. This review examines GAS5 as a therapeutic target and an inducer of apoptosis through various mechanisms, including the role of GAS5-derived small nucleolar RNAs (snoRNAs) in the prevention of carcinogenesis, GAS5 as a microRNA (miRNA) sponge, thereby upregulating several tumor suppressors that promote apoptosis. Moreover, GAS5 is a riborepressor of the glucocorticoid receptor, hindering inhibitors of apoptosis. Additionally, GAS5 sensitizes breast cancer to radiotherapy, chemotherapy and endocrine therapy and alleviates drug resistance either directly through overexpression or indirectly through the administration of drugs that increase its expression, consequently promoting apoptosis. GAS5 is involved in various crucial signaling pathways in breast cancer, such as the PI3K/AKT/mTOR, Wnt/β-catenin, and NF-κB pathways and is itself regulated by many pathways. Recognized as a potent tumor suppressor, GAS5 presents a compelling opportunity for more profound research as a potential game-changing therapeutic target in breast cancer.
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Registered trials
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