ArticleCell death & disease2023
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Recent advances in application of hydrogel-based nanomaterials in breast cancer: from drug delivery, immunotherapy mechanisms to clinical applications.Journal of nanobiotechnology · 2026Pooled it
- Machine learning for discovering anticancer compounds from plants and elucidating their mechanisms.Journal of computer-aided molecular design · 2026Review
- Identification of Antileukemic Compound From Ginger by Integrating UHPLC-MS, Network Pharmacology, Molecular Docking, Molecular Dynamics Simulation, and In Vitro and In Vivo Experimental Validation.Food science & nutrition · 2026Article
- Alternative splicing rewires breast cancer and opens therapeutic avenues.Cell communication and signaling : CCS · 2026Review
- Review
- Nickel Nanoparticles Promote Lung Adenocarcinoma Progression via CDK1-Mediated Fatty Acid Metabolism Regulation.International journal of molecular sciences · 2025Article
- Target identification of natural products in cancer with chemical proteomics and artificial intelligence approaches.Cancer biology & medicine · 2025Review
- Plant-Fungi Mutualism, Alternative Splicing, and Defense Responses: Balancing Symbiosis and Immunity.International journal of molecular sciences · 2025Review
- Ferroptosis: a novel pharmacological mechanism against multiple myeloma.Frontiers in pharmacology · 2025Review
- Apigenin facilitates apoptosis of acute lymphoblastic leukemia cells via AMP-activated protein kinase-mediated ferroptosis.Oncology research · 2025Article
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
- Identification of Tumor-SuppressiveNon-coding RNA · 2024Article
- Mechanisms of RNA alternative splicing dysregulation in triple-negative breast cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- In silico identification of a novel Cdc2-like kinase 2 (CLK2) inhibitor in triple negative breast cancer.Protein science : a publication of the Protein Society · 2024Article
- Role of flavonoids in inhibiting triple-negative breast cancer.Frontiers in pharmacology · 2024Review
- Nature's weapons: Bioactive compounds as anti-cancer agents.AIMS public health · 2024Review
- Apigenin: a natural molecule at the intersection of sleep and aging.Frontiers in nutrition · 2024Review
- Rbm3 deficiency leads to transcriptome-wide splicing alterations.RNA biology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is characterized by its aggressiveness and resistance to cancer-specific transcriptome alterations. Alternative splicing (AS) is a major contributor to the diversification of cancer-specific transcriptomes. The TNBC transcriptome landscape is characterized by aberrantly spliced isoforms that promote tumor growth and resistance, underscoring the need to identify approaches that reprogram AS circuitry towards transcriptomes, favoring a delay in tumorigenesis or responsiveness to therapy. We have previously shown that flavonoid apigenin is associated with splicing factors, including heterogeneous nuclear ribonucleoprotein A2 (hnRNPA2). Here, we showed that apigenin reprograms TNBC-associated AS transcriptome-wide. The AS events affected by apigenin were statistically enriched in hnRNPA2 substrates. Comparative transcriptomic analyses of human TNBC tumors and non-tumor tissues showed that apigenin can switch cancer-associated alternative spliced isoforms (ASI) to those found in non-tumor tissues. Apigenin preferentially affects the splicing of anti-apoptotic and proliferation factors, which are uniquely observed in cancer cells, but not in non-tumor cells. Apigenin switches cancer-associated aberrant ASI in vivo in TNBC xenograft mice by diminishing proliferation and increasing pro-apoptotic ASI. In accordance with these findings, apigenin increased apoptosis and reduced tumor proliferation, thereby halting TNBC growth in vivo. Our results revealed that apigenin reprograms transcriptome-wide TNBC-specific AS, thereby inducing apoptosis and hindering tumor growth. These findings underscore the impactful effects of nutraceuticals in altering cancer transcriptomes, offering new options to influence outcomes in TNBC treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.