ArticleOncology reports2017
Apigenin overcomes drug resistance by blocking the signal transducer and activator of transcription 3 signaling in breast cancer cells.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 70 citations in OpenAlex.
- Flavonoid-modulated JAK-STAT signaling mitigates malignant transformation and drug resistance in breast tumors: A clinically relevant 3PM-guided innovation.Journal of advanced research · 2026Review
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025Review
- Phytoactive Molecules and Nanodelivery Approaches for Breast Cancer Treatment: Current and Future Perspectives.Current pharmaceutical biotechnology · 2025Review
- Naturally Occurring Phytochemicals to Target Breast Cancer Cell Signaling.Applied biochemistry and biotechnology · 2024Review
- Apigenin's Modulation of Doxorubicin Efficacy in Breast Cancer.Molecules (Basel, Switzerland) · 2024Article
- Unveiling the power of flavonoids: A dynamic exploration of their impact on cancer through matrix metalloproteinases regulation.BioMedicine · 2024Review
- p‑STAT3 influences doxorubicin and etoposide resistance of A549 cells grown in anOncology reports · 2023Article
- Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism.Molecules (Basel, Switzerland) · 2023Article
- Reckoning apigenin and kaempferol as a potential multi-targeted inhibitor of EGFR/HER2-MEK pathway of metastatic colorectal cancer identified using rigorous computational workflow.Molecular diversity · 2022Article
- Apigenin Ameliorates Hyperuricemia and Renal Injury through Regulation of Uric Acid Metabolism and JAK2/STAT3 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Chemotherapeutic effects of Apigenin in breast cancer: Preclinical evidence and molecular mechanisms; enhanced bioavailability by nanoparticles.Biotechnology reports (Amsterdam, Netherlands) · 2022Review
- Article
- Comparative Study of Antiproliferative Activity in Different Plant Parts ofTheScientificWorldJournal · 2022Article
- Chemoprotective and chemosensitizing effects of apigenin on cancer therapy.Cancer cell international · 2021Review
- Review
- Apigenin, a Partial Antagonist of the Estrogen Receptor (ER), Inhibits ER-Positive Breast Cancer Cell Proliferation through Akt/FOXM1 Signaling.International journal of molecular sciences · 2021Article
- Apigenin by targeting hnRNPA2 sensitizes triple-negative breast cancer spheroids to doxorubicin-induced apoptosis and regulates expression of ABCC4 and ABCG2 drug efflux transporters.Biochemical pharmacology · 2020Article
- CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020Article
- Natural and herbal compounds targeting breast cancer, a review based on cancer stem cells.Iranian journal of basic medical sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance in chemotherapy is a serious obstacle for the successful treatment of cancer. Drug resistance is caused by various factors, including the overexpression of P‑glycoprotein (P‑gp, MDR1). The development of new, useful compounds that overcome drug resistance is urgent. Apigenin, a dietary flavonoid, has been reported as an anticancer drug in vivo and in vitro. In the present study, we investigated whether apigenin is able to reverse drug resistance using adriamycin‑resistant breast cancer cells (MCF‑7/ADR). In our experiments, apigenin significantly decreased cell growth and colony formation in MCF‑7/ADR cells and parental MCF‑7 cells. This growth inhibition was related to the accumulation of cells in the sub‑G0/G1 apoptotic population and an increase in the number of apoptotic cells. Apigenin reduced the mRNA expression of multidrug resistance 1 (MDR1) and multidrug resistance‑associated proteins (MRPs) in MCF‑7/ADR cells. Apigenin also downregulated the expression of P‑gp. Apigenin reversed drug efflux from MCF‑7/ADR cells, resulting in rhodamine 123 (Rho123) accumulation. Inhibition of drug resistance by apigenin is related to the suppression of the signal transducer and activator of transcription 3 (STAT3) signaling pathway. Apigenin decreased STAT3 activation (p‑STAT3) and its nuclear translocation and inhibited the secretion of VEGF and MMP‑9, which are STAT3 target genes. A STAT3 inhibitor, JAK inhibitor I and an HIF‑1α inhibitor decreased cell growth in MCF‑7 and MCF‑7/ADR cells. Taken together, these results demonstrate that apigenin can overcome drug resistance.
Indexed as
Identifiers
What OpenQuestion holds
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.