Molecular mechanisms underlying mangiferin-induced apoptosis and cell cycle arrest in A549 human lung carcinoma cells
Open accessAbstract
Mangiferin, which is a C‑glucosylxanthone (1,3,6,7-tetrahydroxyxanthone-C2-β-D-glucoside) purified from plant sources, has recently gained attention due to its various biological activities. The present study aimed to determine the apoptotic effects of mangiferin on A549 human lung adenocarcinoma cells. In vitro studies demonstrated that mangiferin exerted growth‑inhibitory and apoptosis-inducing effects against A549 cells. In addition, mangiferin exhibited anti-tumor properties in A549 xenograft mice in vivo. Mangiferin triggered G2/M phase cell cycle arrest via downregulating the cyclin-dependent kinase 1-cyclin B1 signaling pathway, and induced apoptotic cell death by inhibiting the protein kinase C-nuclear factor-κB pathway. In addition, mangiferin was able to enhance the antiproliferative effects of cisplatin on A549 cells, thus indicating the potential for a combined therapy. Notably, mangiferin exerted anticancer effects in vivo, where it was able to markedly decrease the volume and weight of subcutaneous tumor mass, and expand the lifespan of xenograft mice. The present study clarified the molecular mechanisms underlying mangiferin-induced antitumor activities, and suggested that mangiferin may be considered a potential antineoplastic drug for the future treatment of cancer.
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MGF decreases CDK1/cyclin B1 activity, alters CDK1 phosphorylation, and engages ATR-dependent Chk1 activation in other tumor cell lines.
“This outcome is consistent with reports of decreased CDK1/cyclin B1 activity, altered phosphorylation of CDK1 with reduced activating phosphorylation and increased inhibitory phosphorylation, and engagement of checkpoint signaling, including ATR-dependent Chk1 activation, in other tumor cell lines exposed to MGF (56,57).”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [56]
The Results section reports reduced CDK1 (cdc2) and cyclin B1 protein expression after mangiferin treatment in A549 cells, supporting downregulation of that pathway. It does not report a direct activity measurement, CDK1 phosphorylation changes, or ATR-dependent Chk1 activation; those terms were also searched in our copy. The study’s cell-line finding cannot by itself establish those mechanisms in other tumor cell lines. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThis evidence supports multilevel regulation of the CDK1/cyclin B1 axis by MGF.
“This evidence supports multilevel regulation of the CDK1/cyclin B1 axis by MGF.”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [56]
The Results section reports that mangiferin reduced cdc2 (CDK1) and cyclin B1 protein levels in A549 cells and was associated with G2/M arrest. This supports regulation of the axis, but the paper does not establish regulation at multiple levels beyond those protein-expression measurements. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAcross tumor cell systems, the functional consequence of MGF exposure remains G2/M arrest, with reduced proliferation and increased susceptibility to apoptosis.
“However, across tumor cell systems, the functional consequence remains G2/M arrest, with reduced proliferation and increased susceptibility to apoptosis.”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [56]
The Discussion reports G2/M arrest, growth inhibition and apoptosis after mangiferin treatment in A549 lung carcinoma cells. It does not establish that these effects occur across tumor cell systems. Page numbers are not provided in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn HeLa and HT29 cells, MGF suppression of NF-κB coincides with improved responses to oxaliplatin and reduced drug resistance.
“In HeLa and HT29 cells, this suppression coincides with improved responses to oxaliplatin and reduced drug resistance.”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [56]
The Discussion (page not provided) reports that mangiferin suppresses PKC–NF-κB signaling in A549 lung carcinoma cells. The Results (page not provided) report enhanced antiproliferative effects when mangiferin is combined with cisplatin in A549 cells. The paper does not support the claimed findings in HeLa or HT29 cells, improved responses to oxaliplatin, or reduced drug resistance. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMangiferin inhibits expression of RelA and RelB, activates IκB and suppresses phosphorylation of NF-κB kinase, thereby inhibiting transcriptional activity of NF-κB and inducing apoptosis in tumor cells.
“It was demonstrated that mangiferin inhibits the expression of RelA and RelB, activates inhibitor of NF-κB (IκB) and suppresses the phosphorylation of NF-κB kinase, thereby inhibiting the transcriptional activity of NF-κB and inducing apoptosis tumor cells (54)(55)(56).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [55]
The Results section, “Mangiferin induces apoptosis in A549 cells via inhibition of the PKC-NF-κB pathway” (page not provided), reports reduced NF-κB protein expression after mangiferin treatment; the Discussion links suppression of that pathway to apoptosis in A549 cells. The paper does not report reduced RelA or RelB expression, IκB activation, NF-κB kinase phosphorylation, or a direct measurement of NF-κB transcriptional activity. (LLM, conf=0.88)
Experimental — accuracy not yet measured
In A549 lung cancer cells, MGF increases the antiproliferative impact of chemotherapy in association with G2/M arrest and inhibition of the PKC-NF-κB axis.
“In A549 lung cancer cells, MGF increases the antiproliferative impact of chemotherapy in association with G2/M arrest and inhibition of the PKC-NF-κB axis (56).”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [56]
In human lung carcinoma A549 cells, mangiferin exhibits antineoplastic properties by inducing G2/M phase cell cycle arrest via downregulation of CDK1-cyclin B1 and inducing apoptotic cell death by inhibiting PKC-NF-κB.
“Similarly, in human lung carcinoma A549 cells, mangiferin exhibits antineoplastic properties, by inducing G2/M phase cell cycle arrest via downregulation of the cyclin-dependent kinase 1-cyclin B1 signaling pathway and inducing apoptotic cell death by inhibiting the PKC-NF-κB pathway (55).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [55]
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- Authors
- SHI, W., DENG, J., TONG, R., YANG, Y., HE, X., LV, J., WANG, H., DENG, S., QI, P., ZHANG, D., & WANG, Y.
- Affiliations
- Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital (CN)
- Guangxi University of Chinese Medicine (CN)
- ORCID
- Venue
- Molecular Medicine Reports
- Publisher
- Spandidos Publications
- Published
- 2016-02-29
- Volume
- 13
- Issue
- 4
- Pages
- 3423-3432
- ISSN
- 1791-2997 (ISSN-L)
- 1791-3004
- PMC
- PMC4805064
- OpenAlex
- W2282580521
- Cited by
- 50
- References
- 28
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 3 · 2019: 3 · 2018: 8 · 2017: 5 · 2016: 1
- FWCI
- 11.65
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Molecular Medicine Reports (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81271049)
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Mangiferin and Mango Extracts
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Natural Compound Pharmacology Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioactive natural compounds
- Keywords
- mangiferin, apoptosis, cell cycle arrest, G2/M cell cycle arrest, cyclin-dependent kinase 1, cyclin B1, protein kinase C, NF-κB signaling, cisplatin combination therapy, lung adenocarcinoma, A549 cells, anticancer activity, xenograft tumor growth
- MeSH terms
- A549 Cells, Animals, Antineoplastic Agents, Cisplatin, Drug Therapy, Combination, Humans, Lung Neoplasms, Male, Mice, Inbred C57BL, Mice, Nude, Protein Kinase C, Transplantation, Heterologous, Signal Transduction, CDC2 Protein Kinase, NF-kappa B, Apoptosis, Cyclin B, Xanthones, Mice, Membrane Potential, Mitochondrial, M Phase Cell Cycle Checkpoints
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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