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Morinda citrifolia (Noni) Juice Suppresses A549 Human Lung Cancer Cells via Inhibiting AKT/Nuclear Factor-κ B
Ling-di Ma1,2, Gui-Bin Lin3, Lu-Bo Yang4
1Laboratory Center, the Third People's Hospital of Huizhou, Affiliated Hospital of Guangzhou Medical University, Huizhou, Guangdong Province, 516002, China. lingdimawsh@126.com.
Objective:
To study the mechanism of the anti-tumor effect of Morinda citrifolia (noni).
Methods:
The influences of noni juice on cell proliferation, apoptosis, invasion, migration and the activity of AKT/nuclear factor- κ B (NF- κ B) signaling pathway in A549 human lung cancer cells were detected by MTT, cell counting kit-8, colony formation, Annexin V/PI double labeling, transwell, scratch test and immunoblotting assay, respectively. A549 cells were inoculated into the right axilla of nude mice, followed by noni juice treatment. The body weight of the nude mice was weighed, and the tumor volume and weight were measured. Cell proliferation and expression of apoptosis-related proteins were measured by immunohistochemistry, and the activity of NF- κ B signaling pathway was measured by immunoblotting.
Results:
The in vitro studies showed that noni juice inhibited the A549 cells proliferation, migration and invasion. Noni juice also promoted cells apoptosis in A549 cells. Immunoblotting assay showed that the phosphorylation level of AKT, p50, and STAT3 proteins was inhibited to different extents after noni juice treatment. The in vivo studies showed that noni juice effectively suppressed tumor formation of A549 cells in nude mice. Noni juice treatment inhibited the expression of Ki67, PCNA, and Bcl-2 protein in the tumor; while promoted the expression of caspase-3 protein. Additionally, we also found that noni juice treatment could restrain the activity of AKT/NF- κ B signaling pathway in the tumor tissue.
Conclusion:
Noni juice inhibited the proliferation of A549 lung cancer cells, induced apoptosis, and inhibited cell invasion and migration via regulating AKT/NF- κ B signaling pathway.
Insights
Noni juice demonstrates anti-tumor effects by inhibiting lung cancer cell proliferation and migration. It also promotes apoptosis and regulates the AKT/NF-κB signaling pathway, offering potential therapeutic benefits.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Morinda citrifolia (noni) is traditionally used for medicinal purposes.
- Lung cancer remains a leading cause of cancer-related mortality worldwide.
- Understanding the molecular mechanisms of natural compounds is crucial for developing novel cancer therapies.
Purpose of the Study:
- To elucidate the anti-tumor mechanism of noni juice in A549 human lung cancer cells.
- To investigate the effect of noni juice on cancer cell proliferation, apoptosis, invasion, and migration.
- To determine the impact of noni juice on the AKT/nuclear factor-κB (NF-κB) signaling pathway.
Main Methods:
- In vitro assays (MTT, CCK-8, colony formation, Annexin V/PI, transwell, scratch) were used to assess noni juice effects on A549 cells.
- Immunoblotting and immunohistochemistry were employed to analyze protein expression and signaling pathway activity.
- In vivo studies involved inoculating A549 cells in nude mice and administering noni juice to evaluate tumor growth and related markers.
Main Results:
- Noni juice significantly inhibited A549 cell proliferation, migration, and invasion in vitro.
- Noni juice induced apoptosis in A549 cells and suppressed tumor formation in vivo.
- Noni juice treatment downregulated the phosphorylation of AKT, p50, and STAT3, and modulated apoptosis-related proteins (Ki67, PCNA, Bcl-2, caspase-3) in tumor tissues.
- Noni juice restrained the activity of the AKT/NF-κB signaling pathway in both in vitro and in vivo models.
Conclusions:
- Noni juice exhibits potent anti-cancer properties against A549 lung cancer cells.
- The anti-tumor effects are mediated through the inhibition of cell proliferation, invasion, and migration, coupled with the induction of apoptosis.
- Noni juice exerts its effects, at least in part, by regulating the AKT/NF-κB signaling pathway.
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