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Apigenin as an anticancer agent
Muhammad Imran1, Tanweer Aslam Gondal2, Muhammad Atif3
1University Institute of Diet and Nutritional Sciences, Faculty of Allied Health Sciences, The University of Lahore-Lahore, Lahore, Pakistan.
Abstract:
Apigenin is an edible plant-derived flavonoid that has been reported as an anticancer agent in several experimental and biological studies. It exhibits cell growth arrest and apoptosis in different types of tumors such as breast, lung, liver, skin, blood, colon, prostate, pancreatic, cervical, oral, and stomach, by modulating several signaling pathways. Apigenin induces apoptosis by the activation of extrinsic caspase-dependent pathway by upregulating the mRNA expressions of caspase-3, caspase-8, and TNF-α. It induces intrinsic apoptosis pathway as evidenced by the induction of cytochrome c, Bax, and caspase-3, while caspase-8, TNF-α, and B-cell lymphoma 2 levels remained unchanged in human prostate cancer PC-3 cells. Apigenin treatment leads to significant downregulation of matrix metallopeptidases-2, -9, Snail, and Slug, suppressing invasion. The expressions of NF-κB p105/p50, PI3K, Akt, and the phosphorylation of p-Akt decreases after treatment with apigenin. However, apigenin-mediated treatment significantly reduces pluripotency marker Oct3/4 protein expression which might be associated with the downregulation of PI3K/Akt/NF-κB signaling.
Insights
Apigenin, a plant flavonoid, shows anticancer effects by inducing cell death and inhibiting invasion in various cancers. It modulates key signaling pathways like PI3K/Akt/NF-κB, offering potential therapeutic benefits.
Area of Science:
- Oncology
- Molecular Biology
- Natural Products Chemistry
Background:
- Apigenin is a plant-derived flavonoid with documented anticancer properties.
- It affects multiple signaling pathways involved in cancer progression.
Purpose of the Study:
- To investigate the molecular mechanisms of apigenin's anticancer effects.
- To analyze its impact on apoptosis, invasion, and key signaling pathways in cancer cells.
Main Methods:
- Apigenin treatment of human prostate cancer PC-3 cells.
- Analysis of mRNA and protein expression for apoptosis markers (caspases, TNF-α, cytochrome c, Bax, Bcl-2).
- Assessment of invasion-related proteins (MMPs, Snail, Slug) and signaling pathways (NF-κB, PI3K/Akt).
Main Results:
- Apigenin induced apoptosis via extrinsic (caspase-3, -8, TNF-α) and intrinsic (cytochrome c, Bax) pathways.
- It suppressed invasion by downregulating matrix metallopeptidases-2, -9, Snail, and Slug.
- Apigenin reduced NF-κB, PI3K, Akt, and p-Akt levels, and decreased Oct3/4 expression.
Conclusions:
- Apigenin exhibits potent anticancer activity by inducing apoptosis and inhibiting invasion.
- Its effects are mediated through modulation of caspase-dependent and independent pathways.
- Apigenin's downregulation of PI3K/Akt/NF-κB signaling and Oct3/4 suggests a role in suppressing cancer stemness.
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