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Apigenin Suppresses MED28-Mediated Cell Growth in Human Liver Cancer Cells
Jou-Chia Chou1, Chen-Chia Liu1, Ming-Fen Lee1
1Department of Nutrition, China Medical University, Taichung 406040, Taiwan.
Journal of Agricultural and Food Chemistry
|April 15, 2024
Summary
Apigenin, a flavonoid, inhibits liver cancer progression by downregulating MED28 expression and suppressing AKT/mTOR signaling. This suggests apigenin
Area of Science:
- Molecular Oncology
- Cancer Chemoprevention
Background:
- Flavonoids, like apigenin, show promise in cancer chemoprevention.
- Liver cancer has a poor prognosis despite therapeutic advances.
- The role of Mediator subunit 28 (MED28) in liver cancer is currently unknown.
Purpose of the Study:
- To investigate the role of apigenin and MED28 in liver cancer.
- To explore their involvement in the AKT/mammalian target of rapamycin (mTOR) signaling pathway.
Main Methods:
- Utilized CLUE software to assess compound-genetic perturbagen connectivity.
- Analyzed The Cancer Genome Atlas Liver Cancer (TCGA-LIHC) dataset for MED28 expression.
- Performed MED28 knockdown and apigenin treatment in HepG2 and Huh 7 liver cancer cell lines.
Main Results:
- Higher MED28 expression correlated with poorer survival and advanced tumor stage/grade.
- MED28 knockdown induced cell cycle arrest and suppressed AKT/mTOR signaling.
- Apigenin mimicked MED28 knockdown effects, inhibiting MED28 expression and AKT/mTOR signaling.
Conclusions:
- MED28 is linked to liver cancer progression and survival via AKT/mTOR signaling.
- Apigenin inhibits liver cancer cell growth by targeting MED28-mediated mTOR signaling.
- Apigenin shows potential as an adjuvant therapy or chemopreventive agent for liver cancer.
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