ReferenceID 4534
Anticancer Effects and Molecular Mechanisms of Apigenin in Cervical Cancer Cells
Cancers (Basel)
Cervical cancer is the fourth most frequent malignancy in women. Apigenin is a natural plant-derived flavonoid present in common fruit, vegetables, and herbs, and has been found to possess antioxidant and anti-inflammato
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Record Fields
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- Reference Id
- 4534
- Evidence Id
- 21124
- Core Evidence Id
- 21124
- Source Reference Id
- 2344
- Herb2 Reference Id
- HBREF003141
- Subject Paper Key
- HBIN016408_35406599
- Pubmed Id
- 35406599
- Doi
- 10.3390/cancers14071824
- Paper Title
- Anticancer Effects and Molecular Mechanisms of Apigenin in Cervical Cancer Cells
- Paper Abstract
- Cervical cancer is the fourth most frequent malignancy in women. Apigenin is a natural plant-derived flavonoid present in common fruit, vegetables, and herbs, and has been found to possess antioxidant and anti-inflammatory properties as a health-promoting agent. It also exhibits important anticancer effects in various cancers, but its effects are not widely accepted by clinical practitioners. The present study investigated the anticancer effects and molecular mechanisms of apigenin in cervical cancer in vitro and in vivo. HeLa and C33A cells were treated with different concentrations of apigenin. The effects of apigenin on cell viability, cell cycle distribution, migration potential, phosphorylation of PI3K/AKT, the integrin β1-FAK signaling pathway, and epithelial-to-mesenchymal transition (EMT)-related protein levels were investigated. Mechanisms identified from the in vitro study were further validated in a cervical tumor xenograft mouse model. Apigenin effectively inhibited the growth of cervical cancer cells and cervical tumors in xenograft mice. Furthermore, the apigenin down-regulated FAK signaling (FAK, paxillin, and integrin β1) and PI3K/AKT signaling (PI3K, AKT, and mTOR), inactivated or activated various signaling targets, such as Bcl-2, Bax, p21 cip1 , CDK1, CDC25c, cyclin B1, fibronectin, N-cadherin, vimentin, laminin, and E-cadherin, promoted mitochondrial-mediated apoptosis, induced G2/M-phase cell cycle arrest, and reduced EMT to inhibit HeLa and C33A cancer cell migration, producing anticancer effects in cervical cancer. Thus, apigenin may act as a chemotherapeutic agent for cervical cancer treatment.
- Journal
- Cancers (Basel)
- Publish Year
- 2022
- Experiment Subject
- mouse; c33a cells; hela; women
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Cervical Tumor; Cancers; Cervical Cancer; C33a Cancer; Malignancy; Cervical Tumors
- Paper Title Cn
- Paper Title En
- Anticancer Effects and Molecular Mechanisms of Apigenin in Cervical Cancer Cells
- Bilingual Status
- semi_complete