ArticleOpen life sciences2024
Apigenin 7-glucoside impedes hypoxia-induced malignant phenotypes of cervical cancer cells in a p16-dependent manner.
Article in Open life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Juniperus phoenicea extract-loaded nanostructured lipid carriers for potent antimicrobial and anticancer combination therapy.AMB Express · 2026Article
- Comparative Evaluation of the Cytotoxic Effect of Dysphania ambrosioides Extracts Against Human Breast and Cervical Cancer Cells.Chemistry & biodiversity · 2026Article
- Unveiling the anti-cancer properties of apigenin via targeting different molecular signatures: A Review.Molecular biology reports · 2026Review
- Genome-wide identification of UDP-glycosyltransferase gene family inFrontiers in plant science · 2026Article
- The Role of the NO/cGMP Pathway and SKCa and IKCa Channels in the Vasodilatory Effect of Apigenin 7-Glucoside.Molecules (Basel, Switzerland) · 2025Article
- Curcumin, EGCG and apigenin in cervical cancer: mechanistic insights and therapeutic potential.Frontiers in pharmacology · 2025Review
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Authors and funding
5 authors.
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Abstract
Apigenin 7-glucoside (A7G) can suppress cell proliferation and trigger apoptosis in cervical cancer cells. Considering that hypoxia is associated with the malignant phenotypes in cervical cancer, this study aimed to uncover whether A7G exhibits suppressive effects on the hypoxia-induced malignant phenotype of cervical cancer cells (HeLa cells). Compared to normoxia, hypoxia can enhance the malignant phenotypes of HeLa cells, including cell proliferation, reduced sensitivity against chemotherapeutic agents (oxaliplatin and paclitaxel), cancer stemness, migration, and invasion. A7G intervention (20, 40, and 60 μM) could impair these malignant phenotypes of HeLa cells and upregulate the expression level of total and nuclear p16 proteins. Molecular docking analysis showed the interaction between anion exchanger 1 and A7G. In p16-silencing HeLa cells, the anticancer effects of A7G were absent. Therefore, hypoxia derives malignant phenotypes of HeLa cells, which could be impeded by A7G in a p16-dependent manner.
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