What question did this study set out to answer?

This study aims to evaluate how pomegranate seed extract (PSE) and ellagic acid (EA) affect specific microRNAs and cancer cell death in breast cancer cells.

May 13, 2026Open Access

Effects of pomegranate seed extract and ellagic acid on miR-16-5p and miR-34a-5p expression, cell cycle, and apoptosis in MCF-7 cells

Key Points

This study aims to evaluate how pomegranate seed extract (PSE) and ellagic acid (EA) affect specific microRNAs and cancer cell death in breast cancer cells.
MCF-7 breast cancer cells were encapsulated in 3D alginate scaffolds for treatment with PSE, EA, or both.
Cell viability was assessed using the MTT assay, while apoptosis was measured via flow cytometry.
Gene expression levels were analyzed using real-time PCR for specific microRNAs and genes.
The combination of PSE and EA significantly increased miR-16-5p and miR-34a-5p expression.
BCL-2 was downregulated, while SIRT1 and CCND1 expression decreased in treated MCF-7 cells.
Both antioxidants led to increased cell population in the G1 phase and reduced malondialdehyde levels.

Abstract

Background and purpose: The expression of Homo sapiens (has)-miR-16-5p and hsa-miR-34a-5p with anti-tumor effects is downregulated in cancer cells. To maintain these gene expressions in cancer cells, we evaluated the effects of pomegranate seed extract (PSE) and ellagic acid (EA) on hsa-miR-16-5p and hsa-miR- 34a-5p expression, cell cycle regulation, and apoptotic induction in the MCF-7 cells encapsulated in the alginate hydrogel, a 3D culture system. Experimental approach: MCF-7 cells were encapsulated in 3-D alginate scaffolds and cultured (experimental groups: EA, PSE, EA and PSE, and the control group). Cell viability (using MTT assay), cell apoptosis (via flow cytometry), the level of malondialdehyde (MDA), and the expression levels of hsa-miR-16-5p, hsa-miR- 34a-5p, B-cell lymphoma 2 (BCL-2), cyclin D1 (CCND1), and sirtuin 1 (SIRT1) were measured (via real-time PCR). Findings/Results: The combination of PSE and EA exhibited the greatest effects on MCF-7 cells. EA and PSE increased the expression of hsa-miR-16-5p and hsa-miR-34a-5p and decreased the expression of the SIRT1 and CCND1 genes. In addition, the antiapoptotic BCL-2 gene was downregulated in the experimental group. Both antioxidants significantly increased the population of MCF-7 cells in the G1 phase. Additionally, antioxidants reduce the level of MDA in cancer cells. Conclusion and implications: EA and PSE antioxidants increased hsa-miR-16-5p and hsa-miR-34a-5p expression, induced apoptosis, decreased cell proliferation, and stopped cancer cells in the G1 phase. Therefore, they can be considered promising compounds for helping the treatment of breast cancer.

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