# Effects of royal jelly on ovary cancer cells proliferation and apoptosis

**Authors:** Ender Deniz Asmaz, Sabire Güler, Berrin Zık

PMC · DOI: 10.1007/s12032-025-02638-z · Medical Oncology (Northwood, London, England) · 2025-03-04

## TL;DR

This study explores how royal jelly affects the growth and death of ovarian cancer cells, finding that high doses can inhibit cancer cell proliferation and induce apoptosis.

## Contribution

The study identifies that 50 mg/ml royal jelly for 72 hours induces apoptosis in ovarian cancer cells, suggesting potential as an alternative treatment.

## Key findings

- 1 mg/ml royal jelly for 24 hours had no effect on cell proliferation or apoptosis.
- 50 mg/ml royal jelly for 72 hours inhibited cancer cell proliferation and induced apoptosis.
- Royal jelly's effects were confirmed using multiple methods including TUNEL, Ki-67, and cleaved-Caspase-3/PARP.

## Abstract

The aim of the present study is to investigate the proliferative or apoptotic effects of different doses and durations of Royal jelly (RJ) on serous type epithelial ovarian cancer, which is the most common epithelial ovarian cancer. For this purpose, cells of the Skov-3 human ovarian adenocarcinoma cell line were grown in McCoy medium and seeded in 6-well plates. RJ was prepared as a stock solution (1000 mg RJ/10 ml dH2O) and 1, 5, 10, 20, and 50 mg/ml RJ doses from the prepared stock solution were added to the medium for 24, 48, and 72 h incubated. After the treatment of RJ, the cell viability test (Tripan Blue), Ki-67 to determine the proliferative effect, cleaved-Caspase-3 and cleaved PARP expressions to determine its apoptotic effect were examined by immunocytochemical and immunofluorescence methods. In addition, findings were supported by the TUNEL method. As a result of the experiments, it was determined that 1 mg/ml and 24 h treatment of RJ did not affect cell proliferation and apoptosis, but generally, 50 mg/ml of RJ for 72 h inhibited proliferation in cancer cells and induced apoptosis. The use of royal jelly both monotherapeutically and in combination as an alternative treatment for ovarian cancer may provide the basis for new experimental protocols.

## Linked entities

- **Proteins:** Mki67 (antigen identified by monoclonal antibody Ki 67)
- **Diseases:** ovary cancer (MONDO:0008170)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** PARP1 (poly(ADP-ribose) polymerase 1) [NCBI Gene 142] {aka ADPRT, ADPRT 1, ADPRT1, ARTD1, PARP, PARP-1}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}
- **Diseases:** ovarian adenocarcinoma (MESH:D010051), cancer (MESH:D009369), epithelial ovarian cancer (MESH:D000077216)
- **Chemicals:** McCoy medium (-), RJ (MESH:C058787)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** Skov-3 — Homo sapiens (Human), Ovarian serous cystadenocarcinoma, Cancer cell line (CVCL_0532)

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11880105/full.md

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Source: https://tomesphere.com/paper/PMC11880105