Background Breast cancer is one of the most common types of cancer in women worldwide. Anti-apoptotic activity of cancer cells is considered the main reason for drug resistance in BC which reduces the 5-year survival rate of patients and is still considered the main obstacle for cancer therapy. Stigmasterol (SS) is natural phytosterols compound in the plant which has been proved to play an important role to lower cholesterol and inducing anti-inflammatory, and anticancer properties. Methods In this, study, we aimed to evaluate the effect of SS on the expression of anti-apoptotic genes (Bcl-2 and BCL-XL), and also evaluate its effects on cell apoptosis and cell viability using MCF-7 cell line as well as evaluating its effect on tumor growth of spontaneous breast tumor (SMMT) in vivo. Result SS significantly decreased the expression of Bcl-2 and BCL-XL genes (*P < 0.05), induced apoptosis, and reduced cell proliferation in MCF-7 cell lines. Our in vivo study also indicated that SS could inhibit tumor size after treatment with (0, 10, 20 µM) compared to the normal control. Conclusion SS can be suggested as a potential agent in BC cancer treatment or as an adjuvant based on its ability to decrease the expression of Bcl-2 and BCL-XL genes and induce apoptosis.

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Background The expression of miR-382-5p is dysregulated in various cancers, and its aberrant expression has been linked to cancer progression and metastasis. In this study, we aimed to estimate the expression level of miR-382-5p in breast cancer (BC) tissues and cell lines, as well as evaluate its biological function in tumorigenesis. Methods First, qRT-PCR was used to detect miR-382-5p expression in both BC tissues and cell lines. Next, the effects of miR-382-5p on cell proliferation and invasion were studied using the CCK-8 assay, transwell assay, and invasion assay. The association between miR-382-5p and its target (PTEN) was investigated using bioinformatics tools and confirmed using a luciferase assay. The Spearman correlation analysis was used to determine the relationship between miR-382-5p and PTEN. Finally, the analysis of signaling networks was visualized. Results Our findings showed that overexpression of miR-382-5p in both BC tissues and cell lines increased cell viability and invasive ability via PTEN depletion, whereas PTEN up-regulation via plasmid transfection suppressed miR-382-5p proliferation and invasive effect on BC cells. Furthermore, the upregulation of miR-382-5p was associated with a poor prognosis and patient outcomes. Conclusions As a result of our findings, knocking down miR-382-5p could be considered a potential target for BC treatment.