What question did this study set out to answer?

This study aims to explore the effects and mechanisms of deoxyshikonin in breast cancer cells.

April 6, 2026Open Access

Deoxyshikonin inhibits the proliferation, invasion, and tumor immune microenvironment in breast cancer cells by inactivating the PI3K/AKT/NF-κB pathway

Key Points

This study aims to explore the effects and mechanisms of deoxyshikonin in breast cancer cells.
Utilized human breast cancer cell lines MDA-MB-231 and BT549.
Measured cell viability and apoptosis using Cell Counting Kit-8 and flow cytometry.
Assessed expression of apoptosis-related factors and proteins via Western blot analysis.
Conducted Transwell experiments to evaluate cell invasion ability.
Performed in vivo analysis using a xenograft mouse model.
Deoxyshikonin inhibited cell proliferation and enhanced apoptosis in breast cancer cells.
Reduced cell invasion in both MDA-MB-231 and BT549 cells was observed.
Downregulated expression of IL-10, TGF-, and proteins in the PI3K/AKT/NF-kB pathway.
Significant reduction in tumor volume and weight in xenograft models was noted.
DSK effectively inactivated the PI3K/AKT/NF-kB pathway.

Abstract

BACKGROUND/OBJECTIVES: Deoxyshikonin (DSK) has been reported to inhibit tumor growth in various types of cancers, but its roles and action mechanisms in breast cancer (BC) are unclear.This study examined the anti-cancer function and mechanism of DSK in BC.MATERIALS/METHODS: MDA-MB-231 and BT549, human BC cells, were used.The cell viability and apoptosis levels were examined using Cell Counting Kit-8 experiments and flow cytometry, respectively.The expression of apoptosis-related factors (Ki-67, Bax, and Bcl-2), CD206, CD168, and proteins involved in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor (NF)-B pathway was evaluated by Western blot analysis.The cell invasion ability was determined using the Transwell experiment.The levels of interleukin (IL)-10 and transforming growth factor (TGF)- were detected using an enzyme-linked immunosorbent assay.The in vivo functions of DSK were assessed using a xenograft mouse model.RESULTS: DSK inhibited cell proliferation, enhanced cell apoptosis, and reduced the cell invasion of MDA-MB-231 and BT549 cells.DSK also reduced the levels of CD206 and CD168 proteins, as well as IL-10 and TGF- in phorbol 12-myristate 13-acetate-induced THP-1 cells.DSK downregulated the expression of the phosphorylated (p)-PI3K, p-AKT, and p-NF-B proteins in cells.These effects were reversed by 740 Y-P (PI3K/AKT activator).In addition, DSK significantly reduced the tumor volume and weight in a xenograft mouse model.DSK increased the level of cell apoptosis and decreased the expression of Ki-67 and CD206 in subcutaneous tumor tissue.DSK also inactivated the PI3K/AKT/NF-B pathway proteins.CONCLUSION: DSK inhibits the proliferation, invasion, and tumor immune microenvironment of BC cells by inactivating the PI3K/AKT/NF-B pathway, indicating that DSK may be a potential therapeutic option for BC treatment.

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