article · International Journal of Molecular Sciences
Hinokitiol, a compound found in cupressaceous plants, was investigated for its effects on breast cancer cells. Researchers used three breast cancer cell lines and found that hinokitiol significantly reduced their viability in a dose-dependent manner. The compound enhanced apoptosis by increasing specific protein levels and induced dysfunction in autophagy. Furthermore, hinokitiol suppressed the formation and size of cancer cell spheres by reducing the expression of CD44 and key transcription factors. These findings suggest that hinokitiol could be a potential therapeutic agent for breast cancer, acting as an inhibitor of stemness progression. Further research and clinical studies are needed to explore its full therapeutic potential.
Breast cancer is a major global health concern, with tumour relapse and metastasis often linked to cancer stemness. This research identifies hinokitiol as a potential new therapeutic agent that can inhibit this stemness progression, offering a novel approach to combat breast cancer and improve treatment outcomes.
This research identifies hinokitiol as a potential therapeutic agent for breast cancer, specifically targeting stemness progression. It could lead to the development of new drugs for breast cancer treatment, particularly for patients experiencing relapse or metastasis. This is early-stage research, with findings demonstrated in cell lines, and requires further research and clinical studies before it can be considered for real-world application.
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Breast cancer (BC) represents one of the most prevalent malignant threats to women globally. Tumor relapse or metastasis is facilitated by BC stemness progression, contributing to tumorigenicity. Therefore, comprehending the characteristics of stemness progression and the underlying molecular mechanisms is pivotal for BC advancement. Hinokitiol (β-thujaplicin), a tropolone-related compound abundant in the heartwood of cupressaceous plants, exhibits antimicrobial activity. In our study, we employed three BC cell lines (MDA-MB-231, MCF-7, and T47D) to assess the expression of stemness-, apoptosis-, and autophagy-related proteins. Hinokitiol significantly reduced the viability of cancer cells in a dose-dependent manner. Furthermore, we observed that hinokitiol enhances apoptosis by increasing the levels of cleaved poly-ADP-ribose polymerase (PARP) and phospho-p53. It also induces dysfunction in autophagy through the upregulation of LC3B and p62 protein expression. Additionally, hinokitiol significantly suppressed the number and diameter of cancer cell line spheres by reducing the expression of cluster of differentiation44 (CD44) and key transcription factors. These findings underscore hinokitiol's potential as a therapeutic agent for breast cancer, particularly as a stemness-progression inhibitor. Further research and clinical studies are warranted to explore the full therapeutic potential of hinokitiol in the treatment of breast cancer.
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DOI: 10.3390/ijms25073904
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