Abstract

Prostate cancer (PC) is one of the most common challenges endangering public health worldwide. Therefore, finding effective ways to prevent and treat this disease can significantly reduce the detrimental effects of PC. Baicalein is a compound derived from the root of Scutellaria baicalensis. This compound possesses anticancer potential because numerous studies have confirmed its effectiveness in improving leukemia, breast, liver, colon, skin, and bladder cancers. In this study, we focused on reviewing the latest research on the therapeutic effects of baicalein in treating PC. According to our findings in this review, baicalein, by affecting various signaling pathways such as the CDK6 / FOXM1, the Bax/Bcl-2, the Notch1 / NF-κB, and the PARP / caspase-3, inducing cell death, and halting cellular growth in cancer cells, can be an appealing therapeutic approach in treating PC.

Keywords:Prostate cancer; Baicalin; Therapeutic effects; Signaling pathways; Mechanisms

Introduction

Prostate cancer (PC) is the most common cancer diagnosed in men worldwide and a leading cause of cancer-related death, with about 313,780 new cases and approximately 35,770 deaths projected in the United States in 2025 [1]. It originates in the prostate gland and varies from slow-growing tumors to aggressive forms. Early detection through screening methods like PSA testing and MRI improves outcomes [2]. Treatment options include surgery, radiation, hormone therapy, and newer targeted therapies. New treatments for advanced PC have been developed in recent years, and researchers are trying to find new therapies to cure this disease [3]. Baicalin can be mentioned among the substances whose therapeutic properties have attracted the attention of researchers in the treatment of PC in recent years. Baicalin is the name of a substance obtained from the root of a plant called Scutellaria baicalensis. This substance has been used as a medicine in Chinese medicine since ancient times. Today, various kinds of research have shown that baicalin can have an anti-cancer effect in the treatment of different cancers, such as hepatocellular cancer, bladder cancer, and PC [4,5]. In this study, we aim to review the latest research on the therapeutic mechanism of baicalin in PC.

Mechanisms

Research has shown that baicalin can regulate various cell activities, such as proliferation, apoptosis, and cell growth, in cancer cells. Processes that are regulated through different signaling pathways, such as the Cyclin-Dependent Kinase 6 (CDK6) / Forkhead Box M1 (FOXM1), the Bax (Bcl-2 Associated X Protein) / B-cell lymphoma 2 (Bcl-2), the Notch1 / Nuclear Factor kappa-light-chain-enhancer of activated B (NF-κB), and the Poly ADP-ribose polymerase (PARP) / Cysteine-aspartic protease 3 (caspase-3) [6]. Ziqiang Yu et al. demonstrated in their study that baicalin significantly inhibits tumor growth, cell proliferation, and cell cycle progression in PC3 and LNCaP PC cells by downregulating the CDK6 / FOXM1 signaling pathway [7].

In another research, Baicalin treatment in testosterone-induced Benign prostate hyperplasia (BPH) rats reduced prostate enlargement, suppressed dihydrotestosterone (DHT) production, and inhibited 5α reductase Type II activity. In vitro, baicalin decreased proliferation markers and androgen receptor expression in DHT-stimulated PC line. Mechanistically, baicalin promoted apoptosis by restoring the Bax/Bcl-2 ratio and activating caspase pathways, suggesting it may be a promising natural therapy for BPH [8]. In a study, researchers show that baicalin induced G1 cell cycle arrest and apoptosis at higher concentrations and reduced androgen receptor expression in PC cells [9]. In research conducted on mice, Wu et al. showed that baicalin reduces CD133, CD44, ALDH1 proteins and mRNA expression by inhibiting the Notch1 / NF-κB signaling pathway and inhibits the growth of PC cells [10]. L. Chan et al. investigated the effects of baicalin on PC cell lines (DU145, PC-3, LNCaP, CAHPV- 10). Baicalin inhibited cell proliferation, with DU145 being the most sensitive and LNCaP the most resistant. At 150 μM, baicalin caused 50% growth inhibition in DU145. Apoptosis was confirmed through nuclear fragmentation, TUNEL labeling, DNA fragmentation, caspase-3 activation, and PARP cleavage. The findings suggest baicalin’s potential as an anti-tumor agent for PC, particularly androgen-independent types, by inducing apoptosis. The study highlights Baicalin’s promise for complementary PC therapies [11]. In another study, Miocinovic et al. investigated the effects of baicalin on human PC cells (DU-145, PC-3) and angiogenesis. In vitro, its dose-dependently inhibited cancer cell proliferation, induced apoptosis, and reduced endothelial cell sprouting. In vivo, oral baicalein significantly reduced tumor growth in SCID mice with DU-145 xenografts, though escalation did not enhance efficacy. The findings suggest baicalein and baicalin may serve as dual-action agents, targeting both tumor cells and angiogenesis, offering potential for PC therapy, particularly in androgen-insensitive cases [12].

Conclusion

In conclusion, baicalin can be effective in the treatment of PC and enhance the chances of survival of millions of people who are suffering from this disease. In a way that this substance affects various signaling pathways responsible for regulating cellular processes such as cell growth and apoptosis, it can potentially contribute to the destruction of cancer cells and improve the disease. Hopefully, further research on the anticancer effects of this substance will shed light on new aspects of the therapeutic mechanisms of baicalin in improving PC.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Funding

The authors reported no funding associated with the work featured in this article.

References

 

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