The roles of CDR1, CDR2, and MDR1 in kaempferol-induced suppression with fluconazole-resistant Candida albicans. . ???aop.label???. doi: 10.3109/13880209.2015.1091483

Lung cancer is one of the most prevalent malignancies worldwide. Despite the undeniable progress in lung cancer research made over the past decade, it is still the leading cause of cancer-related deaths and continues to challenge scientists and researchers engaged in searching for therapeutics and drugs. The tumor microenvironment (TME) is recognized as one of the major hallmarks of epithelial cancers, including the majority of lung cancers, and is associated with tumorigenesis, progression, invasion, and metastasis. Targeting of the TME has received increasing attention in recent years. Natural products have historically made substantial contributions to pharmacotherapy, especially for cancer. In this review, we emphasize the role of the TME and summarize the experimental proof demonstrating the antitumor effects and underlying mechanisms of natural products that target the TME. We also review the effects of natural products used in combination with anticancer agents. Moreover, we highlight nanotechnology and other materials used to enhance the effects of natural products. Overall, our hope is that this review of these natural products will encourage more thoughts and ideas on therapeutic development to benefit lung cancer patients.

Vulvovaginal candidiasis (VVC) is an inflammatory disease of the vagina mainly caused by Candida albicans (C. albicans), which affects around three-quarters of all women during their reproductive age. Although some antifungal drugs such as azoles have been applied clinically for many years, their therapeutic value is very limited due to the emergence of drug-resistant strains. Previous studies have shown that the adhesion of C. albicans to vaginal epithelial cells is essential for the pathogenesis of VVC. Therefore, preventing the adhesion of C. albicans to vaginal epithelial cells may be one of the most effective strategies for the treatment of VVC. Berberine (BBR) is a biologically active herbal alkaloid that was used to treat VVC. However, so far, its mechanism has remained unclear. This study shows BBR significantly inhibits the adhesion of C. albicans to vaginal epithelial cells by reducing the expressions of ICAM-1, mucin1, and mucin4 in vaginal epithelial cells, which play the most important role in modulating the adhesion of C. albicans to host cells, and balancing IL-2 and IL-4 expressions, which play a key effect on regulating the inflammatory response caused by C. albicans infection. Hence, our findings demonstrate that BBR may be a potential therapeutic agent for VVC by interfering with the adhesion of C. albicans to vaginal epithelial cells and represents a new pathway for developing antifungal therapies agents from natural herbs.

Pathogenic fungi represent a growing concern for human health, necessitating a deeper understanding of their molecular mechanisms of virulence to formulate effective antifungal strategies. Recent research has increasingly highlighted the role of phospholipid components in fungal cell membranes, which are not only vital for maintaining cellular integrity but also significantly influence fungal pathogenicity. This review focuses on the impact of membrane phospholipid composition on fungal growth, morphogenesis, stress responses, and interactions with host cells. To be specific, membrane phospholipid composition critically influences fungal virulence by modulating growth dynamics and morphogenesis, such as the transition from yeast to hyphal forms, which enhances tissue invasion. Additionally, phospholipids mediate stress adaptation, enabling fungi to withstand host-derived oxidative and osmotic stresses, crucial for survival within hostile host environments. Phospholipid asymmetry also impacts interactions with host cells, including adhesion, phagocytosis evasion, and the secretion of virulence factors like hydrolytic enzymes. These adaptations collectively enhance fungal pathogenicity by promoting colonization, immune evasion, and damage to host tissues, directly linking membrane architecture to infection outcomes. By elucidating the molecular mechanisms involved, we aim to underscore the potential of targeting phospholipid metabolic pathways as a promising avenue for antifungal therapy. A comprehensive understanding of how membrane phospholipid composition regulates the virulence of pathogenic fungi can provide valuable insights for developing novel antifungal strategies.