Melanoma, a type of skin cancer originating from melanocytes, represents a significant public health concern according to the World Health Organization. It is one of the most commonly diagnosed cancers worldwide, particularly affecting populations in Europe and North America, with an increasing incidence in Asia. The rise emphasizes the need for diversified treatment approaches. Conventional treatments for melanoma, including immunotherapy, chemotherapy, and targeted therapies like the FDA-approved Opdivo and Relatlimab, often come with severe side effects and high relapse rates. Consequently, natural products have gained considerable attention for their potential to enhance therapeutic outcomes and reduce adverse effects. This systematic review evaluates the anti-cancer properties of natural products against melanoma, examining 52 studies from PubMed and Google Scholar. Our analysis focuses on the antioxidant, anti-angiogenesis, anti-metastatic, and apoptosis-inducing activities of these compounds, also discussing the regulatory factors involved. The findings advocate for intensified research into natural products as complementary agents in melanoma treatment, aiming to improve efficacy and patient quality of life. Further in vitro, in vivo, and clinical trials are essential to validate their effectiveness and integrate them into standard care protocols.

Although immunotherapy has become the standard of treatment for non-small cell lung cancer (NSCLC), only a limited number of patients benefit from it clinically because of the resistance to immunotherapeutic agents. Of late, the usefulness of herbal medicines in combination with immunotherapy has been investigated. Bojungikki-Tang (BJIKT) is a widely used traditional herbal medicine. It synergistically enhances the antitumor effects of chemotherapy and regulates the immune responses in cancer, but its antitumor effect with immunotherapy in NSCLC is unclear. In this study, we investigated the combined effects of BJIKT and an anti-PD-1 antibody in a KLN205-DBA/2 syngeneic lung cancer model. Immunohistochemistry and flow cytometry analyses were performed to analyze the changes in immune cells in the tumor microenvironment. BJIKT plus an anti-PD-1 antibody treatment significantly inhibited tumor growth, unlike the respective monotherapies. Compared to monotherapy, the combination treatment resulted in a higher population of CD8⁺ cytotoxic T cells and a lower number of Ki67⁺ cells in the tumor tissues. Furthermore, the combination treatment decreased the proportion of myeloid-derived suppressor cells but increased the proportion of M1-like macrophages compared to that observed with monotherapy. Cytokine analysis showed that the combination treatment increased the levels of T helper type 1-related cytokines. Network pharmacology analysis revealed that BJIKT might regulate multiple signaling pathways related to immune function and tumor progression in NSCLC. These findings indicate that the combination treatment with BJIKT and an anti-PD-1 antibody effectively suppresses tumor growth by regulating immune function and may be an alternative therapeutic option for the treatment of NSCLC.

Redox dysregulation, ferroptosis evasion, and immune suppression are major barriers in cancer therapy. SH003, a multi-herbal formulation standardized under GMP conditions and evaluated in early-phase clinical studies (NCT03081819; KCT0004770), demonstrated a favorable safety profile supporting its translational potential. Preclinical studies reveal that SH003 disrupts mitochondrial homeostasis, triggers endoplasmic reticulum stress apoptosis, and sensitizes resistant tumors to ferroptosis via suppression of the SLC7A11–GPX4 axis and NRF2 destabilization. In parallel, SH003 remodels tumor immunity by attenuating STAT3-driven PD-L1 signaling, promoting macrophage repolarization, and enhancing cytotoxic lymphocyte activity. Exosome-associated microRNAs further suggest SH003’s role in redox–immune communication, although functional validation is pending. Collectively, SH003 represents a clinically tested phytomedicine that integrates ferroptosis induction with immune modulation, offering a biomarker-informed approach to precision oncology.

Paclitaxel (PTX) is widely used for gastric cancer treatment; however, PTX resistance (PTXR) significantly limits clinical efficacy. To investigate the pot

Background: The compound 4′-O-methylbroussochalcone B (4′-O-M) is a chalcone-type flavonoid isolated from Psoralea corylifolia , a traditional Asian medicinal herb. While studies have reported its antioxidant and anti-inflammatory activities, its effects on macrophage inflammatory signaling and NLRP3 inflammasome activation remain unclear. Therefore, in this in vitro study, we aimed to clarify the anti-inflammatory actions and underlying molecular mechanisms of 4′-O-M in lipopolysaccharide (LPS)/adenosine triphosphate (ATP)-stimulated J774A.1 macrophages, with a particular emphasis on mitochondrial reactive oxygen species (mtROS)-dependent NLRP3 inflammasome activation and MAPK/NF-κB signaling pathways. Methods: J774A.1 macrophages were pretreated with graded concentrations of 4′-O-M, followed by LPS priming and ATP stimulation to activate the inflammasome. Levels of nitric oxide (NO), prostaglandin E ₂ (PGE ₂ ), and cytokines (interleukin [IL]-6, tumor necrosis factor-α [TNF-α], IL-1β, IL-18) in J774A.1 macrophages were quantified by ELISA. MAPK/NF-κB phosphorylation and inflammasome-related proteins (NLRP3, ASC, caspase-1, IL-1β, gasdermin D) were assessed by immunoblotting. mtROS production was evaluated using the MitoSOX™ Red assay. Results: 4′-O-M markedly reduced LPS-induced inflammatory mediators, suppressing NO and PGE ₂ production and IL-6 and TNF-α secretion by inhibiting MAPK and NF-κB phosphorylation. As the response progressed to the inflammasome activation stage, 4′-O-M further reduced IL-1β and IL-18 release and limited caspase-1 activation. Additionally, 4′-O-M decreased the production of mtROS, an upstream signal associated with NLRP3 activation, suggesting that this reduction may contribute to its inhibitory effects on the inflammasome pathway. Conclusion: 4′-O-M mitigates macrophage inflammatory responses in vitro via the dual suppression of MAPK/NF-κB-mediated priming and mtROS-dependent NLRP3 inflammasome activation. Thus, 4′-O-M is a promising natural scaffold for developing therapeutics targeting inflammasome-driven inflammatory diseases.