As two pivotal regulatory factors in cancer biology, oxidative stress and inflammation interact dynamically through complex network mechanisms to influence tumor initiation, progression, and treatment resistance. Oxidative stress induces genomic instability, oncogenic signaling activation, and tumor microenvironment (TME) remodeling via the abnormal accumulation of reactive oxygen species (ROS) or reactive nitrogen species (RNS). Conversely, inflammation sustains malignant phenotypes by releasing pro-inflammatory cytokines and chemokines and promoting immune cell infiltration. These processes create a vicious cycle via positive feedback loops whereby oxidative stress initiates inflammatory signaling, while the inflammatory milieu further amplifies ROS/RNS production, collectively promoting proliferation, migration, angiogenesis, drug resistance, and immune evasion in tumor cells. Moreover, their crosstalk modulates DNA damage repair, metabolic reprogramming, and drug efflux pump activity, significantly impacting the sensitivity of cancer cells to chemotherapy, radiotherapy, and targeted therapies. This review systematically discusses these advances and the molecular mechanisms underlying the interplay between oxidative stress and inflammation in cancer biology. It also explores their potential as diagnostic biomarkers and prognostic indicators and highlights novel therapeutic strategies targeting the oxidative stress–inflammation axis. The goal is to provide a theoretical framework and translational roadmap for developing synergistic anti-tumor therapies.

Colorectal cancer (CRC) is the third most common malignant tumor worldwide, with morbidity and mortality rates increasing annually. Consequently, the development of safe and effective natural anti-tumor drugs has become a critical research focus. Lignin, a polyphenolic polymer abundant in nature, possesses a unique chemical structure that imparts antioxidant, anti-inflammatory, and tumor cell-related bioactivities, demonstrating remarkable potential in the prevention and treatment of CRC. In this study, we investigated the anti-tumor cell effects of coffee grounds lignin nanoparticles (CLN), prepared using aqueous ethanol extraction from coffee waste, against three CRC cell lines (HCT116, HT29, SW620). The results indicated that CLN potently inhibited the proliferation of all three CRC cell lines mentioned above. This research supports the transformation of lignin from natural products into innovative anti-colorectal cancer agent, offering new insights for the development of novel therapeutic strategies characterized by low toxicity and high efficacy. As research advances and technology continues to innovate, lignin-based nanoparticles emerge as key natural products in CRC therapy, offering new hope for patients and paving the way for the application of natural products in cancer therapy.

(E)-Flavokawain A (FKA), the primary chalcone constituent of Piper methysticum, exhibits diverse pharmacological properties and holds significant potential for therapeutic development. Objectives: This study aims to investigate the anti-colorectal cancer effects and mechanisms of FKA. Methods: Using AOM/DSS-induced colorectal cancer models in C57 mice, the research examines the impact of different FKA doses, employing 16S rRNA and metabolomics to explore the potential mechanism. Results: The findings indicated that FKA significantly inhibited the progression of colorectal cancer in C57 mice by modulating the composition of the gut microbiota. This modulation involved the suppression of endotoxin secretion by pathogenic bacteria and the concurrent augmentation of beneficial bacteria. Furthermore, in the context of metabolic pathways, FKA regulates lipid metabolism and arachidonic acid metabolism, thereby mitigating the inflammatory transformation associated with colorectal cancer. Conclusions: These findings provide valuable insights supporting the potential of FKA as a viable preventive strategy against CRC.

Hepatocellular carcinoma (HCC) is a highly lethal malignancy presenting a considerable challenge due to limited therapeutic options. This study investigates the anti‐cancer mechanisms of Lupeol, a natural triterpenoid. Our results demonstrated that Lupeol exhibited significant anti‐proliferative effects on HepG2 cells with an IC ₅₀ of 42.82 μM at 24 h. Furthermore, Lupeol treatment significantly inhibited cell migration and suppressed the secretion of exosomes, as evidenced by the downregulation of exosome markers (CD63, TSG101) ( p < 0.05). Mechanistic analysis revealed that Lupeol induces autophagy, marked by the upregulation of LC3‐II and Beclin‐1. Importantly, blocking autophagy with the inhibitor 3‐MA prevented the Lupeol‐induced reduction of CD63 and restored exosome secretion ( p < 0.05). These findings suggest that Lupeol inhibits HCC progression by inducing autophagy to suppress exosome secretion, rather than merely acting as a correlative factor. This study elucidates a novel mechanism where Lupeol redirects multivesicular bodies toward the autophagic‐lysosomal pathway, highlighting its potential as an effective therapeutic strategy for HCC.

Harmful algal blooms have occurred more frequently in recent decades and threaten aquaculture, tourism and human health. As a promising control method, most studies on allelopathic mechanisms have focused on the physiological effects on harmful algae. This study employed a multiomics approach to investigate the allelopathic response of the dinoflagellate Scrippsiella acuminata to the allelochemical protocatechuic acid, a phenolic compound known for its inhibitory effects on algal growth. Using transcriptomic, proteomic, and metabolomic analyses, we identified significant changes in gene expression (5247 upregulated and 81 downregulated), protein expression (56 upregulated and 49 downregulated), and metabolite profiles (320 upregulated and 168 downregulated) in response to allelochemical stress. Transcriptomic data revealed an upregulation of genes associated with antioxidant systems and energy metabolism, suggesting a potential antioxidant response to protocatechuic acid exposure. Proteomic analysis highlighted the impact on photosynthesis, energy metabolism, and genetic information processing, with a particular emphasis on the modulation of lipid and carbohydrate metabolism to adapt to stress. Metabolomic profiling corroborated these findings, demonstrating shifts in lipid and amino acid metabolism indicative of an adaptive strategy for energy storage and maintenance of cellular homeostasis under allelochemical stress. Notably, alterations in photosynthesis-related proteins and metabolites indicated a direct effect of protocatechuic acid on the photosynthetic machinery, potentially impairing algal growth and energy production. In conclusion, our multiomics analysis provides a comprehensive view of the complex response of S. acuminata to allelochemical stress, revealing the intricate interplay among genetic, proteomic, and metabolic adjustments. These insights contribute to the understanding of allelopathic interactions and offer potential avenues for the development of novel strategies to manage harmful algal blooms.