Yiyi Fuzi Baijiang Decoction (YFBD), an ancient prescription developed by the ancient Chinese physician, Zhang Zhongjing, has shown remarkable effects in treating ulcerative colitis (UC). However, there are few studies on its mechanism. This study was designed to explore the potential mechanism of YFBD in treating UC. The principal ingredients of YFBD were analyzed using high-performance liquid chromatography (HPLC). Dextran sulfate sodium- (DSS-) induced mice and lipopolysaccharide- (LPS-) stimulated RAW264.7 cells were used in the study. The body weight and disease activity index (DAI) of mice were recorded and analyzed for 10 days. After sacrifice, the colonic tissues were harvested. The colon length was measured, and the histopathological changes were observed by hematoxylin and eosin staining. The levels of inflammatory cytokines in mice colons and RAW246.7 cells were determined by real-time quantitative PCR and immunofluorescence. The effects of YFBD on the TLR4-mediated PI3K/Akt and NF-κB pathways were determined by western blot analysis. HPLC identified five compounds in YFBD: chlorogenic acid, caffeic acid, benzoylmesaconine, benzoyl aconitine, and quercetin. YFBD alleviated weight loss, colon shortening, and colonic histopathological lesion in mice. Meanwhile, it decreased the DAI and histological score of mice with UC. In addition, YFBD remarkably decreased the levels of interleukin- (IL-) 6, IL-1β, and tumor necrosis factor (TNF)-α in the colons of DSS-induced mice and LPS-stimulated RAW246.7 cells. Furthermore, the expression of key proteins in TLR4-mediated PI3K/Akt and NF-κB pathways significantly decreased with YFBD treatment. In conclusion, YFBD had protective effects on mice with UC, which was in part related to its anti-inflammatory effects and downregulation of TLR4-mediated PI3K/Akt and NF-κB pathways.

Cholesterol metabolism reprogramming helps tumor cells meet their high energy and biosynthetic needs. Many studies link high cholesterol levels to a higher risk of cancers, such as breast, prostate, and colorectal cancer. Dysregulated cholesterol metabolism contributes to cancer development and progression. Various non-coding RNAs (ncRNAs), such as miRNAs, lncRNAs, circRNAs, piRNAs, and tRNAs, are key players in this process. However, systematic reviews of ncRNAs’ functions in cholesterol metabolism and their impact on tumor progression are limited. This review aims to address this gap by summarizing the current understanding of how ncRNAs govern cholesterol metabolism in cancer. We provide a comprehensive overview of cholesterol metabolism reprogramming in tumor progression through its influence on growth, metastasis, drug resistance, and immune evasion. Moreover, we summarize recent advances in understanding how ncRNAs regulate cholesterol metabolism in cancer, highlighting potential therapeutic targets for cancer treatment.

Stimulus-responsive sonodynamic immunotherapy is a promising non-invasive strategy that combines ultrasound-activated Sonodynamic therapy (SDT) with a smart stimulus-responsive nanodelivery system to overcome the limitations of traditional cancer therapies. By utilizing signals from the tumor microenvironment (TME), such as acidic pH, high glutathione (GSH) levels, enzyme overexpression, and hypoxia, stimulus-responsive nanosonic sensitizers enable precise, on-demand release and deep tumor penetration. Ultrasound activation generates reactive oxygen species (ROS) and cavitation effects, inducing immunogenic cell death (ICD), characterized by damage-associated molecular patterns (DAMPs) and exposure/release of tumor-associated antigens (TAAs). This approach can transform “cold” tumors into “hot” tumors, promoting dendritic cell maturation, cytotoxic T lymphocyte (CTL) infiltration, and systemic antitumor immunity, including remote effects and long-term immune memory. When combined with immune checkpoint blockade (ICB), chemodynamic therapy (CDT), gas therapy, photothermal (PTT)/photodynamic therapy (PDT), or gene therapy, stimulus-responsive sonodynamic immunotherapy can significantly improve tumor suppression rates, reduce metastasis, and minimize systemic toxicity. Despite significant progress in preclinical studies, clinical translation still faces numerous challenges, including low ICD efficiency in hypoxic tumors, TME heterogeneity, parameter standardization, and optimization of the dual role of High migration group box 1 (HMGB1). This review summarizes the mechanisms, stimulus-response strategies, multimodal synergistic effects, and current clinical progress of stimulus-responsive sonodynamic immunotherapy, highlighting its opportunities and key challenges in future precision cancer treatment.

Lipid metabolism reprogramming is one of the most prominent characteristics of cancer, but it is still unclear which regulatory pathways underlie this process in cancer cells. Circular RNAs (circRNAs) represent a novel category of non‐coding RNAs with multifaceted regulatory functions. While the biological roles of circRNAs in cancer have been elucidated, there remains a dearth of knowledge regarding their involvement and regulatory mechanisms in lipid metabolism within the context of cancer. This article provides an overview of the regulatory roles and specific mechanisms of circRNAs in cancer lipid metabolism reprogramming. By elucidating these mechanisms, it enhances our comprehension of the metabolic rewiring driving tumour development and uncovers new avenues for targeted therapy.