Colorectal cancer (CRC) is one of the most common malignant carcinomas. CRC is characterized by asymptomatic onset, and most patients are already in the middle and advanced stages of disease when they are diagnosed. Inflammatory bowel disease (IBD) and the inflammatory-cancer transformation of advanced colorectal adenoma are the main causes of CRC. There is an urgent need for effective prevention and intervention strategies for CRC. In recent years, rapid research progress has increased our understanding of gut microbiota. Meanwhile, with the deepening of research on the pathogenesis of colorectal cancer, gut microbiota has been confirmed to play a direct role in the occurrence and treatment of colorectal cancer. Strategies to regulate the gut microbiota have potential value for application in the prevention and treatment of CRC. Regulation of gut microbiota is one of the important ways for natural products to exert pharmacological effects, especially in the treatment of metabolic diseases and tumours. This review summarizes the role of gut microbiota in colorectal tumorigenesis and the mechanism by which natural products reduce tumorigenesis and improve therapeutic response. We point out that the regulation of gut microbiota by natural products may serve as a potential means of treatment and prevention of CRC.

Colorectal cancer (CRC) is a common cancer of the digestive system that endangers human health. Immunotherapy is widely used in the treatment of patients with cancer. Some patients with dMMR/MSI-H CRC benefit from treatments that use immune checkpoint inhibitors, but most CRC patients are not sensitive to immunotherapy. Furthermore, internal resistance and immune escape lead to a reduced immunotherapy response. Therefore, the development of an effective combination therapy to improve the response rate to immunotherapy is a goal of cancer research. Natural products are potential candidates for comprehensive cancer treatments due to their wide range of immunomodulatory effects through multifactorial underlying mechanisms. In this review, we summarize the challenges in the treatment of CRC and assess the immunomodulatory effects of natural products and their active components. Our work suggests that natural products represent potential options for combined CRC immunotherapy.

In lean individuals, NAFLD is not a benign disease,and these patients have longterm morbidity and mortality similar to those of their nonlean counterparts.It is urgent to find biomarkers for noninvasive and early detection. miRNAs are useful biomarkers for detection.The aims of this study were to investigate the potential role of serum miRNAs in the detection of lean NAFLD and to explore the possible pathogenesis of lean NAFLD.Here, a total of 498 patients with NAFLD and 98 healthy controls were included to compare the clinical characteristics of lean NAFLD patients(BMI < 23 kg/m2),nonlean NAFLD patients(BMI ≥ 23kg/m2) and normal healthy individuals.A total of fourteen serum samples were collected for high-throughput profiling to identify altered miRNA expression patterns in lean NAFLD.The candidate miRNA miR-4488 was identified by filtering based on studies in a second independent cohort(31LNs,62NLNs and 72HIs) that included qRT-PCR analysis.GO enrichment, KEGG enrichment, and PPI network analyses were performed to investigate the potential molecular mechanism of miR-4488 in lean NAFLD. miR-4488 was selected as the candidate biomarker for lean NAFLD. The serum level of miR-4488 was increased in LNs compared to HIs(P < 0.0001) and to NLNs(P = 0.025).miR-4488 had acceptable performance in predicting[area under the curve(AUC) = 0.794,0.698]lean NAFLD. Moreover,GO and KEGG enrichment analyses revealed that the differentially expressed target genes were mainly involved in choline metabolism in cancer, the TNF signaling pathway and the p53 signaling pathway.PPI analysis identified ARHGAP1, SLC10A1 and SIX5 as the hub genes.Taken together, our findings indicate that serum miR-4488 is a potential biomarker for diagnosing and predicting the pathogenetic mechanisms of lean NAFLD.