Accumulating evidence indicates that the gut microbiota can promote or inhibit colonic inflammation and carcinogenesis. Promotion of beneficial gut bacteria is considered a promising strategy to alleviate colonic diseases including colitis and colorectal cancer. Interestingly, dietary polyphenols, which have been shown to attenuate colitis and inhibit colorectal cancer in animal models and some human studies, appear to reach relatively high concentrations in the large intestine and to interact with the gut microbial community. This review summarizes the modulatory effects of polyphenols on the gut microbiota in humans and animals under healthy and diseased conditions including colitis and colitis-associated colorectal cancer (CAC). Existing human and animal studies indicate that polyphenols and polyphenol-rich whole foods are capable of elevating butyrate producers and probiotics that alleviate colitis and inhibit CAC, such as Lactobacillus and Bifidobacterium. Studies in colitis and CAC models indicate that polyphenols decrease opportunistic pathogenic or proinflammatory microbes and counteract disease-induced dysbiosis. Consistently, polyphenols also change microbial functions, including increasing butyrate formation. Moreover, polyphenol metabolites produced by the gut microbiota appear to have anticancer and anti-inflammatory activities, protect gut barrier integrity, and mitigate inflammatory conditions in cells and animal models. Based on these results, we conclude that polyphenol-mediated alteration of microbial composition and functions, together with polyphenol metabolites produced by the gut microbiota, likely contribute to the protective effects of polyphenols on colitis and CAC. Future research is needed to validate the causal role of the polyphenol–gut microbiota interaction in polyphenols’ anti-colitis and anti-CAC effects, and to further elucidate mechanisms underlying such interaction.

Glioma is one of the most common primary malignancies of the central nervous system, which has aggressive clinical behavior and a poorer prognosis. MicroRNAs (miRs) are a class of small noncoding RNAs that function as mediators of gene expression, which can be sponged by circRNA provided with a closed circular structure. Dysregulations of circular RNAs (circRNAs) and miRs have been implicated in the development and progression of glioma. In the current study, we investigated the role of circular RNA hsa_circ_0076248 in mediating the oncogenesis of glioma by sponging miR‐181a to modulate silent information regulator 1 (SIRT1) expression in vitro and in vivo. The quantitative real‐time polymerase chain reaction results showed that the expression of miR‐181a was significantly decreased in glioma tissues and cell lines compared with normal brain tissues and normal gliocyte, respectively, and the expression of hsa_circ_0076248 and SIRT1 demonstrated the opposite. Bioinformatics analysis identified hsa_circ_0076248 could sponge miR‐181a, and miR‐181a could target the mRNA of SIRT1. Our results verified that downregulating hsa_circ_0076248 or upregulating miR‐181a could depress the proliferation and invasion of glioma in vitro and in vivo. The experiment also showed that downregulating hsa_circ_0076248 or upregulating miR‐181a could remarkably promote the temozolomide chemotherapy sensitivity. Furthermore, Western blot analysis testified that downregulating hsa_circ_0076248 or upregulating miR‐181a could promote the expression of p53 and SIRT1. In summary, our study sheds light on the regulatory mechanism of hsa_circ_0076248 in glioma growth and invasion via sponging miR‐181a, which downregulates the SIRT1 expression and also suggests that hsa_circ_0076248, miR‐181a, and SIRT1 may serve as potential therapeutic targets for glioma.

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Radioresistance‐induced residual and recurrent tumours are the main cause of treatment failure in nasopharyngeal carcinoma (NPC). Thus, the mechanisms of NPC radioresistance and predictive markers of NPC prognosis and radioresistance need to be investigated and identified. In this study, we identified RPA3 as a candidate radioresistance marker using RNA‐seq of NPC samples. In vitro studies further confirmed that RPA3 affected the radiosensitivity of NPC cells. Specifically, the overexpression of RPA3 enhanced radioresistance and the capacity for DNA repair of NPC cells, whereas inhibiting RPA3 expression sensitized NPC cells to irradiation and decreased the DNA repair capacity. Furthermore, the overexpression of RPA3 enhanced RAD51 foci formation in NPC cells after irradiation. Immunohistochemical assays in 104 NPC specimens and 21 normal epithelium specimens indicated that RPA3 was significantly up‐regulated in NPC tissues, and a log‐rank test suggested that in patients with NPC, high RPA3 expression was associated with shorter overall survival (OS) and a higher recurrence rate compared with low expression (5‐year OS rates: 67.2% versus 86.2%; 5‐year recurrence rates: 14.8% versus 2.3%). Moreover, TCGA data also indicated that high RPA3 expression correlated with poor OS and a high recurrence rate in patients with head and neck squamous cell carcinoma (HNSC) after radiotherapy. Taken together, the results of our study demonstrated that RPA3 regulated the radiosensitivity and DNA repair capacity of NPC cells. Thus, RPA3 may serve as a new predictive biomarker for NPC prognosis and radioresistance to help guide the diagnosis and individualized treatment of patients with NPC.