No abstract

No abstract

Colorectal cancer (CRC) is the most commonly diagnosed tumor worldwide. However, the molecular mechanisms and biological processes of CRC remain unknown. The present study used reverse transcription-quantitative polymerase chain reaction to determine the expression levels of microRNA (miR)-296 in CRC cell lines and tissues. In addition, a miR-296 mimic was transfected into CRC cells, and the effects of miR-296 on cell proliferation and apoptosis were explored by MTT assay and flow cytometry. Luciferase assays were also performed to validate arrestin β1 (ARRB1) as a miR-296 target in SW480 and HCT-116 cells. The results demonstrated that miR-296 is a critical tumor suppressor which was downregulated in CRC patients. Increased expression levels of miR-296 were positively associated with a longer survival time of CRC patients. In addition, it was demonstrated that ARRB1 is a direct downstream target of miR-296. Upregulation of miR-296 in SW480 and HCT-116 cells resulted in suppressed cell growth and increased cell apoptosis through an ARRB1-dependent mechanism. Furthermore, the molecular mechanisms underlying the antitumor effect of miR-296 in CRC are at least in part due to the inactivation of the RAC-α serine/threonine-protein kinase (AKT) signaling pathway induced by the suppression of ARRB1 expression. Overall, the present study, to the best of the author's knowledge, is the first to demonstrate that the miR-296-ARRB1-AKT signaling pathway forms a critical feedback loop and mediates CRC carcinogenesis, and these findings may introduce a potential therapeutic strategy for the treatment of CRC.

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) with a complex aetiology that commonly recurs. Most drugs for UC treatment interfere with metabolism and immune responses, often causing some serious adverse reactions. Therefore, the development of alternative treatments, including nutritional supplements and probiotics, have been one of the main areas of current research due to fewer side effect. As both a Chinese medicine and a food, edible bird’s nest (EBN) has high nutritional value. Modern pharmacological studies have shown that it has anti-inflammatory, immunoregulatory, antiviral and neuroprotective effects. In this study, UC was induced with dextran sulfate sodium (DSS) to investigate the protective effect of EBN on colitis mice and the related mechanism. The body weight, faecal morphology and faecal occult blood results of mice were recorded every day from the beginning of the modelling period. After the end of the experiment, the length of the colon was measured, and the colon was collected for histopathological detection, inflammatory factor detection and immunohistochemical detection. Mouse spleens were dissected for flow cytometry. The results showed that in mice with colitis, EBN improved symptoms of colitis, reduced colonic injury, and inhibited the increases in the levels of the pro-inflammatory cytokines IL-1β and TNF-α. The T helper 17 (Th17)/regulatory T (Treg) cell balance was restored by decreasing the expression of IL-17A and IL-6 in intestinal tissues, increasing the expression of TGF-β, and decreasing the number of Th17 cells in each EBN dose group. These findings suggest that EBN has a protective effect on DSS-mediated colitis in mice, mainly by restoring the Th17/Treg cell balance.

Researchers have demonstrated that long non-coding RNAs (lncRNAs) are vital in colorectal cancer (CRC) progression. Here, we aimed to explore the function of lncRNA PAX6 upstream antisense RNA (PAUPAR) in the development of CRC. In the present study, PAUPAR and microRNA (miR)-17-5p expression levels in CRC tissues and cells were examined using quantitative real-time polymerase chain reaction (qRT-PCR). Western blot analysis was adopted to examine ZNF750 expression at the protein level in CRC cells. CRC cell proliferation was examined by colony formation experiment and 5-Bromo-2-deoxyUridine (BrdU) experiment. CRC cell migration and invasion were assessed by Transwell experiments. Apoptosis was measured using the TUNEL experiment. The targeting relationship between PAUPAR and miR-17-5p was confirmed using dual-luciferase reporter gene and RNA immunoprecipitation (RIP) experiments. We demonstrated that PAUPAR was markedly down-modulated in CRC, and its low expression was significantly related to increased T stage and local lymph node metastasis. Knockdown of PAUPAR enhanced CRC cell proliferation, migration and invasion, and restrained apoptosis relative to controls, whereas PAUPAR overexpression caused the opposite effects. Moreover, rescue experiments showed that miR-17-5p inhibitor could reverse the role of PAUPAR knockdown on the malignant phenotypes of CRC cells. Additionally, PAUPAR could positively regulate the expression of ZNF750 via repressing miR-17-5p. Taken together, these findings suggest that PAUPAR/miR-17-5p/ZNF750 axis is a novel mechanism implicated in CRC progression.