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Glycyrrhiza Uralensis Polysaccharide (GCP), as a macromolecular polysaccharide extracted from the Traditional Chinese Medicine (TCM) - Licorice has been proved to inhibit tumor growth in vitro and in vivo; however, the specific anti-tumor mechanism of GCP needs to be further investigated. In this study, we explore the anti-tumor mechanism of GCP from the angle of gut microbiota. Colon carcinoma cells (CT-26) were used to set up a tumor-bearing mouse model. After 14 days of GCP treatment, the weights of tumors were significantly reduced. In addition, HE staining of tissue sections reflected that GCP could effectively inhibit tumor metastasis. 16SrRNA high-throughput sequencing of fecal samples showed a significant change between the model group and GCP group in the composition of gut microbiota. Subsequently, gut microbiota depletion and fecal transplantation experiments further confirmed the relationship between the anti-tumor effects of GCP and gut microbiota. Following depletion of gut microbiota, GCP cannot inhibit tumor growth. Fecal transplantation experiments found that transplanting the feces of GCP-treated mice, to a certain extent, could inhibit tumor growth and metastasis. These results indicate that Glycyrrhiza Polysaccharides exert anti-tumor effects by affecting gut microbiota composition. Keywords: Glycyrrhiza Uralensis Polysaccharides, Gut microbiota, Cancer, TCM, Anti-tumor

Long non-coding RNAs (lncRNAs) are involved in development of non-small cell lung cancer (NSCLC) by interacting with microRNAs (miRNAs) and/or mRNAs. However, the function of most lncRNAs in NSCLC remains unclear. Reverse transcription-quantitative PCR (RT-qPCR) and western blot were applied for detection of mRNA/miRNA and protein level. Interaction between LncRNA small nucleolar RNA host gene 14 (SNHG14) and miR-382-5p was validated by dual luciferase reporter assay. Cell proliferation and apoptosis was detected using Cell Counting Kit 8 (CCK8) and Flow cytometry, while cell migration and invasion was detected by scratch assay and Transwell assay. SNHG14 was upregulated in NSCLC tissues and cell lines. SNHG14 silencing reduced proliferation, migration and invasion, and induced apoptosis in A549 cells. SNHG14 was negatively correlated with miR-382-5p in NSCLC tissues, SNHG14 and miR-382-5p negatively regulated each other in A549 cells. SNHG14 promoted expression of miR-382-5p target genes, including LIM-only protein 3 (LMO3) and SET domain containing lysine methyltransferase 8 (SETD8), in A549 cells. miR-382-5p inhibition reversed SNHG14 knockdown-induced increase in apoptosis and decrease in proliferation, migration and invasion. SNHG14 was correlated with SETD8 and LMO3 in NSCLC tissues. Collectively, SNHG14 promoted NSCLC proliferation, migration and invasion, while inhibited apoptosis by sponging miR-382-5p in A549 cells. [ABSTRACT FROM AUTHOR]