We aimed at the effects of long non-coding RNA (lncRNA) SNHG5 on proliferation, metastasis and migration of colorectal cancer (CRC) cells. We also investigated regulatory relationships among miR-132-3p, SNHG5 and CREB5 and their roles in CRC. 25 pairs of samples containing CRC tissues and matched para-tumor tissues were obtained to examine SNHG5, miR-132-3p and CREB5 expression by qRT-PCR or Western blot. The targeted relationship between miR-132-3p and SNHG5 or CREB5 was confirmed by dual luciferase report assay as well as RNA pull down assay. The expression of SNHG5, miR-132-3p and CREB5 in CRC cells were regulated by cell transfection. CRC cellular proliferation was assayed by CCK-8 and meanwhile flow cytometry was adopted to observe apoptosis. Metastasis and migration of CRC cells were determined respectively by means of Transwell assay and scratch test. The effects of SNHG5 on CRC were researched in vivo, too. SNHG5 or CREB5 was up-regulated in CRC tissues and cells, whereas miR-132-3p was down-regulated. Overexpression of SNHG5 and CREB5 resulted in the enhancement of proliferation, metastasis, migration and the inhibition of apoptosis in CRC cells, while miR-132-3p led to the opposite result. LncRNA SNHG5 promoted proliferation, migration and metastasis of CRC cells but inhibited apoptosis by modulating miR-132-3p/CERB5.

Objectives Circular RNAs (circRNAs) exist extensively in the eukaryotic genome. The study aimed to identify the role of hsa_circ_0008365 (Circ‐SERPINE2) in gastric carcinoma (GC) cells and its downstream mechanisms. Materials and methods Gene Expression Omnibus (GEO) database was applied to screen differentially expressed circRNAs. CircInteractome, TargetScan and miRecords websites were used to predict target relationships. qRT‐PCR and RNase R treatment were utilised to detect molecule expression and confirm the existence of circ‐SERPINE2. RNA pull‐down assay and dual‐luciferase reporter assay were performed for interaction between circRNA and miRNA or mRNA. EdU assay, colony formation assay, and flow cytometry for apoptosis and cell cycle detections were utilised to assess cell function. Western blot and immunohistochemistry (IHC) assays were applied for detection of proteins in tissues or cells. Results Circ‐SERPINE2 and YWHAZ were upregulated, and miR‐375 was downregulated in GC tissues and cells. Circ‐SERPINE2 and YWHAZ targetedly bound to miR‐375. Circ‐SERPINE2 promoted cell proliferation and cell cycle progress and inhibited cell apoptosis by sponging miR‐375 and regulating YWHAZ expression in vitro. Circ‐SERPINE2 repressed solid tumour growth through enhancing miR‐375 expression and reducing YWHAZ expression in vivo. Conclusions Circ‐SERPINE2 is a novel proliferative promoter through the regulation of miR‐375/ YWHAZ . Circ‐SERPINE2/miR‐375/ YWHAZ axis might provide a novel therapeutic target of GC.

Gastric cancer (GC) is a common heterogeneous disease. The critical roles of microRNA‐340 (miR‐340) in the development and progression of GC were emphasized in accumulating studies. This study aims to examine the regulatory mechanism of miR‐340 in GC cellular processes. Initially, microarray technology was used to identify differentially expressed genes and regulatory miRs in GC. After that, the potential role of miR‐340 in GC was determined via ectopic expression, depletion, and reporter assay experiments. Expression of secreted phosphoprotein 1 (SPP1), miR‐340, phosphatidylinositol 3‐kinase/protein kinase B (PI3K/AKT) pathway, and epithelial–mesenchymal transition (EMT)‐related genes was measured. Moreover, to further explore the function of miR‐340 in vivo and in vitro, proliferation, apoptosis, migration, invasion, and tumorigenic capacity were evaluated. SPP1 was a target gene of miR‐340 which could then mediate the PI3K/AKT signaling pathway by targeting SPP1 in GC. Furthermore, miR‐340 levels were reduced and SPP1 was enriched in GC tissues and cells, with the PI3K/AKT signaling pathway being activated. Inhibitory effects of upregulated miR‐340 on SPP1 and the PI3K/AKT signaling pathway were confirmed in vivo and in vitro. Overexpression of miR‐340 or the silencing of SPP1 inhibited GC cell proliferation, invasion, migration, and EMT process, but promoted apoptosis of GC cells. Typically, targeting of SPP1 by miR‐340 may contribute to the inhibition of proliferation, migration, invasion, and EMT of GC cells via suppression of PI3K/AKT signaling pathway.

ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression through activating ZEB1-induced EMT.

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Circular RNAs (circRNAs) function as modulators of microRNAs (miRNAs) and are often involved in cancer progression. This study aims to investigate the underlying mechanism by which circRNA hsa‐circ‐000684 promotes the progression of gastric cancer (GC). Expression of hsa‐circ‐000684 and that of ZEB1 mRNA were elevated while microRNA‐186 (miR‐186) expression was downregulated in GC cell lines and clinical tissues. In addition, the effects of hsa‐circ‐000684 on the proliferation, migration, invasion, and tube formation of GC cells were examined through gain‐and loss‐of‐function experiments. Furthermore, we introduced tumor xenografts into nude mice to better understand these effects in vivo. Either knockdown of hsa‐circ‐000684 or upregulation of miR‐186 inhibited GC cell proliferation, migration, invasion, and tube formation in vitro, and reduced the xenograft tumor growth in nude mice. Moreover, we found that hsa‐circ‐000684 and ZEB1 directly bound to miR‐186. Hsa‐circ‐000684 increased the expression of ZEB1 by binding to miR‐186. The tumor suppressive effects of hsa‐circ‐000684 knockdown were reversed by inhibition of miR‐186. Collectively, our data show that hsa‐circ‐000684 reduces the miR‐186 expression which leads to an increase in the ZEB1 expression and, consequently, promotion of GC progression.

Background/Objectives Colon polyps (CP) is a chronic disease prevalent in the middle-aged adults. To improve the diagnosis, treatment and prevention of CP incidence, we explored the disease-specific and gender-dependent features of gut-microbiome in Chinese CP patients. Methods We enrolled 124 CP patients (40 females and 84 males) that contain 89 single polyps cases and 35 multiple polyps cases. Their basic information, blood chemistry and gut microbiome were analyzed to find out disease-specific and gender-dependent features. Results We found that smaller blood platelet size was associated with multiple colon polyps type (χ2 p < 0.05). Less breakfast frequency and more alcohol intake showed logistic association with disadvantageous blood biochemistry, including serum triglyceride level, low-density lipoprotein, high-density lipoprotein and fasted blood glucose levels (Chi square p < 0.01). CP patients had significantly higher gut-microbiome diversity than alcoholic fatty liver diseases (n = 12) but less than that observed in the ulcerative colitis (UC) patients (n = 20). Bioinformatics analysis showed that CP gut-microbiome is linked with higher cancer risk than UC. The gut-microbiome of CP patients are featured by Prevotellaceae and Paraprevotellaceae. We further found that inflammatory/infectous related Alcaligenaceae, Enterobacteriaceae and Erysipeltrichaceae were abundant in male CP patients, whereas neutral/beneficial Barnesiellaceae, Lachnospiraceae, Odoribacteraceae and Rikenellaceae were abundant in female CP patients. Conclusion To summarize, gut-microbiome demonstrated to be highly gender-dependent and disease-specific in CP patients and our data provides valuable reference to the gut-microbiome centered treatment of CP patients of different genders.