Circular RNA (circRNA) participates in a variety of pathophysiological processes, including the development of gastric cancer (GC). However, the role of circ_0006089 in GC progression and its underlying molecular mechanism need to be further revealed.Quantitative real-time PCR was utilized for detecting circ_0006089, microRNA (miR)-361-3p and transforming growth factor-β1 (TGFB1) expression. The interaction between miR-361-3p and circ_0006089 or TGFB1 was confirmed using a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. Cell proliferation, metastasis, apoptosis, and angiogenesis were determined using colony formation assay, EdU assay, transwell assay, flow cytometry, and tube formation assay. Cell glycolysis was evaluated by detecting glucose consumption, lactate production, and ATP levels. In addition, western blot (WB) analysis was used to measure protein expression.Xenograft tumor models were used to assess the effect of circ_0006089 knockdown on GC tumorigenesis. circ_0006089 had been found to be upregulated in GC tissues and cells, and it could act as an miR-361-3p sponge. circ_0006089 knockdown suppressed GC proliferation, metastasis, glycolysis, angiogenesis, and increased apoptosis, while this effect could be revoked by miR-361-3p inhibitor. TGFB1 was targeted by miR-361-3p, and its overexpression reversed the effects of miR-361-3p on GC cell function. Also, circ_0006089 promoted TGFB1 expression via sponging miR-361-3p. Animal experiments showed that silenced circ_0006089 inhibited GC tumorigenesis through the miR-361-3p/TGFB1 pathway. Our results revealed that the circ_0006089/miR-361-3p/TGFB1 axis contributed to GC progression, confirming that circ_0006089 might be a potential therapeutic target for GC.

<b><i>Background:</i></b> Accumulating evidence indicates that micro­RNAs play a key role in tumor progression and prognosis. However, the overall biological role and clinical significance of microRNA-552 (miR-552) in the pathogenesis of gastric cancer (GC) remain unclear. <b><i>Methods:</i></b> miR-552 expression was measured in 122 pairs of cancerous and noncancerous tissues and cell lines by quantitative real-time polymerase chain reaction. The relationship between miR-552 and the clinical parameters of patients was analyzed by the χ² test; Kaplan-Meier analysis and multivariate Cox regression analysis were used to predict the overall survival time and prognosis of patients with different expression of miR-552. Finally, CCK-8 and Transwell were used to detect the changes in cell proliferation, migration, and invasion ability. <b><i>Results:</i></b> miR-552 was expressed at markedly high levels in GC tissues compared to normal tissues and in some GC cell lines (<i>p</i> &#x3c; 0.001). The upregulation of miR-552 was significantly associated with tumors with advanced TNM stage (<i>p</i> = 0.026), lymph node metastasis (<i>p</i> = 0.018), intestinal metaplasia (<i>p</i> = 0.044), and genomically stable subtype (<i>p</i> = 0.035). Moreover, GC patients with high miR-552 expression showed shorter overall survival (log-rank test, <i>p</i> = 0.011) than those with low expression. Meanwhile, miR-552 was an independent prognostic factor for GC patients (HR 5.657, 95% CI 1.619–19.761, <i>p</i> = 0.007). Finally, miR-552 overexpression promoted the proliferation, migration, and invasion of GC cells (<i>p</i> &#x3c; 0.01). <b><i>Conclusion:</i></b> Taken together, our results indicate that miR-552, as an oncogene of GC, can promote cell proliferation, migration, and invasion, and miR-552 may be a novel prognostic biomarker for GC.

The present study was conducted to investigate the effects of dietary yeast (Saccharomyces cerevisiae) cell walls (YCW) from the yeast extract industry on performance and immune function of cyclosporine A (CSA)-treated, immunosuppressed broiler chickens. A total of 240 day-old male broilers were allocated randomly into four treatments: (1) non-challenged control; (2) non-challenged control þ 0·3 % YCW; (3) CSA-challenged group; (4) CSA-challenged þ 0·3 % YCW. On days 1-4 and 22-25 of age, broilers were subcutaneously injected with CSA or sterile saline. The results showed that supplementation of YCW significantly improved daily weight gain (DWG) during the starter (days 1 -21, P,0·01), finisher (days 22-42, P, 0·01) and overall (days 1-42, P, 0·05) periods compared with the control birds, but had no effect on feed conversion ratio (FCR, P.0·05). Compared with the CSA-treated birds, YCW alleviated the decrease of DWG (P,0·01) and increase of FCR (P,0·05) caused by CSA challenge at different periods and cumulatively. On days 21 and 42, YCW mitigated the CSA-induced decrease of peripheral blood lymphocyte blastogenic response (P,0·01). In addition, YCW improved the relative weights of the bursa of Fabricius (P, 0·01) and thymus (P, 0·01) and up-regulated the splenic expression of pro-inflammatory cytokines IL-1b (P,0·01) and IL-6 (P, 0·01) on day 42 compared with the CSA-treated birds. These results indicate that YCW supplementation has beneficial effects in attenuating the immunosuppressive effects of CSA challenge, therefore improving growth performance of broiler chickens.

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