Background Previous data have shown that circular RNA (circRNA) is a key regulator in papillary thyroid cancer (PTC). However, the role and the detailed mechanism of circ_0027446 in PTC progression have not been reported. Methods Circ_0027446, miR-129–5p, claudin 1 (CLDN1), C-myc and MMP2 expression were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), Western Blot or immunohistochemistry (IHC) assay. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Cell proliferation was investigated by 5-Ethynyl-2′-deoxyuridine (EdU) assay and cell colony formation assay. Cell apoptosis , invasion and migration were assessed by flow cytometry analysis, transwell assay and wound-healing assay, respectively. Dual-luciferase reporter assay was conducted to identify the associations among circ_0027446, miR-129–5p and CLDN1. The effect of circ_0027446 on PTC cell malignancy in vivo was revealed by a xenograft mouse model assay. Results Circ_0027446 and CLDN1 expression were significantly upregulated, while miR-129–5p expression was downregulated in PTC tissues and cells. High circ_0027446 expression was closely associated with the poor prognosis of PTC patients . Circ_0027446 depletion inhibited PTC cell proliferation, migration and invasion but increased cell apoptosis. In addition, circ_0027446 acted as a miR-129–5p sponge, and miR-129–5p bound to CLDN1. Moreover, miR-129–5p inhibitors attenuated circ_0027446 depletion-induced effects in PTC cells. CLDN1 also participated in the regulation of miR-129–5p in PTC cell tumor properties. Importantly, circ_0027446 mediated CLDN1 expression by interacting with miR-129–5p. In vivo data showed that the decreased expression of circ_0027446 led to delayed tumor formation. Conclusion Circ_0027446 contributed to PTC cell tumor properties by regulating the miR-129–5p/CLDN1 pathway, showing circ_0027446 might be a therapeutic target in PTC.
Chen Yang,Pei Luo,Shi-jian Chen,Zhi-chao Deng,Xin-liang Fu,Dan-ning Xu,Yun-bo Tian,Yun-mao Huang,Wen-jun Liu
ABSTRACT Resveratrol, a natural antioxidant, anti-inflammatory plant extract, was found to have a protective effect in poultry subjected to heat stress. In this study, we strove to characterize resveratrol on intestinal of duck exposed to acute heat stress and investigate the underlying mechanism. A total of 120 Shan-ma ducks (60 days old) were randomly divided into 2 groups. The control group was fed a basal diet, and the resveratrol group was fed a basal diet supplemented with 400 mg/kg resveratrol. Animals in 2 groups were kept at a temperature of 24°C ± 2°C for 15 d. Then, animals of both groups were placed in an artificial climate room at 39°C. Twelve ducks of each group were sacrificed for sampling at 0, 30, and 60 min, respectively. Results indicated that resveratrol increased the ratio of villus height to crypt depth, increased the number of goblet cells, and reduced the histopathological damage of jejunum caused by acute heat stress. Furthermore, the gene expression of heat shock proteins ( HSP60, HSP70 , and HSP90 ) and tight junction proteins ( CLDN1 and OCLN ) was significantly increased in the resveratrol group compared to that in the control groups. Simultaneously, resveratrol significantly activated the SIRT1-NRF1/NRF2 signaling pathways, improved ATP level of jejunum, and increased SOD and CAT antioxidant enzymes activities. In addition, we found that the NF-κB / NLRP3 inflammasome signaling pathways were repressed under acute heat stress. Meanwhile, supplement resveratrol further inhibited the NLRP3 inflammasome pathway, decreased protein level of NLRP3 and caspase1 p20, reduced the secretion of IL-1β. Taken together, our results indicate that resveratrol against the oxidative damage and inflammation injury in duck jejunum induced by heat stress via active SIRT1 signaling pathways.
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