New Findings What is the central question of this study?This study was designed to investigate the molecular mechanism and biological roles of long non‐coding RNA activated by transforming growth factor‐β (lncRNA ATB) in the progression of cervical cancer. What is the main finding and its importance?Our study provided new insight into the cross‐talk between lncRNA ATB, miR‐144 and ITGA6, shedding light on the therapy for cervical cancer. Abstract The present study was designed to investigate the molecular mechanism and biological roles of long non‐coding RNA activated by transforming growth factor‐β (lncRNA ATB) in the progression of cervical cancer. The expression levels of lncRNA ATB, miR‐144 and integrin α6 (ITGA6) were detected in human cervical cancer cell lines using quantitative real‐time PCR and western blotting. Cell viability was quantified by MTT assay at 12, 24, 36, 48 and 72 h after transfection, and cell invasion was determined by the Transwell migration assay. The association among lncRNA ATB, miR‐144 and ITGA6 was disclosed by a dual‐luciferase reporter assay. We found that lncRNA ATB was highly expressed in human cervical cancer cell lines. Further investigation indicated that lncRNA ATB functioned as a competitive endogenous RNA (ceRNA) for miR‐144 to promote cervical cancer cell proliferation and invasion. We demonstrated that ITGA6 was a direct target of miR‐144, and lncRNA ATB facilitated the proliferation and invasion of cervical cancer cells via the miR‐144/ITGA5 axis. In conclusion, the lncRNA ATB/miR‐144/ITGA6 axis might be a promising therapeutic target for cervical cancer.

Recently, our group has developed a therapeutic hypertensive vaccine against angiotensin (Ang) II type 1 receptor (AT1R) named ATRQβ-001. To explore its potential effectiveness on streptozotocin-induced diabetic nephropathy, male Sprague Dawley rats were randomly divided into two groups: a control and a diabetic model. After 1 week, the diabetic rats were divided into four subgroups (each with 15 rats) for 14-week treatments with saline, olmesartan, ATRQβ-001, and Qβ virus-like particle (VLP), respectively. In addition to lower blood pressure, ATRQβ-001 vaccination ameliorated biochemical parameter changes of renal dysfunction, mesangial expansion, and fibrosis through inhibiting oxidative stress, macrophage infiltration, and proinflammatory factor expression. Furthermore, ATRQβ-001 vaccination suppressed renal Ang II-AT1R activation and abrogated the downregulation of angiotensin-converting enzyme 2-Ang (1–7), similar to olmesartan treatment, while no obvious feedback activation of circulating or local renin-angiotensin system (RAS) was only observed in vaccine group. In rat mesangial cells, the anti-ATR-001 antibody inhibited high glucose-induced transforming growth factor-β1 (TGF)-β1/Smad3 signal pathway. Additionally, no significant immune-mediated damage was detected in vaccinated animals. In conclusion, the ATRQβ-001 vaccine ameliorated streptozotocin-induced diabetic renal injury via modulating two RAS axes and inhibiting TGF-β1/Smad3 signal pathway, providing a novel, safe, and promising method to treat diabetic nephropathy.Key messagesOveractivation of RAS plays a crucial role in the development of the DN.Our aim was to verify the effectiveness of ATRQβ-001 vaccine in STZ-induced DN.The ATRQβ-001 modulated two RAS axes and inhibited TGF-β1/Smad3 signal pathway.The vaccine therapy may provide a novel, safe, and promising method to treat DN.Electronic supplementary materialThe online version of this article (doi:10.1007/s00109-015-1343-6) contains supplementary material, which is available to authorized users.

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