Long non-coding RNA gastric cancer associated transcript 3 (GACAT3), is a newly identified non-coding RNA, which has been found to be involved in the tumorigenesis of gastric cancer. However, the biological function of GACAT3 in liver cancer remains unclear. The present study aimed to determine the expression level and function of GACAT3 in liver cancer. The authors cultured liver cancer cells in vitro and GACAT3 was silenced in the cells. Cell proliferation, apoptosis and migration were determined by MTT assay, flow cytometric analysis and transwell assay, respectively. It was demonstrated that GACAT3 was upregulated in liver cancer tissues. The inhibition of GACAT3 decreased the ability of hepatoma cells to proliferate and migrate, and increased apoptosis of the cells. These findings provide the first evidence, to the best of our knowledge, of the exact role of GACAT3 in liver cancer, suggesting GACAT3 as a potential target for liver cancer therapy in the future.
BackgroundIslet transplantation is increasingly used in the diabetic patients to control the blood glucose level. However, the functional output of transplanted islets remains hampered due to the local inflammation, loss of islets, etc. To that end, in this study we explored to enhance the functional output of transplanted islets in diabetic mice by employing a drug-eluting scaffold with a payload of interleukin 4 (IL-4).ResultsAccording to the in vitro studies, the scaffold showed no cytotoxicity, a rapid release of IL-4 within a week and the IL-4 retained its bioactivity. During the 4-week time window after the islet transplantation, in vivo studies showed that the levels of blood insulin and C-peptide 2 in diabetic mice in the drug-eluting scaffold group significantly increased since week 2, which effectively reduced the blood glucose level. In addition, these mice demonstrated a stronger capability to withstand a rapid glucose spike as evidenced by the tolerance of sudden oral glucose challenge test result. A further mechanistic study suggested that the enhanced functional output could be attributed to the M2 polarization of macrophages as evidenced by the increase of CD163+/CD68+ macrophages in the islet tissues. A M2 polarization of macrophages is widely believed to exert an anti-inflammatory influence on local tissues, which could accelerate the resolution of local inflammation following the islet transplantation.ConclusionOur study shed a new light on the hyperglycemia management of diabetic patients following the islet transplantation.
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