ST8SIA6-AS1 Promotes the Epithelial-to-Mesenchymal Transition and Angiogenesis of Pituitary Adenoma.

To investigate the effect of long noncoding RNA ST8SIA6-AS1 on the epithelial-to-mesenchymal transition (EMT) and angiogenesis of pituitary adenoma and its possible mechanism. The expression levels of ST8SIA6-AS1 and HOXA9 in noninvasive pituitary adenoma and invasive pituitary adenoma were detected using qRT-PCR. sh-ST8SIA6-AS1 transfection silenced the expression of ST8SIA6-AS1 in GH3 and GTI-1 cells. The effects of ST8SIA6-AS1 on the proliferation, invasion, angiogenesis, and EMT of GH3 and GTI-1 pituitary adenoma cells were detected. The migration ability of cells was detected through scratch assay. Dual luciferase analysis verified the targeting relationship between ST8SIA6-AS1 and miR-5195-3p. ST8SIA6-AS1 and HOXA9 were highly expressed in invasive pituitary adenoma. In pituitary adenomas, miR-5195-3p directly targeted HOXA9. miR-5195-3p is the target gene of ST8SIA6-AS1. ST8SIA6-AS1 knockdown inhibited the proliferation, invasion, angiogenesis, and EMT of pituitary adenoma. HOXA9 expression mediates the biological effect of ST8SIA6-AS1. ST8SIA6-AS1 targets miR-5195-3p to regulate the expression of HOXA9 and promote the EMT of pituitary adenomas.

lncRNA KCNQ1OT1 Promotes EMT, Angiogenesis, and Stemness of Pituitary Adenoma by Upregulation of RAB11A.

This study is aimed at investigating the effect and mechanism of long noncoding RNA (lncRNA) KCNQ1OT1 on pituitary adenoma (PA). The KCNQ1OT1 expression in invasive and noninvasive PA tissues was detected by real-time fluorescence quantitative polymerase chain reaction (qPCR). The effects of KCNQ1OT1 on the proliferation of PA cells, namely, GH3 and HP75, were detected by CCK-8 experiment. The Transwell assay detected the effect of KCNQ1OT1 on the invasion of GH3 and HP75 cells. The effect of KCNQ1OT1 on the clonal formation ability was detected by clonal formation experiment. The double luciferase reporter assay and the miRNA pull down assay verified the binding of KCNQ1OT1 to miR-140-5p. Meanwhile, the regulatory effect of miR-140-5p on RAB11A was verified. qPCR results showed that KCNQ1OT1 was significantly increased in invasive PA compared with noninvasive PA tissues. Knockdown KCNQ1OT1 inhibited PA cell stemness, angiogenesis, and EMT. In addition, knockdown KCNQ1OT1 inhibited the proliferation, invasion, and clonal formation of PA. miR-140-5p is the target gene of KCNQ1OT1. miR-140-5p targets RAB11A directly. RAB11A can mediate the biological effects of KCNQ1OT1. Meanwhile, lncRNA KCNQ1OT1 can promote the EMT and cellular stemness of PA. Its mechanism of action is realized by inhibiting miR-140-5p. This result can provide a molecular basis for the further study of PA.

Tanshinone IIA Ameliorate Coxsackie Virus B3-Induced Viral Myocarditis through the Inhibition of Inflammation and Modulation T Helper 1/T Helper 2 Balance in Mice.

To investigate the effect of Tanshinone IIA (TSA) on viral myocarditis (VMC). VMC animal model was established using BALB/c mice by intraperitoneally injecting Coxsackie virus B3 (CVB3). The mice were randomly divided into control group, model group, and TSA group. We detected the survival rate, the heart weight to body weight (HW/BW) ratio and hemodynamic and cardiac function parameters. The pathological features of VMC were measured through H&E staining. The expression of serum enzyme, inflammatory cytokines, and T helper (Th)1/Th2 markers was also investigated. TSA remarkably alleviated CVB3-caused myocardial injury, decreased the HW/BW ratio, and improved survival rate. TSA obviously improved hemodynamic parameters and reversed the damage to the heart pump function. Furthermore, the serum levels of lactate dehydrogenase, creatine kinase, and Th1 cytokines in the TSA group were significantly lower than those in the VMC group, and TSA treatment significantly improved the pathological condition. The interferon-gamma (IFN-γ) and interleukin-2 (IL-2) levels in VMC model group was higher than control group, and lower levels of IL-4 and IL-10 were identified. However, TSA treatment elevated IL-4 and IL-10 levels and decreased IFN-γ and IL-2 levels. TSA could effectively protect the myocardium against CVB3-induced myocarditis by the inhibition of inflammation and modulation Th1/Th2 balance in mice.

Identification of quantitative trait loci for the dead leaf rate and the seedling dead rate under alkaline stress in rice.

The quantitative trait loci (QTLs) for the dead leaf rate (DLR) and the dead seedling rate (DSR) at the different rice growing periods after transplanting under alkaline stress were identified using an F(2:3) population, which included 200 individuals and lines derived from a cross between two japonica rice cultivars Gaochan 106 and Changbai 9 with microsatellite markers. The DLR detected at 20 days to 62 days after transplanting under alkaline stress showed continuous normal or near normal distributions in F(3) lines, which was the quantitative trait controlled by multiple genes. The DSR showed a continuous distribution with 3 or 4 peaks and was the quantitative trait controlled by main and multiple genes when rice was grown for 62 days after transplanting under alkaline stress. Thirteen QTLs associated with DLR were detected at 20 days to 62 days after transplanting under alkaline stress. Among these, qDLR9-2 located in RM5786-RM160 on chromosome 9 was detected at 34 days, 41 days, 48 days, 55 days, and 62 days, respectively; qDLR4 located in RM3524-RM3866 on chromosome 4 was detected at 34 days, 41 days, and 48 days, respectively; qDLR7-1 located in RM3859-RM320 on chromosome 7 was detected at 20 days and 27 days; and qDLR6-2 in RM1340-RM5957 on chromosome 6 was detected at 55 days and 62 days, respectively. The alleles of both qDLR9-2 and qDLR4 were derived from alkaline sensitive parent "Gaochan106". The alleles of both qDLR7-1 and qDLR6-2 were from alkaline tolerant parent Changbai 9. These gene actions showed dominance and over dominance primarily. Six QTLs associated with DSR were detected at 62 days after transplanting under alkaline stress. Among these, qDSR6-2 and qDSR8 were located in RM1340-RM5957 on chromosome 6 and in RM3752-RM404 on chromosome 8, respectively, which were associated with DSR and accounted for 20.32% and 18.86% of the observed phenotypic variation, respectively; qDSR11-2 and qDSR11-3 were located in RM536-RM479 and RM2596-RM286 on chromosome 11, respectively, which were associated with DSR explaining 25.85% and 15.41% of the observed phenotypic variation, respectively. The marker flanking distances of these QTLs were quite far except that of qDSR6-2, which should be researched further.