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Clear cell renal cell carcinoma (ccRCC) represents approximately 70% of RCC,as the most frequent histological subtype of RCC. MiR-138-5p, a tumor-related microRNA (miRNA), has been reported to be implicated in the diverse types of human malignancies, but its role in ccRCCremains unclear.

The study was designed to investigate the functional behaviors and regulatory mechanisms of miR-138-5p in ccRCC.

Quantitative real-time PCR and western blotting analyses were performed to determine the expression of miR-138-5p and TMEM40 in ccRCC tissues. Pearson’s correlation coefficient was utilized to evaluate the correlation between miR-138-5p and TMEM40 expression. The function of miR-138-5p and TMEM40 in the cell proliferation, migration and invasion of ccRCC cells (786-O and ACHN) was assessed by CCK-8, colony formation, wound healing and transwell assay, respectively. A luciferase reporter assay was performed to confirm the direct binding of miR-138-5p to the target gene TMEM40.

We found the expression of miR-138-5p was significantly down-regulated, while TMEM40 was remarkably up-regulated in ccRCC tissues. TMEM40 expression was discovered to be inversely correlated with miR-138-5p expression in ccRCC tissues. Functional studies demonstrated that miR-138-5p overexpression or TMEM40 knockdown significantly suppressed ccRCC cell proliferation, migration and invasion in vitro. Notably, we experimentally confirmed that miR-138-5p directly recognizes the 3′-UTR of the TMEM40 transcript and down-regulated its expression in ccRCC cells.

Taken together, our findings provide the first clues regarding the role of miR-138-5p as a tumor suppressor in ccRCC by directly targeting of TMEM40.

Taken together, our findings provide the first clues regarding the role of miR-138-5p as a tumor suppressor in ccRCC by directly targeting of TMEM40.

Vs is an important aquaculture pathogen that can infect a broad host of marine organisms. In our previous study, an antagonistic bacterium

sp. V33 that possessed inhibitory effects on the growth and virulence of a pathogenic isolate

Vs was identified.

Here, we further explored the antagonistic substances and antagonistic effects from the viewpoint of iron competition.

The main antagonistic substances in the supernatants from

sp. V33 were identified using the bioassay-guided method. The response of

Vs under the challenge of cell-free supernatant from

sp. V33 was determined via sodium dodecyl sulfate-polyacrylamide gel electrophoresis and real-time reverse-transcription PCR.

The main antagonisticsubstances produced by

sp. V33 have low molecular weights, are water soluble, and are heat-stable substances. Meanwhile, the iron uptake rate of

sp. V33 was higher than that of

Vs. In the presence of cell-free supernatant from

sp. V33, expressions of two functional genes, viuB and asbJ related to ferric uptake processes in

Vs, were up-regulated, whereas furVs coding the ferric uptake repressor was suppressed below 0.5-fold. One gene coding phosphopyruvate hydratase does not change at mRNA level, but was up-regulated at protein level.

Our results suggested that antagonistic effect of

sp. V33 on the pathogenic isolate

Vs was partially due to the stronger ability of

sp. Vorinostat V33 to seize iron. This cell-free supernatant from

sp. V33 created an iron-limited milieu for

Vs, which led to the changed expression profiles of genes that were related to iron uptake in

Vs.

Our results suggested that antagonistic effect of Vibrio sp. V33 on the pathogenic isolate V. splendidus Vs was partially due to the stronger ability of Vibrio sp. V33 to seize iron. This cell-free supernatant from Vibrio sp. V33 created an iron-limited milieu for V. splendidus Vs, which led to the changed expression profiles of genes that were related to iron uptake in V. splendidus Vs.

Characterizing the structure and function of superoxide dismutase (SOD), as an antioxidant enzyme providing opportunities for its application in food supplements.

In this study, the features of the Manganese-SOD of

(SDLL), subsp.

MG1363, as probiotic bacteria, were determined on the basis of the computational methods.

The protein’s physicochemical properties and the prediction of its secondary structure were determined via the ProtParam server and the GOR program respectively. Moreover, the 3D structures of the proteins were constructed via the MODELLER on the basis of the homology method and the threading algorithm MUSTER. On the other hand, the structural stability of the models was assayed under the quasi-physiological conditions by the GROMACS program via the GROMOS96 43a1 force field in Linux system. Finally, using the Molecular Docking Studies, the functionality features of the models were predicted through their affinity with the corresponding substrates.

The results revealed the physicocs.

In general, the study provides a new model of SDLL with certain thermostable features, and a new mutant with suitable stability and functionality on the basis of the direct mutagenesis being used in different applications.

MiR-103a-3p is a small non-coding RNA and has been reported to be involved in osteogenic proliferation and differentiation, but the role of miR-103a-3p in human osteoarthritis (OA) remains unclear.

In this study, we aimed to explore its function and molecular target in chondrocytes during OA pathogenesis.

Total 12 experimental OA rat models, together with 12 rats without knee OA lesions were established and cartilage samples were collected. Chondrocytes were treated with LPS

. MiR-103a-3p expression was detected in articular cartilage tissues and chondrocytes using quantitative real-time PCR. Knee OA chondrocytes were transfected with miR-103a-3p mimics, and siHMGB1, respectively. Then cellular proliferation, apoptosis, apoptosis related factors and inflammatory cytokines were analyzed by MTT, flow cytometry, western blot, caspase-3 activity and ELISA, respectively. Potential targets of miR-103a-3p were predicted using series of bioinformatics analysis, then confirmed by luciferase reporter assay.

We first found miR-103a-3p was significantly down-regulated in the articular cartilage tissues from experimental OA rats, as well as in chondrocytes treated with LPS

.