[Retracted] MicroRNA­199a­3p inhibits ovarian cancer cell viability by targeting the oncogene YAP1.

Following the publication of the above article, the authors have submitted a request that it be retracted on account of the fact that, when requested to do so, the first author was unable to provide the original data for this article. The Editor of Molecular Medicine Reports has agreed with the request that this article be retracted. Note that all the authors agree with the decision to retract this article. The Editor and the authors regret any inconvenience that this retraction will cause to the readership of the Journal. [Molecular Medicine Reports 23: 237, 2021; DOI: 10.3892/mmr.2021.11876].

Effect of MgO and Fe2O3 dual sintering aids on the microstructure and electrochemical performance of the solid state Gd0.2Ce0.8O2-δ electrolyte in intermediate-temperature solid oxide fuel cells.

Solid state electrolytes have been intensively studied in the solid oxide fuel cells (SOFCs). The aim of this work is to investigate the effects of MgO and Fe2O3 dual sintering aids on the microstructure and electrochemical properties of solid state Gd0.2Ce0.8O2-δ (GDC) electrolytes, which are prepared by a sol-gel method with MgO and Fe2O3 addition to the GDC system. It is found that the addition of MgO and Fe2O3 can reduce the sintering temperature, increase densification and decrease the grain boundary resistance of the electrolyte. The 2 mol% MgO and 2 mol% Fe2O3 co-doped GDC (GDC-MF) exhibits the highest grain boundary conductivity. At 400°C, the grain boundary conductivity and total conductivity of GDC-MF are 15.89 times and 5.56 times higher than those of GDC. The oxygen reduction reaction (ORR) rate at the electrolyte/cathode interface of GDC-MF is 47 % higher than that of GDC. Furthermore, the peak power density of a single cell supported by GDC-MF is 0.45 W cm-2 at 700°C, 36.7% higher than that of GDC. Therefore, the GDC-MF should be a promising electrolyte material for intermediate-temperature solid oxide fuel cells (IT-SOFCs).

Retraction Note: MicroRNA-199a-5p suppresses the cell growth of colorectal cancer by targeting oncogene Caprin1.

[This retracts the article DOI: 10.1007/s13205-020-02433-9.].

Heterointerface Effect in Accelerating the Cathodic Oxygen Reduction for Intermediate-Temperature Solid Oxide Fuel Cells.

A solid-state mixing method was adopted to prepare a new Pr0.8Sr0.2Fe0.7Ni0.3O3-δ-Pr1.2Sr0.8Fe0.4Ni0.6O4+δ (PSFN113-214) composite cathode oxide for the solid oxide fuel cells (SOFCs). Herein, heterointerface engineering was investigated for the performance enhancement. It was found that the oxygen vacancy content could be increased by mixing the PSFN214 with PSFN113, which gave rise to the formation of a heterostructure, and resulted in the promotion of oxygen ion transport as well as the specific surface area. The optimum mixing ratio 5:5 resulted in the highest oxygen vacancy content and the largest specific surface area, indicating the strongest interface effect. Polarization resistance of PSFN113-214 (5:5) was 0.029 Ω cm2 at 800°C, which was merely 24% of PSFN113 and 39% of PSFN214. The corresponding maximum power density was 0.699 W cm-2, which was nearly 1.44 times of PSFN113 and 1.24 times of PSFN214. Furthermore, the voltage attenuation rate after 100 h was merely 0.0352% h-1. Therefore, the new PSFN113-214 composite could be a prospective cathode oxide for SOFCs.

MicroRNA­199a­3p inhibits ovarian cancer cell viability by targeting the oncogene YAP1.

MicroRNA­199a­3p (miR­199a­3p) is aberrantly expressed in various types of cancer where it exhibits a tumor suppressive role. However, the biological role of miR­199a­3p in ovarian cancer (OC) remains unclear. The present study aimed to investigate whether miR­199a­3p was a tumor suppressor in OC and to identify the possible mechanisms. It was found that miR­199a­3p expression was significantly downregulated in the tumor tissues and blood samples of patients with OC, as well as in three OC cell lines. In addition, its low expression was closely associated with International Federation of Gynecology and Obstetrics disease stage, histological grade and lymph node metastasis. It was demonstrated that overexpression of miR­199a­3p inhibited the viability and promoted apoptosis of OV90 and SKOV­3 cells. In addition, Yes­associated protein 1 (YAP1), a well­known oncogene, was identified as a direct target of miR­199a­3p in OC cells. Additionally, it was observed that YAP1 was significantly increased and inversely correlated with miR­199a­3p expression in OC tissues. Notably, YAP1 overexpression abrogated the tumor suppressive effects of miR­199a­3p in vitro. Collectively, the present results indicated that miR­199a­3p suppressed viability in OC cells, at least partly via inhibiting the YAP1 oncogene, suggesting that miR­199a­3p may act as a biomarker and therapeutic target for patients with OC.

MicroRNA-199a-5p suppresses the cell growth of colorectal cancer by targeting oncogene Caprin1.

MicroRNAs-199a-5p (miR-199a-5p) plays critical regulatory roles in various types of human cancers. However, the biological function and regulatory mechanisms of miR-199a-5p in colorectal cancer (CRC) remain unclear. The aim of this study was to investigate the role of miR-199a-5p in CRC and possible mechanisms of its action. The expression of miR-199a-5p in CRC tumor tissues was validated using quantitative real-time PCR (qRT-PCR). The effects of miR-199a-5p on cell proliferation and apoptosis were evaluated in vitro. Then, the association of miR-199a-5p and its downstream target was investigated in both cell line and clinical specimens. Furthermore, gain- and loss-of-function studies of cytoplasmic activation/proliferation-associated protein-1 (Caprin1) were performed to assess whether the suppressive effect of on CRC cells were via targeting Caprin1. Using a microarray platform, we focused on miR-199a-5p for further research, which was one of the most markedly downregulated miRNAs in CRC tumor tissues. Functionally, the overexpression of miR-199a-5p inhibited proliferation and induced apoptosis in both HTC116 and SW480 cells. Furthermore, cytoplasmic activation/proliferation-associated protein-1 (Caprin1), a well-known oncogene, was directly targeted by miR-199a-5p. It was also observed that Caprin1 was upregulated, and inversely correlated with miR-199a-5p levels in CRC tissues. Further investigations revealed that knockdown of Caprin1 by siRNA has similar role with miR-199a-5p overexpression in CRC cells, suggesting the oncogenic role of Caprin1 in CRC. In the contrast, we found that overexpression of Caprin1 reversed the suppressive effects of miR-199a-5p on CRC cells. Collectively, our study suggests that miR-199a-5p/Caprin1 axis may serve as potential therapeutic targets for the treatment of CRC.