Mechanisms by which silencing long-stranded noncoding RNA KCNQ1OT1 alleviates myocardial ischemia/reperfusion injury (MI/RI)-induced cardiac injury via miR-377-3p/HMOX1.

BACKGROUND: The key complication of myocardial infarction therapy is myocardial ischemia/reperfusion injury (MI/RI), and there is no effective treatment. The present study elucidates the mechanism of action of lncRNA KCNQ1OT1 in alleviating MI/RI and provides new perspectives and therapeutic targets for cardiac injury-related diseases. METHODS: An ischemia/reperfusion (I/R) injury model of human adult cardiac myocytes (HACMs) was constructed, and the expression of KCNQ1OT1 and miR-377-3p was determined by RT‒qPCR. The levels of related proteins were detected by western blot analysis. Cell proliferation was detected by a CCK-8 assay, and cell apoptosis and ROS content were determined by flow cytometry. SOD and MDA expression as well as Fe2+ changes were detected by related analysis kits. The target binding relationships between lncRNA KCNQ1OT1 and miR-377-3p as well as between miR-377-3p and heme oxygenase 1 (HMOX1) were verified by a dual-luciferase reporter gene assay. RESULTS: Myocardial ischemia‒reperfusion caused oxidative stress in HACMs, resulting in elevated ROS levels, increased Fe2+ levels, decreased cell viability, and increased LDH release (a marker of myocardial injury), and apoptosis. KCNQ1OT1 and HMOX1 were upregulated in I/R-induced myocardial injury, but the level of miR-377-3p was decreased. A dual-luciferase reporter gene assay indicated that lncRNA KCNQ1OT1 targets miR-377-3p and that miR-377-3p targets HMOX1. Inhibition of HMOX1 alleviated miR-377-3p downregulation-induced myocardial injury. Furthermore, lncRNA KCNQ1OT1 promoted the level of HMOX1 by binding to miR-377-3p and aggravated myocardial injury. CONCLUSION: LncRNA KCNQ1OT1 aggravates ischemia‒reperfusion-induced cardiac injury via miR-377-3P/HMOX1.

Recycling and reutilization of smelting dust as a secondary resource: A review.

Smelting dust is a toxic waste produced in metal-mineral pyrometallurgical processes. To eliminate or reduce the adverse environmental impacts of smelting dust, valuable components need to be selectively separated from the toxic components present in the waste. This paper reviews the chemical composition, phase composition and particle size distribution characteristics of smelting dust, and the results show that smelting dust has excellent physicochemical characteristics for recovering valuable metals. The process flow, critical factors, development status, advantages and disadvantages of traditional technologies such as pyrometallurgy, hydrometallurgy and biometallurgy were discussed in depth. Conventional treatment methods typically prioritize separating and reclaiming specific elements with high concentrations. However, these methods face challenges such as excessive chemical usage and limited selectivity, which can hinder the sustainable utilization of smelting dust. With the increasing scarcity of resources and strict environmental requirements, a single treatment process can hardly fulfil the demand, and a physical field-enhanced technology for releasing and separating valuable metals is proposed. Through analysing the effect of electric field, microwave and ultrasound on recovering valuable metals from smelting dust, the enhancement mechanism of physical field on the extraction process was clarified. This paper aimed to provide reference for the resource utilization of smelting dust.

Harmless and resourceful utilization of solid waste: Multi physical field regulation in the microbiological treatment process of solid waste treatment.

Solid waste (SW) treatment methods mainly include physical, chemical, and biological methods, while physical and chemical methods have advantages such as fast effectiveness and short treatment time, but have high costs and were prone to secondary pollution. Due to the advantages of mild conditions and environmental protection, microbial methods have attracted the attention of numerous researchers. Recently, promotion of biological metabolic activity in biotreatment technology by applying multiple physical conditions, and reducing the biochemical reaction energy base to promote the transfer of protons and electrons, has made significant progress in harmless and resourceful utilization of SW. This paper main summarized the harmless and resourceful treatment methods of common bulk SW. The research of physical field-enhanced microbial treatment of inorganic solid waste (ISW) and organic solid waste (OSW) was discussed. The advantages and mechanisms of microbial treatment compared to traditional SW treatment methods were analyzed. The multi-physical field coupling enhanced microbial treatment technology was proposed to further improving the efficiency of large-scale treatment of bulk SW. The application prospects and potential opportunities of this technology were analyzed. Novel research ideas for the large-scale harmless and resourceful treatment of bulk SW were provided.

Potential Therapeutic Effects of Policosanol from Insect Wax on Caenorhabditis elegans Models of Parkinson's Disease.

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide. The standard treatments for PD focus on symptom relief rather than attempting to address the underlying degenerative processes completely. This study aimed to evaluate the potential therapeutic effects of policosanol derived from insect wax (PIW) by investigating improvements in disease symptoms represented in Caenorhabditis elegans models of PD. For our assessments, we used the following three models: NL5901, which is a transgenic model for α-synuclein aggregation; wild-type N2 induced with 6-hydroxydopamine (6-OHDA); and 6-OHDA-induced BZ555 as a model for loss of dopaminergic neurons (DNs). Specifically, we examined the effects of PIW treatment on α-synuclein aggregation, the loss of DNs, lipid abundance, and the lifespan of treated organisms. Further, we examined treatment-related changes in the levels of reactive oxygen species (ROS), malondialdehyde (MDA), adenosine triphosphate (ATP), glutathione S-transferase (GST), and superoxide dismutase (SOD), as well as the mRNA production profiles of relevant genes. A 10 µg/mL dose of PIW reduced the aggregation of α-synuclein in NL5901 and suppressed the loss of DNs in 6-OHDA-induced BZ555. Overall, PIW treatment decreased ROS and MDA levels, restored lipid abundance, and prolonged the lifespans of worms in all the three models, which may be associated with changes in the expression profiles of genes related to cell survival and oxidative stress response pathways. Our findings show that PIW alleviated the symptoms of PD in these models, possibly by regulating the stress responses initiated by injuries such as α-synuclein aggregation or 6-OHDA treatment.

Electrolytic Corrosion Behavior of 20 Cu-20 Ni-54 NiFe2O4-6 NiO Cermet with Interpenetrating Structure at 880 °C and 960 °C.

Here, 20 Cu-20 Ni-54 NiFe2O4-6 NiO (wt%) cermets were prepared via the powder metallurgy process, and the electrolytic corrosion behavior of the cermets at 880 °C and 960 °C was studied through the microstructure analysis by SEM and EDS. Results show that the ceramic phase is seriously affected by chemical corrosion at 880 °C electrolysis, and it is difficult to form a dense ceramic surface layer. A dense ceramic surface layer is formed on the bottom of the anode electrolyzed at 960 °C, and the dense layer thickens with the extension of the electrolysis time. The formation of the dense surface layer is mainly caused by the oxidation of Ni. The oxidation rate of the metallic phase and the corrosion rate of the ceramic phase have an important effect on the formation of the dense layer. In the corrosion process of NiFe2O4 phase, preferential corrosion of Fe element occurs first, and then NiO phase is precipitated from NiFe2O4 phase. After the NiO is dissolved and corroded, the NiFe2O4 grains collapse and the ceramic phase peels off from the anode.

Long Noncoding RNA CASC2 Facilitated Wound Healing through miRNA-155/HIF-1α in Diabetic Foot Ulcers.

Diabetic foot ulcers (DFU) are among the serious complications which are closely linked to diabetes mellitus. However, there is still a lack of accurate and effective standard prevention and treatment programs for DFU. In this manuscript, we have investigated the function of lncRNA cancer susceptibility candidate 2 (CASC2)/miR-155/hypoxia-inducible factor 1-alpha (HIF-1α) in the wound healing of DFU. We have analyzed lncRNA CASC2`s expression in the marginal tissues of ulcers in patients and mice with DFU. Additionally, the interaction relationship and mechanism between lncRNA CASC2, miR-155, and HIF-1α were determined, which proved the effects of lncRNA CASC2/miR-155/HIF-1α on fibroblasts apoptosis, proliferation, and migration. According to our study, the lncRNA CASC2's expression was low in the tissues of ulcers of DFU mice and patients. lncRNA CASC2's overexpression promoted fibroblasts migration, proliferation, and inhibited apoptosis and was beneficial for the healing of wounds, preferably in the DFU mice. In addition, lncRNA CASC2 directly targets miR-155 and HIF-1α functions as miR-155's target gene. Overexpression of miR-155 abrogated the function of lncRNA CASC2. Similarly, HIF-1α's inhibition has reversed the effect of miR-155 downregulation on fibroblasts. In general, overexpression of lncRNA CASC2 facilitated wound healing through miR-155/HIF-1α in DFU.

[Corrigendum] FNDC3B promotes epithelial­mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment.

After the publication of the article, and also the publication of a Corrigendum (see doi: 10.3892/or.2020.7744), there are further errors in the published paper that the authors wish to correct in a subsequent corrigendum. In the printed version of Fig. 5, the "NC" images were mistakenly presented in the data panels showing the results of the TCA8113 and TSCCA invasion assay experiments. Furthermore, in Fig. 4A and 6A, the ß­actin control bands were erroneously selected for these figures. The corrected versions of Figs. 4, 5 and 6 are shown opposite and on the next page, incorporating the correct data for Figs. 4A, 5 and 6A. These further corrections do not affect the results and conclusions of this work. The authors all agree to this Corrigendum, and are grateful to the Editor of Oncology Reports for allowing them to have the opportunity to correct these additional errors. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [the original article was published in Oncology Reports 39: 1853­1859, 2018; DOI: 10.3892/or.2018.6231].

[Corrigendum] FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment.

During the preparation of the above article, the authors inadvertently selected an incorrect pair of data panels for Fig. 5B. Essentially, in the published version of Fig. 5B, the images were presented incorrectly for the NC migration and KD#3 migration and invasion data panels associated with the TSCCA cell Transwell assay experiments. Furthermore, in Fig. 7A, the GAPDH control bands were erroneously selected for the figure. Figs. 5 and 7 as they should have appeared in the Journal are shown opposite, incorporating the correct data for Figs. 5B and 7A. These errors did not affect either the results or the conclusions of this work. The authors all agree to this Corrigendum, and thank the Editor of Oncology Reports for allowing them to have the opportunity to present their corrected data. Furthermore, the authors apologize to the readership for any inconvenience these errors may have caused. [the original article was published in Oncology Reports 39: 1853­1859, 2018; DOI: 10.3892/or.2018.6231].

Identification of prognostic biomarkers in colorectal cancer using a long non-coding RNA-mediated competitive endogenous RNA network.

Colorectal cancer (CRC) is a highly malignant gastrointestinal tumor accompanied by poor prognosis. Long non-coding RNA (lncRNA) plays an important role in the progression and physiology of tumors as it competes with endogenous RNAs, including miRNA and mRNA. In the present study, a multi-step computational method was used to build a CRC-related functional lncRNA-mediated competitive endogenous RNA (ceRNA) network (LMCN). lncRNAs with more degrees and betweenness centrality (BC) were screened out as hub lncRNAs. Then functional enrichment analyses of lncRNAs were carried out from the Gene Ontology (GO) and Reactome pathway databases based on the 'guilt by association' principle. As a result, lncRNAs in the LMCN displayed specific topological characteristics in accordance with the regulatory correlation of coding mRNAs in CRC pathology. HCP5, EPB41L4A-AS1, SNHG12, and LINC00649 were screened out as hub lncRNAs which were more significantly related to the development and prognosis of CRC. The hub lncRNAs in CRC were obviously involved in functions of cell cycle arrest, vacuolar transport, histone modification, and in pathways of GPCR, signaling by Rho GTPases, axon guidance pathways, meaning that they might be potential biomarkers for diagnosis, evaluation and gene-targeted therapy of CRC. Thus, the LMCN construction method could accelerate lncRNA discovery and therapeutic development in CRC.

FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment.

The primary reasons for the treatment failure of patients with oral tongue squamous cell carcinoma (OTSCC) are metastasis and tumor recurrence. Identifying the exact mechanisms underlying metastasis is a key point in improving patient prognosis. It has been reported that a hypoxic microenvironment plays an important role during the metastasis of malignancies. We found that the expression of fibronectin type III domain containing 3B (FNDC3B) is positively correlated with lymph node metastasis and advanced cTNM stage of OTSCC by IHC assay and correlation analysis. Furthermore, we found that knockdown of FNDC3B could suppress the migratory and invasive abilities of OTSCC cells. In addition, treating OTSCC cells with CoCl2 (a hypoxia mimetic agent) upregulated the mRNA and protein expression of FNDC3B via HIF-1α. Moreover, the resultant increase in FNDC3B expression significantly induced epithelial-mesenchymal transition (EMT) in OTSCC cells. The present study elucidated the important role played by FNDC3B in OTSCC metastasis and indicates FNDC3B as a potential target for the treatment of OTSCC metastasis. However, many questions remain to be explored.