Erratum: CircRNA_100395 inhibits cell proliferation and metastasis in ovarian cancer via regulating miR-1228/p53/epithelial-mesenchymal transition (EMT) axis: Erratum.

[This corrects the article DOI: 10.7150/jca.35041.].

Curcumin Antagonizes Glucose Fluctuation-Induced Renal Injury by Inhibiting Aerobic Glycolysis via the miR-489/LDHA Pathway.

It has been considered that glucose fluctuation (GF) plays a role in renal injury and is related to diabetic nephropathy (DN) development. But the mechanism is still unclear. Aerobic glycolysis has become a topical issue in DN in recent years. There is an internal connection between GF, aerobic glycolysis, and DN. Curcumin (Cur) is a principal curcuminoid of turmeric and possesses specific protective properties in kidney functions. Cur also participates in the regulation of aerobic glycolysis switch. In this study, we first measured the levels of aerobic glycolysis and evaluated Cur's inhibitory ability in a cell model of HEK-293 under the condition of oscillating high glucose. The results indicated that GF exacerbated inflammation injury, oxidative stress, and apoptosis in HEK-293 cell, while Cur alleviated this cytotoxicity induced by GF. We found that GF increased aerobic glycolysis in HEK-293 cells and Cur presented a dose-dependent weakening effect to this exacerbation. Next, we built a panel of 17 miRNAs and 8 lncRNAs that were previously reported to mediate the Warburg effect. Our RT-qPCR results indicated that GF reduced the miR-489 content in the HEK-293 cell model and Cur could prevent this downregulation. Then, we planned to explore the character of miR-489 in Cur-triggered attenuation of the Warburg effect under GF condition. Our findings presented that Cur prevented GF-triggered aerobic glycolysis by upregulating miR-489 in HEK-293 cells. Next, we choose the miR-489/LDHA axis for further investigation. We confirmed that Cur prevented GF-triggered aerobic glycolysis via the miR-489/LDHA axis in HEK-293 cells. In conclusion, this study presented that Cur prevented GF-triggered renal injury by restraining aerobic glycolysis via the miR-489/LDHA axis in the HEK-293 cell model.

High-order orbital angular momentum generation in a helically twisted pig-nose-shaped core microstructured optical fibers.

We propose a helically twisted pig-nose-shaped core microstructured optical fiber (HPC-MOF) for orbital angular momentum (OAM) mode generation. It comprises seven air-hole rings hexagonally arranged with two air holes and one air-hole ring replaced, forming two cores in a line 3 µm from the fiber center and one ring-shaped core. The fiber is helically twisted along the rotation axis. In this fiber, supermodes in inner dual-core can be coupled to high-order modes in outer ring-core, yielding OAM ring-shaped modes at different certain wavelengths, and various OAM modes at different twist rates were investigated in this paper. We demonstrate the distinct coupling differences of symmetric and antisymmetric supermodes in inner dual-core when the supermode coupled to ring-core mode. A modal matching rule is presented to characterize the coupling differences, which is suitable for describing supermode coupling characteristics in HPC-MOFs. Compared to conventional methods, these properties indicate that the fiber can generate higher-order OAM modes and more easily integrate into all-fiber optical communication systems, with potential in OAM generators, light-controlling devices, and integrated optics applications.

CircRNA_100395 inhibits cell proliferation and metastasis in ovarian cancer via regulating miR-1228/p53/epithelial-mesenchymal transition (EMT) axis.

Purpose: Circular RNAs (circRNAs) have been reported to regulate the incidence of tumor by regulating the transcriptional level and post-transcriptional level of tumor-related genes, and are significantly correlated with tumor metastasis and progression. CircRNA_100395 (circ_100395) has been reported to suppress lung cancer cell proliferation, and might act as an oncogene in deveopment of various cancers. However, the expression and function of circ_100395 in ovarian cancer has not been systematically researched. Methods: The expression of circ_100395 in ovarian cancer tissues was detected by Real-time Quantitative polymerase chain reaction (RT-qPCR), while the relationship between circ_100395 expression and clinicopathological characteristics was further analyzed. After increasing the expression of circ_100395 by plasmid transfection in ovarian cancer cells, we further investigated the cell proliferation, invasion and migration by cell counting kit-8 (CCK-8), and Transwell assays. Epithelial-mesenchymal transition (EMT) pathway was also measured by western blotting. In addition, the relationship among circ_100395, miR-1228 and p53 in ovarian cancer, was explored by luciferase reporter assay. Results: The expression of circ_100395 was found to be significantly down-regulated in ovarian cancer, while low expression of circ_100395 was highly correlated with the poor outcomes. In addition, upregulation of circ_100395 could significantly inhibit tumor growth, metastasis and EMT signaling pathway in ovarian cancer. Furthermore, the expression level of circ_100395 was negatively correlated with the expression of miR-1228, and with the addition of miR-1228 could reverse anti-cell proliferation effect induced by circ_100395 in ovarian cancer cells. In addition, p53 might be the key target of circ_100395 / miR-1228 axis in ovarian cancer. Conclusion: CircRNA_100395 could inhibit cell growth and metastasis of ovarian cancer cells via regulating the miR-1228/p53/EMT axis.

Upregulation of SNHG14 suppresses cell proliferation and metastasis of colorectal cancer by targeting miR-92b-3p.

Ample evidence have demonstrated that long noncoding RNAs small nucleolus RNA host gene 14 (SNHG14) serves as a master regulator in various cancers. However, the exact mechanism of SNHG14 in colorectal cancer (CRC) remains unknown. In the present study, we concentrate on the potential function of SNHG14 in the pathogenesis of CRC. From the quantitative reverse transcription-polymerase chain reaction results, SNHG14 was found to be downregulated in CRC tissues compared with the normal mucous samples, and its low expression was significantly correlated with poor clinical outcomes. Overexpression of SNHG14 inhibited cell growth, induced cell apoptosis, suppressed migration and invasion by inhibiting epithelial-mesenchymal transition process. Furthermore, mechanistic studies revealed that miR-92b-3p could rescue the CRC progress induced by SNHG14. Consequently, SNHG14 exhibited low expression in CRC tissues and involved in CRC progression and metastasis by competing for miR-92b-3p, and SNHG14 could be used as a valuable biomarker and therapeutic target for CRC.

Serum YKL-40 positively correlates with MMP-9 and CRP in patients with acute ST segment elevation myocardial infarction following emergency treatment.

OBJECTIVE: To investigate the role of YKL-40 in ST segment elevation myocardial infarction (STEMI) and its relationship to C-reactive protein (CRP) and matrix metalloproteinase-9 (MMP-9). METHODS: This prospective study included 358 STEMI patients who were sent to the Emergency Department of our hospital from April 2014 to December 2017. Serum levels of YKL-40, CRP and MMP-9 were determined using commercially available Enzyme linked immunosorbent assay (ELISA) kits. Major adverse cardiovascular events (MACE) and overall survival time were analyzed. RESULTS: GRACE scores (P < .001) and the levels of YKL-40 (P < .001), MMP-9 (P < .001), and CRP (P < .001) were significantly higher in deceased patients compared to those that survived. The levels of CRP (P = .007) and MMP-9 (P = .022) were significantly higher in the high YKL-40 group. The GRACE scores were also significantly elevated (P = .011, 95% CI 2.1 (-9.7 to -1.3)). Cumulative MACE rates and cardiac death rates were significantly higher in the high YKL-40 group (P < .001, 95% CI 3.9 (1.9-8.2)). Overall survival times were significantly longer in patients with lower YKL-40 levels (P < .0001). CONCLUSION: Elevated YKL-40 levels positively correlate with CRP and MMP-9 levels and are associated with clinical outcomes including MACE and 6-month survival in STEMI patients.