Circ_0014130 is involved in the drug sensitivity of colorectal cancer through miR-197-3p/PFKFB3 axis.

BACKGROUND AND AIM: Colorectal cancer (CRC) is one of the most deadly cancers in the world, with few treatments and a poor prognosis. In recent years, many circular RNAs have been studied in CRC, but the role of circ_0014130 in CRC has not been investigated. Therefore, this research is designed to investigate the impact of circ_0014130 on the resistance of 5-fluorouracil (5-FU) in CRC. METHODS: Quantitative real-time polymerase chain reaction was conducted to assess the expression of circ_0014130, microRNA-197-3p (miR-197-3p), and 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 3 (PFKFB3). The expression of PFKFB3 protein was detected by Western blot. The effect of cric_0014130 on drug resistance in CRC was verified by Cell Counting Kit-8 assay, clone formation assay, Transwell, and flow cytometry. The effect of circ_0014130 on tumor growth was evaluated by xenograft tumor model in vivo. RESULTS: Circ_0014130 and PFKFB3 were increased, while miR-197-3p was reversed in CRC tissues and cells. Knocking down circ_0014130 can promote cell apoptosis, inhibit the proliferation of CRC cells, and reduced the IC50 of 5-FU. In addition, miR-197-3p inhibitors reversed the effect of si-circ_0014130 on CRC cells. Similarly, overexpression of PFKFB3 can regulate CRC cell behavior and 5-FU resistance caused by miR-197-3p. Finally, decrease of circ_0014130 was demonstrated to enhance the resistance of 5-FU in CRC tissues in vivo. CONCLUSION: Circ_0014130 modulates 5-FU resistance in CRC by modulating the miR-197-3p/PFKFB3 axis, which is helpful for drug chemotherapy in CRC.

Circular RNA circPLK1 promotes breast cancer cell proliferation, migration and invasion by regulating miR-4500/IGF1 axis.

BACKGROUND: Circular RNAs (circRNAs) can regulate gene expression in different malignancies. However, the biological functions of circRNA polo-like kinase-1 (circPLK1) in the tumorigenesis of breast cancer (BC) and its potential mechanisms have not been well elucidated yet. METHODS: The expression levels of circPLK1, microRNA-4500 (miR-4500), insulin-like growth factor 1 (IGF1) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell viability, cell cycle distribution, cell migration and invasion were determined by Cell Counting Kit-8 (CCK-8) assay, flow cytometry and transwell assay, respectively. Western blot assay was used to analyze the protein levels of cyclin-dependent kinase (CDK) 4 and CDK-6. The relationship between miR-4500 and circPLK1 or IGF1 was predicted by starBase v3.0 and verified by dual-luciferase reporter assay and RNA pull-down assay. The mice xenograft model was established to investigate the roles of circPLK1 in vivo. RESULTS: CircPLK1 and IGF1 were upregulated and miR-4500 was downregulated in BC tissues and cells. Interference of circPLK1 inhibited BC cell growth, migration and invasion, which was reversed by overexpression of IGF1. Moreover, circPLK1 could directly bind to miR-4500 and IGF1 was verified as a direct target of miR-4500. Furthermore, IGF1 overexpression abated the inhibitory effects of miR-4500 upregulation on proliferation, migration and invasion of BC cells. Mechanically, circPLK1 was a sponge of miR-4500 to regulate IGF1 expression in BC cells. Besides, circPLK1 knockdown suppressed tumor growth via upregulating miR-4500 and downregulating IGF1. CONCLUSIONS: CircPLK1 silence inhibited BC cell growth, migration and invasion by regulating miR-4500/IGF1 axis, suggesting circPLK1/miR-4500/IGF axis might be a potential therapeutic target.

Curcumin suppresses lung cancer progression via circRUNX1 mediated miR-760/RAB3D axis.

BACKGROUND: Curcumin is a natural chemical component that has an anticancer effect. The aim of this study was to explore the potential molecular mechanism of curcumin regulating lung cancer (LC) progression. METHODS: The expression of circRUNX1, miR-760 and Ras-like GTPase 3D (RAB3D) was detected by qRT-PCR. Cell proliferation were determined by CCK8 assay and colony formation assay. Cell apoptosis, migration and invasion were detected by flow cytometry, wound healing and transwell assays. Protein levels were examined by western blot (WB) analysis. RNA interaction was confirmed by dual-luciferase reporter assay. LC xenograft tumors were constructed using BALB/c nude mice. RESULTS: CircRUNX1 was upregulated in LC and its expression could be inhibited by curcumin. Curcumin reduced LC cell proliferation, metastasis, and accelerate apoptosis, while circRUNX1 overexpression reversed these effects. MiR-760 was confirmed to be a target of circRUNX1, which could reverse the effects of circRUNX1 on curcumin-treated LC cell functions. RAB3D was a target of miR-760, and its knockdown reversed the promotion effect of miR-760 inhibitor on the progression of curcumin-treated LC cells. CONCLUSION: Curcumin suppressed LC progression via circRUNX1/miR-760/RAB3D axis.

Creating a pseudometallic state of K+ by intercalation into 18-crown-6 grafted on polyfluorene as electron injection layer for high performance PLEDs with oxygen- and moisture-stable Al cathode.

Polymer light-emitting diodes (PLEDs) suffer from inadequate lifetimes because of the use of environmentally sensitive metals as the cathodes. We present the use of water/methanol-soluble polyfluorene grafted with 18-crown-6 chelating to K(+) as the electron-injection layer (EIL) for deep-blue-emission PLEDs, allowing the use of environmentally stable Al as the cathode since electron donation from the 18-crown-6 can reduce K(+) to a stable "pseudometallic state", enabling it to act as an intermediate step for electron injection. Furthermore, when poly(ethylene oxide) was blended into the EIL to provide hole blocking (HB), the device exhibited the highest performance reported to date for a deep-blue-emission PLED based on a conjugated polymer as the emitting layer, with a brightness of 54,800 cd/m(2) and an external quantum efficiency of 5.42%. The use of such an EI-HB layer opens a broad avenue leading toward industrialization of PLEDs.

Enhancing Absorption Performance of CO2 by Amine Solution through the Spiral Wired Channel in Concentric Circular Membrane Contactors.

The CO2 absorption rate by using a Monoethanolamide (MEA) solution through the spiral wired channel in concentric circular membrane contactors under both concurrent-flow and countercurrent-flow operations was investigated experimentally and theoretically. The one-dimensional mathematical modeling equation developed for predicting the absorption rate and concentration distributions was solved numerically using the fourth Runge-Kutta method under various absorbent flow rate, CO2 feed flow rate and inlet CO2 concentration in the gas feed. An economical viewpoint of the spiral wired module was examined by assessing both absorption flux improvement and power consumption increment. Meanwhile, the correlated average Sherwood number to predict the mass-transfer coefficient of the CO2 absorption mechanisms in a concentric circular membrane contactor with the spiral wired annulus channel is also obtained in a generalized and simplified expression. The theoretical predictions of absorption flux improvement were validated by experimental results in good agreements. The amine solution flowing through the annulus of a concentric circular tube, which was inserted in a tight-fitting spiral wire in a small annular spacing, could enhance the CO2 absorption flux improvement due to reduction of the concentration polarization effect. A larger concentration polarization coefficient (CPC) was achieved in the countercurrent-flow operations than that in concurrent-flow operations for various operations conditions and spiral-wire pitches. The absorption flux improvement for inserting spiral wire in the concentric circular module could provide the maximum relative increment up to 46.45%.

Down-regulation of circ-PTN suppresses cell proliferation, invasion and glycolysis in glioma by regulating miR-432-5p/RAB10 axis.

BACKGROUND: Circular RNAs (circRNAs) are related to the carcinogenesis of cancers, including glioma. However, the role and mechanism of circRNA pleiotrophin (circ-PTN) remain largely unknown. METHODS: Glioma tissues (n = 30) and normal tissues were obtained. Glioma cell lines LN229 and A172 were cultured for experiments in vitro. circ-PTN, microRNA-432-5p (miR-432-5p) and Ras-related protein Rab-10 (RAB10) levels were examined via quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation, invasion and glycolysis were examined via 3-(4, 5-Dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, colony formation analysis, transwell invasion analysis, specific glucose, lactate or adenosine triphosphate assay kit and western blot. The relationship of miR-432-5p and circ-PTN or RAB10 was analyzed via dual-luciferase reporter analysis. The effect of circ-PTN on glioma development in vivo was explored by a murine xenograft model. RESULTS: circ-PTN expression was enhanced and miR-432-5p abundance was reduced in glioma tissues and cells. circ-PTN silence suppressed cell proliferation, invasion and glycolysis. circ-PTN regulated glioma development by directly sponging miR-432-5p. RAB10 was a target of miR-432-5p and miR-432-5p inhibited cell proliferation, invasion and glycolysis by targeting RAB10. circ-PTN could modulate RAB10 expression via miR-432-5p. circ-PTN knockdown reduced glioma cell xenograft tumor growth in vivo. CONCLUSION: circ-PTN knockdown repressed cell proliferation, invasion and glycolysis in glioma via modulating miR-432-5p and RAB10.