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Supplemental Material, sj-pdf-1-tct-10.1177_15330338211004950 for Knockdown of circ_NEK6 Decreased 131I Resistance of Differentiated Thyroid Carcinoma via Regulating miR-370-3p/MYH9 Axis by Fukun Chen, Shuting Yin, Zhiping Feng, Chao Liu, Juan Lv, Yuanjiao Chen, Ruoxia Shen, Jiaping Wang and Zhiyong Deng in Technology in Cancer Research & Treatment

Recent research has suggested that long non-coding RNA (lncRNA) is involved in the tumorigenesis and development of breast cancer (BC). This meta-analysis aimed to identify the diagnostic role of lncRNAs in BC.All relevant studies were systematically searched through PubMed, Web of Science, Cochrane Library, and EMBASE databases. The diagnostic values of lncRNAs were mainly assessed by pooled sensitivity (SEN), specificity (SPE), and summary receiver operating characteristic area under the curve (SROC AUC). Meta-DiSc 1.4, Review Manager 5.3 and STATA 12.0 were used for statistical analysis.A total of 24 eligible studies were included in this meta-analysis. The pooled SEN, SPE, and AUC were 0.75 (95% CI: 0.68 - 0.81), 0.77 (95% CI: 0.70 - 0.82), and 0.82 (95% CI: 0.79 - 0.86), respectively, suggesting that the lncRNAs test had a high accuracy for the diagnosis of BC. Obvious heterogeneity might come from the dysregulated state of lncRNAs through subgroup and meta-regression analysis (p0.001). Fagan diagram showed clinical value of lncRNAs test in BC.Abnormal expression of lncRNAs exhibits a high efficacy for diagnosing BC, which is promising in clinical application.

Papillary thyroid cancer (PTC) is a common tumor malignancy of the endocrine system worldwide. Recently, circular RNAs (circRNAs) have been reported to participate in diverse pathological processes, especially in tumorigenesis. However, the functional role and mechanism of circRNA pleckstrin and Sec7 domain containing 3 (circ-PSD3) in PTC are still unclear. In this study, qRT-PCR results showed that circ-PSD3 was significantly upregulated in PTC tissues and cell lines. Meanwhile, circ-PSD3 overexpression was positively associated with larger tumor size, TNM stage, and lymph node metastasis. Knockdown of circ-PSD3 suppressed the proliferation and invasion of PTC cells. Besides, circ-PSD3 interacted with miR-7-5p to reduce its expression, and methyltransferase like 7B (METTL7B) was verified as a target gene of miR-7-5p. Functionally, inhibition of circ-PSD3 impeded PTC cell proliferation and invasion via targeting miR-7-5p to downregulate METTL7B expression. Taken together, silencing of circ-PSD3 hampered the proliferation and invasion of PTC cells via upregulating the inhibitory effect of miR-7-5p on METTL7B expression. Therefore, circ-PSD3 could be a potential diagnostic biomarker or molecular treatment target for PTC.

It is difficult to comprehensively master and precisely regulate the external factors distribution of automobile weathering in non-uniform thermal environment as well as the consequent disequilibrium weathering problem, while exploring weather-resistant materials in uniform thermal environment. Thus, a numerical calculation method for the weathering external factors is proposed, on the basis of annual experimental study on the outdoor weathering inconsistencies of auto-parts. The time&ndash, space distribution characteristics and day&ndash, night variation rules of the external factors are studied, and the disequilibrium weathering mechanism among parts is revealed from the perspective of non-uniform distribution of external factors. The laws of automotive physical parameters, orientations and locations, as well as their influences on external factors distribution are analyzed in detail, and hereby the targeted schemes to effectively reduce the local external factor intensity and the thermal gradient between parts are investigated. The method can be used to rapidly predict weathering external factors distribution of vehicle exposed to outdoor in any direction during day and night, so as to provide auto-parts with differentiated test schemes in accelerated tests and IP/DP box tests, and it also contributes to present some pertinence guidance for the accurate regulation of automobile disequilibrium weathering on regions at different levels.

M2-like tumour-associated macrophages (TAMs) have been demonstrated to promote the growth of anaplastic thyroid carcinoma (ATC). However, the underlying mechanism of M2-like TAMs in ATC remains unclear. Thus, in the present study, the role and mechanism of M2-like TAMs in ATC were investigated. M2-like TAMs were induced by treatment with PMA, plus IL-4 and IL-13, and identified by flow cytometry. Transwell and sphere formation assays were applied to assess the invasion and stemness of ATC cells. The expression levels of insulin-like growth factor (IGF)-1 and IGF-2 were examined by ELISA and reverse transcription-quantitative PCR. Proteins related to the epithelial-mesenchymal transition (EMT), stemness and the PI3K/AKT/mTOR pathway were examined via western blotting. Immunohistochemistry (IHC) was used to detect the expression of the M2-like TAM markers CD68 and CD206 in ATC tissues and thyroid adenoma tissues. It was found that treatment with PMA plus IL-4 and IL-13 successfully induced M2-like TAMs. Following co-culture with M2-like TAMs, the invasive ability and stemness of ATC cells were significantly increased. The expression levels of the EMT-related markers N-cadherin and Vimentin, the stemness-related markers Oct4, Sox2 and CD133, and the insulin receptor (IR)-A/IGF1 receptor (IGF1R) were markedly upregulated, whereas E-cadherin expression was significantly decreased. In addition, the production of IGF-1 and IGF-2 was significantly increased. Of note, exogenous IGF-1/IGF-2 promoted the invasion and stemness of C643 cells, whereas blocking IGF-1 and IGF-2 inhibited metastasis and stemness by repressing IR-A/IGF-1R-mediated PI3K/AKT/mTOR signalling in the co-culture system. IHC results showed that the expression of CD68 and CD206 was obviously increased in ATC tissues. To conclude, M2-like TAMs accelerated the metastasis and increased the stemness of ATC cells, and the underlying mechanism may be related to the section of IGF by M2-like TAMs, which activates the IR-A/IGF1R-mediated PI3K/AKT/mTOR signalling pathway.

IgE-mediated activation of Na(+)-H(+) exchanger-1 (Nhe1) induces aortic cell extracellular acidification and promotes cell apoptosis. A pH-sensitive probe pHrodo identified acidic regions at positions of macrophage accumulation, IgE expression, and cell apoptosis in human and mouse abdominal aortic aneurysm (AAA) lesions. Angiotensin-II-induced AAA in Nhe1-insufficient Apoe(−/−)Nhe1(+/−) mice and Apoe(−/−)Nhe1(+/+) littermates tested Nhe1 activity in experimental AAA, because Nhe1(–/−) mice develop ataxia and epileptic-like seizures and die early. Nhe1 insufficiency reduced AAA incidence and size, lesion macrophage and T-cell accumulation, collagen deposition, elastin fragmentation, cell apoptosis, smooth muscle cell loss, and matrix metalloproteinase (MMP) activity. Nhe1 insufficiency also reduced blood pressure and the plasma apoptosis marker translationally controlled tumor protein (TCTP), but did not affect plasma IgE. While pHrodo localized the acidic regions to macrophage clusters, IgE expression, and cell apoptosis in AAA lesions from Apoe(−/−)Nhe1(+/+) mice, such acidic areas were much smaller in lesions from Apoe(−/−)Nhe1(+/–) mice. Nhe1-FcεR1 colocalization in macrophages from AAA lesions support a role of IgE-mediated Nhe1 activation. Gelatin zymography, immunoblot, and RT-PCR analyses demonstrated that Nhe1 insufficiency reduced the MMP activity, cysteinyl cathepsin expression, IgE-induced apoptosis, and NF-κB activation in macrophages and blocked IgE-induced adhesion molecule expression in endothelial cells. A near-infrared fluorescent probe (LS662) together with fluorescence reflectance imaging of intact aortas showed reduced acidity in AAA lesions from Nhe-1-insufficient mice. This study revealed extracellular acidity at regions rich in macrophages, IgE expression, and cell apoptosis in human and mouse AAA lesions and established a direct role of Nhe1 in AAA pathogenesis.

Clinical studies reveal changes in blood eosinophil counts and eosinophil cationic proteins that may serve as risk factors for human coronary heart diseases. Here we report an increase of blood or heart eosinophil counts in humans and mice after myocardial infarction (MI), mostly in the infarct region. Genetic or inducible depletion of eosinophils exacerbates cardiac dysfunction, cell death, and fibrosis post-MI, with concurrent acute increase of heart and chronic increase of splenic neutrophils and monocytes. Mechanistic studies reveal roles of eosinophil IL4 and cationic protein mEar1 in blocking H2O2- and hypoxia-induced mouse and human cardiomyocyte death, TGF-β-induced cardiac fibroblast Smad2/3 activation, and TNF-α-induced neutrophil adhesion on the heart endothelial cell monolayer. In vitro-cultured eosinophils from WT mice or recombinant mEar1 protein, but not eosinophils from IL4-deficient mice, effectively correct exacerbated cardiac dysfunctions in eosinophil-deficient ∆dblGATA mice. This study establishes a cardioprotective role of eosinophils in post-MI hearts., Blood eosinophil (EOS) counts may serve as risk factors for human coronary heart diseases. Here the authors show that increased circulating and myocardial EOS after myocardial infarction play a cardioprotective role by reducing cardiomyocyte death, cardiac fibroblast activation and fibrosis, and endothelium activation-mediated inflammatory cell accumulation.

Aims This study aims to explore the effect and underlying mechanism of zoledronic acid (ZA) on the incidence of thyroid cancer (TC) tumorigenesis. Materials and methods Human mononuclear cells THP-1 were differentiated into M2-like tumor associated macrophages (TAMs) by incubation with PMA followed by additional incubation of IL-4 and IL-13. TC cells TPC-1 and IHH4 were co-cultured with M2-like TAMs. Identification of M2-like TAMs markers were determined by immunohistochemistry or flow cytometry. Cell proliferation, stemness and migration/invasion ability were measured by colony, sphere formation assay and transwell assay, respectively. The expression levels of cell stemness, EMT and Wnt/β-catenin pathway-related factors were verified by qRT-PCR, Western blotting, and immunofluorescence. A subcutaneous tumor model was established in nude mice to examine the in vivo effects of ZA. Key findings M2-like TAMs were enriched in TC tissues, and they promoted the colony/sphere formation, accompanied with a down-regulated expression in E-cadherin and an up-regulated expression in N-cadherin, Vimentin and other stemness-associated markers (CD133, Oct4, c-Myc) in TC cells. The effects were suppressed when ZA co-treatment was given, because ZA inhibited the polarization of M2-like TAMs and β-catenin entry into the nucleus. Moreover, in agreement with in vitro data, ZA also limited subcutaneous tumor formation and macrophage enrichment in nude mice. Significance ZA suppressed M2-like TAMs induced TC cell proliferation, stemness and metastasis through inhibiting M2-like TAMs polarization and Wnt/β-catenin pathway, which sheds light on the mechanisms of TC and provides avenues for the development of clinical therapy to TC.

Exosomes have appeared as fundamental vehicle-modulated crosstalk among various cells in the tumor microenvironment. The systematic understanding of exosomes in gastric cancer (GC) enhances our comprehension about the tumor growth, metastasis, chemoresistance and diagnosis of cancers. The versatile functions of exosomes provide reasonable explanations about the propensity for GC metastasis. The selectively enriched components, especially some exosomal miRNAs, are potential noninvasive biomarkers for sensitive and specific GC diagnosis. Given the characteristics of exosomes, frontier researchers are stimulated to modulate the biogenesis, concentrations or release of exosomes so as to disturb malignant signals between cells. Abnormal expression profiles of exosomal miRNAs afford potential GC therapeutic or diagnostic strategies in future.

Objective: By binding to its high-affinity receptor FcεR1, IgE activates mast cells, macrophages, and other inflammatory and vascular cells. Recent studies support an essential role of IgE in cardiometabolic diseases. Plasma IgE level is an independent predictor of human coronary heart disease. Yet, a direct role of IgE and its mechanisms in cardiometabolic diseases remain incompletely understood. Approach and Results: Using atherosclerosis prone Apoe −/− mice and IgE-deficient Ige −/− mice, we demonstrated that IgE deficiency reduced atherosclerosis lesion burden, lesion lipid deposition, smooth muscle cell and endothelial cell contents, chemokine MCP (monocyte chemoattractant protein)-1 expression and macrophage accumulation. IgE deficiency also reduced bodyweight gain and increased glucose and insulin sensitivities with significantly reduced plasma cholesterol, triglyceride, insulin, and inflammatory cytokines and chemokines, including IL (interleukin)-6, IFN (interferon)-γ, and MCP-1. From atherosclerotic lesions and peritoneal macrophages from Apoe −/− Ige −/− mice that consumed an atherogenic diet, we detected reduced expression of M1 macrophage markers (CD68, MCP-1, TNF [tumor necrosis factor]-α, IL-6, and iNOS [inducible nitric oxide synthase]) but increased expression of M2 macrophage markers (Arg [arginase]-1 and IL-10) and macrophage-sterol-responsive-network molecules (complement C3, lipoprotein lipase, LDLR [low-density lipoprotein receptor]-related protein 1, and TFR [transferrin]) that suppress macrophage foam cell formation. These IgE activities can be reproduced in bone marrow-derived macrophages from wild-type mice, but muted in cells from FcεR1-deficient mice, or blocked by anti-IgE antibody or complement C3 deficiency. Conclusions: IgE deficiency protects mice from diet-induced atherosclerosis, obesity, glucose tolerance, and insulin resistance by regulating macrophage polarization, macrophage-sterol-responsive-network gene expression, and foam cell formation.

Considering the resistance of papillary thyroid cancer (PTC) 131I therapy, this study was designed to find a solution at molecular respect. By probing into lncRNA-NEAT1/miR-101-3p/FN1 axis and PI3K/AKT signaling pathway, this study provided a potential target for PTC therapy. 131I-resistant cell lines were established by continuous treatment with median-lethal 131I. Bioinformatic analysis was applied to filtrate possible lncRNA/miRNA/mRNA and related signaling pathway. Luciferase reporter assay was employed in the verification of the targeting relationship between lncRNA and miRNA as well as miRNA and mRNA. MTT assay and flow cytometry assay were performed to observe the impact of NEAT1/miR-101-3p/FN1 on cell viability and apoptosis in radioactivity iodine (RAI)-resistant PTC cell lines, respectively. Western blot and qRT-PCR were conducted to measure the expression of proteins and mRNAs in RAI-resistant PTC tissues and cells. Meanwhile, endogenous PTC mice model were constructed, in order to verify the relation between NEAT1 and RAI-resistance in vivo. NEAT1 was over-expressed in RAI-resistant PTC tissues and cell lines and could resist RAI by accelerating proliferation accompanied by suppressing apoptosis. It indicated that overexpressed NEAT1 restrained the damage of RAI to tumor in both macroscopic and microcosmic. Besides, NEAT1/miR-101-3p exhibited a negative correlation by directly targeting each other. The expression of FN1, an overexpressed downstream protein in RAI-resistance PTC tissues, could be tuned down by miR-101-3p, while the decrease could be restored by NEAT1. In conclusion, both in vitro and in vivo, NEAT1 suppression could inhibit 131I resistance of PTC by upregulating miR-101-3p/FN1 expression and inactivated PI3K/AKT signaling pathway both in vitro and in vivo.

Backgrounds. Doxorubicin (DOX) is an effective therapeutic drug for malignant tumors; however, its clinical applications were limited by its side effects, especially the cardiotoxicity caused by ROS-mediated p53 and MAPK signal pathways’ activation-induced cell apoptosis. Sanyang Xuedai mixture (SYKT) has been reported as an antioxidant agent and attenuated DOX-induced cardiotoxicity by targeting ROS-mediated apoptosis, but the mechanisms are still not fully delineated. Objective. This study aimed at investigating whether SYKT alleviated DOX-induced cardiotoxicity by inhibiting ROS-mediated apoptosis and elucidating the role of ROS-mediated p53 and MAPK signal pathways’ activation in this process. Materials and Methods. Identification, separation, and culture of mouse primary cardiomyocytes. Cells were treated with DOX (1 μM), SYKT (30 mg/mL), or SYKT coupled with DOX. The p53 inhibitor Pifithrin-α (PFT-α), p38/MAPK inhibitor SB203583 (SB), and JNK inhibitor SP600125 (SP) were used as positive control. Western blot was employed to detected p53 and p38 as well as JNK expressions and the activation and translocation of Bax and cytochrome C. Flow cytometer (FCM) was used to detect the mitochondrial membrane potential and cell apoptosis. Results. After separation and culture, 95% of cells showed positive cTnI expression, which indicated that mouse primary cardiomyocytes were successfully identified in our research. DOX activated p53 and MAPK signal pathways in a time-dependent manner, which were inactivated by being cotreated with SYKT, PFT-α, or SB, respectively. DOX significantly decreased Bax and increased cytochrome c expressions in the cytoplasm, whereas Bax was upregulated and cytochrome c was downregulated in the mitochondria, which were reversed by SYKT treatment. Besides, DOX reduced mitochondria membrane potential (MMP) in cardiomyocytes compared to the control group; SYKT recovered its MMP and attenuated DOX-induced cardiomyocyte injury. Of note, DOX increased the expression levels of cleaved caspase-3 as well as poly ADP-ribose polymerase (PARP) and promoted cell apoptosis, which were also reversed by SYKT treatment. Discussion and Conclusions. Our results indicated that SYKT alleviated DOX-induced cardiotoxicity by inhibiting p53 and MAPK signal pathways’ activation-mediated apoptosis, and it might serve as a potential therapeutic agent for DOX-induced cardiotoxicity.

Structure stability of CeO2 nanoparticles and nanorods were studied for ethanol steam reforming reaction over Ir/CeO2 nanocatalysts. Characterizations of BET, XRD, HRTEM, H2-TPR and H2O-TPD et al. were applied to analyze surface areas, sizes, morphologies, redox properties and water activation of the nanocatalysts. Performance results revealed that reaction patterns of ethanol steam reforming reaction were dependent on the structures of CeO2 supports, originating from different abilities in water activation. After long time stability tests conducted at high temperature of 923 K, the CeO2 nanoparticles maintained original polyhedral shape, while the CeO2 nanorods changed to polyhedrons. The shape variation of the nanorods was supposed to associated with OH groups combination and oxygen exchange in surface crystal planes of ceria nanorods, which diminished oxygen vacancies and reconstructed ceria morphology.

In this study, we aimed at investigating effects of lncRNA ADAMTS9-AS2 on lung cancer progression through regulating miR-223-3p and TGFBR3 expressions. Expressions of ADAMTS9-AS2 in lung cancer tissues and cell lines were determined by reverse transcriptase polymerase chain reaction (qRT-PCR). TargetScan and miRcode were used to predict the targeting relationships, respectively. The luciferase reporter system was used to verify that the relationship among ADAMTS9-AS2, TGFBR3 and miR-223-3p. Western blot assay tested the protein level changes in TGFBR3. Cell proliferation was determined by CCK-8 assay. Cell cycle and cell apoptosis were detected by flow cytometry assay, and migration and invasion were determined by transwell assay. Tumor xenograft model was developed to study the influence of ADAMTS9-AS2 on tumor growth in vivo. qRT-PCR results demonstrated that lncADAMTS9-AS2 was lowly expressed in lung cancer tissues. High expression of ADAMTS9-AS2 in lung cancer cells significantly reduced proliferation ability and inhibited migration, as well as elevating their apoptosis rate. In vivo assay found that ADAMTS9-AS2 suppressed the lung tumor growth. Bioinformatics predicted that miR-223-3p bound directly to the ADAMTS9-AS2 and TGFBR3, which was later confirmed by luciferase reporter system. ADAMTS9-AS2 transfection increased TGFBR3 mRNA and protein expressions in lung cancer cells, but miR-223-3p transfection significantly decreased them. Besides, our results showed that miR-223-3p induced cellular apoptosis while TGFBR3 group showed the complete opposite effect. It was proved that ADAMTS9-AS2 and TGFBR3 were the direct genes of miR-223-3p. MiR-223-3p promotes proliferation, migration and invasion of lung cancer cells by targeting TGFBR3. Therefore, ADAMTS9-AS2, miR-223-3p and TGFBR3 may provide potential targets for the treatment of lung cancer patients. © 2018 IUBMB Life, 70(6):536-546, 2018.

Thyroid carcinoma is primarily treated by surgery combined with radioactive 131iodine (131I) treatment; however, certain patients exhibit resistance to 131I treatment. Previous research indicated that nuclear factor-κB (NF-κB) was associated with resistance to 131I in cancer cells. The present study aimed to investigate the effects of NF-κB on 131I uptake and apoptosis in thyroid carcinoma cells. TPC-1 and BCPAP cell lines were employed as research models in the present study, and the expression of NF-κB was inhibited by RNA interference (RNAi). The ability of TPC-1 and BCPAP cells to uptake 131I was measured and the cell viability was detected by an MTT assay. Finally, the expression of the apoptosis-associated proteins X-linked inhibitor of apoptosis (XIAP), cellular inhibitor of apoptosis protein 1 (cIAP1) and caspase-3 in TCP-1 and BCPAP cells was determined by western blotting. Western blotting results demonstrated that the expression levels of NF-κB in TPC-1 and BCPAP cells were successfully downregulated by RNAi (P0.05). MTT experiments demonstrated that the inhibition of NF-κB expression in combination with radiation (131I treatment) led to a marked reduction in cell viability (P

In this study, potassium persulfate, N,N'-methylene bisacrylamide (MBA), and soluble starch (ST) were in situ cross-linked into porous antimicrobial starch particles containing N-halamine functional groups (PST–MBA–Cl). Then, polyacrylonitrile (PAN)/silica aerogel (SA)/zinc oxide (ZnO) beaded fibers containing PST–MBA–Cl particles were prepared by electrospinning. Scanning electron microscopy results demonstrated the uniform dispersion of the PST–MBA–Cl particles and ZnO on the surface and interior of the beaded fiber when the concentration of the PST–MBA–Cl particles was 15%. The composite beaded fibers prepared after chlorination and soaking in zinc salt solutions of different pH values had a higher degree of interior fluffiness. For the analysis of the effectivity of the prepared particles using 108 CFU/mL gram-positive (S. aureus) and gram-negative (E. coli) bacterial human pathogens, the inhibition zone was 15.97 ± 0.12 and 17.81 ± 0.23 mm, respectively. Meanwhile, the degradation efficiency of PAN and SA for the cationic dye methylene blue (MB) was 88.00% ± 1.83%. The PAN/SA/PST–MBA–Cl/ZnO composite beaded fiber showed good antibacterial properties and a fast recovery rate, and its degradation efficiency for MB was retained at ~80% after five cycles. Thus, the PAN/SA/ PST–MBA–Cl/ZnO beaded fibers can be used as an environment-friendly and reusable adsorbing material for the removal of dyes from industrial wastewater.

Thermal catalysis is the most investigated approach for methane dry reforming (MDR) reaction over Ni-based catalysts. However, sintering and carbon deposition in the conventional approach tend to deactivate the Ni catalysts. Developing new technique to resolve the problems is a hot topic for MDR. Herein, we reported a novel (Ni/CeO2)@SiO2 catalyst for MDR by photothermal catalysis. The catalyst was characterized by BET, XRD, TEM and UV–vis diffuse reflectance spectrum to analysis structural and optical properties, which were applied to build relationship with MDR performance. The results revealed that band gap energy of ceria in the catalyst was significantly narrowed by the tiny size of crystal ceria, leading to strong absorbance of visible solar light. The adsorption considerably promoted activations of CH4 on Ni and CO2 on CeO2, and greatly improved gasification of CHx at Ni-CeO2 boundaries. Along with confinement effect from silica shell, sintering and carbon deposition were both resolved for the (Ni/CeO2)@SiO2 catalyst in photothermal MDR. Consequently, photothermal MDR was higher and more stable than thermal MDR over the catalyst. The work provided a new way of photothermal MDR to enhance activity and stability, and simultaneously resolved problems of sintering and carbon deposition.

All over the world, the nuclear reactor technology has been in the critical stage of transformation and upgrading. Also, there have been the higher requirements for the key technical indicators, such as the power level, the miniaturization and the security. According to analyzing the engineering requirements of typical nuclear reactor devices, the authors demonstrated the scientific problems and the physical mechanisms behind the limitation of thermal-hydraulic parameters, such as the fuel assembly, the steam generator, and the special safe system. Thus, the technical route of heat transfer enhancement was put forward in this paper. The technology of heat transfer enhancement referred to the application of various engineering means to improve the heat transfer performance of component and reduce the power consumption of coolant, the component temperature, as well as the device size. In this paper, the heat transfer enhancement technology was divided into the passive technology and the active technology. Meanwhile, the passive technology could be subdivided into the structure innovation technology and the surface modification technology. The active technology could be subdivided into the magnetic field technology and the electric filed technology. Based on the analyses of this paper, it was considered that the effects of different heat transfer enhancement technologies on the single-phase and two-phase conditions were quite different. Moreover, the corresponding technical development maturity and the manufacturing process were also much different. First of all, the structure innovation technology mainly included two categories: the micro-channel technology and the longitudinal vortex technology. By increasing the specific surface area of thermal component, enhancing the turbulent mixing degree of flow field, and disturbing the near-wall thermal boundary layer, the heat transfer performance of single-phase and two-phase conditions could be significantly improved. The above technology had been widely applied to many heat transfer fields, and the manufacturing technology was mature as well as diversified, which had the strong application prospect in the field of reactor core and heat exchanger without nuclear conditions. It should be noted that the technical difficulty of structure innovation technology lied in the optimization of structure design to obtain the best enhanced heat transfer performance. As for the surface modification technology, it mainly included the surface micro-nano structure technology and the surface coating technology. Moreover, it was suggested that the structural dimensions of above two technologies were far smaller than that of the near-wall thermal boundary layer, and the corresponding effects on the sing-phase heat transfer condition was not obvious. However, the above two technologies could significantly affect the bubble dynamics and the two-phase interface evolution under boiling condition, which could obviously improve the heat transfer performance under two-phase condition. In addition, the magnetic field technology and the electric field technology belonged to the active heat transfer enhancement technology, which relied on the coolant physical properties and the intervention technology of flow field. It should be noted that the above two technologies could effectively improve the heat transfer performance under the single-phase and two-phase conditions. However, this kind of technology was still in the stage of scientific research, and there was no practical engineering application. Based on the current technology development, the application of these two technologies was weak in the reactor core, and the application in non-nuclear environment was also limited.

Carbonation is a typical disease that affects the long-term durability of concrete. In this paper, neural network toolbox in MATLAB software was employed to analyze sample parameters such as CO2 concentration, compressive strength, age and water-cement ratio in concrete carbonation research, and to predict the depth of carbonation. The results show that under the premise of setting reasonable parameters, the sample training results are satisfactory, the average error is about 7%∼14%, which basically meets the precision requirements of the preliminary identification of concrete carbonation depth.

A series of Ce 0.90 Co 0.10 O 2 − δ and Ce 0.90 − x Cu x Co 0.10 O 2 − δ (x = 0.03, 0.07 and 0.10) catalysts synthesized by an alkaline hydrothermal method were utilized as ozonation catalysts for the NO X (x = 1, 2) removal at low temperatures. A novel catalyst-duct separation apparatus for denitrification by catalytic ozonation was developed by our group. Ce 0.83 Cu 0.07 Co 0.10 O 2 − δ exhibits the highest catalytic activity (91.5% removal at 120 °C), whereas Ce 0.80 Cu 0.10 Co 0.10 O 2 − δ presents the lowest (74.1% removal at 120 °C). Only NO 3 − is detected in the tail solutions. The catalytic performance presents a positive relationship with the corresponding OH concentration. OH radical can be “transferred” from catalyst surface to the duct, prolonging activation time through its own reproduction reaction. The surface –OH activation, not the surface –OH density determines the OH concentration in the present method. Ce 0.83 Cu 0.07 Co 0.10 O 2 − δ contains a large number of high-activation bridging –OH, whereas the bridging –OH is absent in Ce 0.80 Cu 0.10 Co 0.10 O 2 − δ . Therefore, Ce 0.83 Cu 0.07 Co 0.10 O 2 − δ shows much higher activation for promoting the formation of OH than Ce 0.80 Cu 0.10 Co 0.10 O 2 − δ .

Co 3 O 4 nanomaterials were synthesized by hydrothermal method and were applied for low temperature CO oxidation and methane combustion. The addition of ethylene glycol and its concentration significantly influenced the size and shape of the Co 3 O 4 oxides. Nanosheets of Co 3 O 4 were synthesized in ethylene glycol solution and nanospheres were formed in water. The activity of oxygen species in the nanosheets and nanospheres were characterized by hydrogen/methane programmed reduction, oxygen programmed desorption and XPS. The results showed that the Co 3 O 4 nanosheets exhibited more active oxygen species than the Co 3 O 4 nanospheres, leading to the higher activity in the oxidative reactions. The study demonstrated the importance of active oxygen species in Co 3 O 4 catalysts to achieve high catalytic performance towards the carbon monoxide and methane elimination at low temperatures.

Iron-responsive element-binding proteins (IRPs) are master regulators of cellular iron homeostasis. Our previous work demonstrated that iron homeostasis is altered in prostate cancer and contributes to prostate cancer progression. Here we report that prostate cancer cells overexpress IRP2 and that overexpression of IRP2 drives the altered iron phenotype of prostate cancer cells. IRP2 knockdown in prostate cancer cell lines reduces intracellular iron and causes cell cycle inhibition and apoptosis. Cell cycle analysis demonstrates that IRP2-depleted prostate cancer cells accumulate in G0/G1 due to induction of p15, p21, and p27. Activation of these pathways is sufficient to significantly reduce the growth of PC3 prostate tumors in vivo. In contrast, IRP1 knockdown does not affect iron homeostasis and only modestly affects cell growth, likely through an iron-independent mechanism. These results demonstrate that upregulation of IRP2 in prostate cancer cells co-opts normal iron regulatory mechanisms to facilitate iron retention and drive enhanced tumor growth.

Background SIX homeobox 3 (SIX3) is a member of the sine oculis homeobox transcription factor family. It plays a vital role in the nervous system development. Our previous study showed that the SIX3 gene is hypermethylated, and its expression is decreased in astrocytoma, but the role of SIX3 remains unknown. Methods Chromatin-immunoprecipitation (ChIP) and luciferase reporter assay were used to confirm the binding of SIX3 to the promoter regions of aurora kinase A (AURKA) and aurora kinase B (AURKB). Confocal imaging and co-immunoprecipitation (Co-IP) were used to detect the interaction between AURKA and AURKB. Flow cytometry was performed to assess the effect of SIX3 on cell cycle distribution. Colony formation, EdU incorporation, transwell, and intracranial xenograft assays were performed to demonstrate the effect of SIX3 on the malignant phenotype of astrocytoma cells. Results SIX3 is identified as a novel negative transcriptional regulator of AURKA and AURKB, and it decreases the expression of AURKA and AURKB in a dose-dependent manner in astrocytoma cells. Importantly, interactions between AURKA and AURKB stabilize and protect AURKA/B from degradation, and overexpression of SIX3 does not affect these interactions; SIX3 also acts as a tumor suppressor, and it increases p53 activity and expression at the post-translational level by the negative regulation of AURKA or AURKB, reduces the events of numerical centrosomal aberrations and misaligned chromosomes, and significantly inhibits the proliferation, invasion, and tumorigenesis of astrocytoma in vitro and in vivo. Moreover, experiments using primary cultured astrocytoma cells indicate that astrocytoma patients with a low expression of SIX3 and mutant p53 are more sensitive to treatment with aurora kinase inhibitors. Conclusion SIX3 is a novel negative transcriptional regulator and acts as a tumor suppressor that directly represses the transcription of AURKA and AURKB in astrocytoma. For the first time, the functional interaction of AURKA and AURKB has been found, which aids in the protection of their stability, and partially explains their constant high expression and activity in cancers. SIX3 is a potential biomarker that could be used to predict the response of astrocytoma patients to aurora kinase inhibitors. Electronic supplementary material The online version of this article (doi:10.1186/s13045-017-0483-2) contains supplementary material, which is available to authorized users.

Ovarian cancer is a lethal malignancy that has not seen a major therapeutic advance in over 30 years. We demonstrate that ovarian cancer exhibits a targetable alteration in iron metabolism. Ferroportin (FPN), the iron efflux pump, is decreased, and transferrin receptor (TFR1), the iron importer, is increased in tumor tissue from patients with high grade but not low grade serous ovarian cancer. A similar profile of decreased FPN and increased TFR1 is observed in a genetic model of ovarian cancer tumor initiating cells (TICs). The net result of these changes is an accumulation of excess intracellular iron and an augmented dependence on iron for proliferation. A forced reduction in intracellular iron reduces the proliferation of ovarian cancer TICs in vitro, and inhibits both tumor growth and intraperitoneal dissemination of tumor cells in vivo. Mechanistic studies demonstrate that iron increases metastatic spread by facilitating invasion through expression of matrix metalloproteases and synthesis of IL6. We show that the iron dependence of ovarian cancer tumor initiating cells renders them exquisitely sensitive in vivo to agents that induce iron-dependent cell death (ferroptosis) as well as iron chelators, and thus creates a metabolic vulnerability that can be exploited therapeutically.

Regulatory T cells (Tregs) play essential roles in obesity and diabetes. Here, we report a role of Tregs in enhancing β3-adrenergic receptor agonist CL316243 (CL)-stimulated thermogenic program in subcutaneous adipose tissue (SAT), but not in visceral fat. CL treatment for 7 days increased SAT adipocyte beiging and thermogenic gene expression in male or female mice. Adoptive transfer of Tregs enhanced this CL activity. Such Treg activity lost in male epididymal white adipose tissue (eWAT) and female gonadal gWAT. Adipocyte culture yielded the same conclusion. Tregs enhanced the expression of CL-induced thermogenic genes in SAT from male and female mice. This activity of Tregs reduced or disappeared in adipocytes from eWAT or gWAT. Both CL and Tregs induced much higher UCP-1 (uncoupling protein-1) expression in SAT from females than that from males. A mechanistic study demonstrated a role of Tregs in suppressing the expression of M1 macrophage markers (Tnfa, Il6, iNos, Ip10) and promoting the expression of M2 macrophage markers (Mrc1, Arg1, Il10) in bone-marrow-derived macrophages or in SAT from male or female mice. In female mice with pre-established obesity, Treg adoptive transfer reduced the gWAT weight in 2 weeks. Together with CL treatment, Treg adoptive transfer reduced the SAT weight and further improved CL-induced glucose metabolism and insulin sensitivity in female obese mice, but did not affect CL-induced body weight loss in male or female obese mice. This study revealed a predominant role of Tregs in female mice in promoting adipocyte beiging and thermogenesis in SAT, in part by slanting M2 macrophage polarization.

Magnetic Ni

This paper presents a calculation method of chromatic aberration of such kinds of optical systems based on the aberration theory of plane-symmetric optical systems, and the analytic expressions of the axial chromatic aberration and chromatic change in the magnification at an image plane of any position are derived. The resultant expressions are used to calculate the chromatic aberration of two single-lens optical systems with a large incidence angle, and the calculation results are compared to the ones obtained from a ray-tracing program to validate the chromatic aberration expressions. The study shows that the calculation accuracy of the chromatic aberration expressions is satisfactory. The analytical analysis of chromatic aberration is helpful in the imaging analysis and design of plane-symmetric optical systems.

Low temperature methane dry reforming by Ni-based catalysts is an economic way to convert greenhouse gases of CH4 and CO2, but carbon deposition is a great challenge. Taking the advantage of mobile oxygen on CeO2, we synthesized a Ni@SiO2@CeO2 catalyst by coating ceria on surface of Ni@SiO2 to reduce carbon deposition. H2 temperature-programmed reduction, X-ray photoelectron spectra and oxygen temperature-programmed desorption demonstrated the high oxygen mobility from ceria in Ni@SiO2@CeO2 catalyst, which significantly reduced carbon deposition and enhanced stability of methane dry reforming reaction. Experimental results revealed that methane dry reforming performance was one and a half times higher, but carbon deposition was one half lower, over the Ni@SiO2@CeO2 catalyst than over the Ni@SiO2 catalyst. The strategy of ceria coating in reducing carbon deposition and enhancing reaction stability could also be applied to other heterogeneous reactions suffering carbon deposition.

Radioresistance is a crucial factor for the failure of iodine 131 (131I)-based radiotherapy for differentiated thyroid carcinoma (DTC). This study aimed to explore the effect of circ_NEK6 on the development of 131I resistance in DTC and its potential mechanism. In this study, we demonstrated that circ_NEK6 expression was significantly elevated in 131I-resistant DTC tissues and cell lines. Knockdown of circ_NEK6 significantly repressed 131I resistance via inhibiting cell proliferation, migration, invasion abilities, and inducing cell apoptosis and DNA damage in 131I-resistant DTC cells. Mechanistically, knockdown of circ_NEK6 suppressed 131I resistance in DTC by upregulating the inhibitory effect of miR-370-3p on the expression of myosin heavy chain 9 (MYH9). In vivo experiments showed that circ_NEK6 inhibition aggravated 131I radiation-induced inhibition of xenograft tumor growth. Taken together, knockdown of circ_NEK6 repressed 131I resistance in DTC cells by regulating the miR-370-3p/MYH9 axis, indicating that circ_NEK6 may act as a potential biomarker and therapeutic target for DTC patients with 131I resistance.

In this paper, copper ferrite(CuFe2O4), prepared by a hydrothermal method, was successfully utilized in catalytic ozonation for NOx removal. CuFe2O4 shows higher activity (83%) than both CuO (79%) and Fe2O3 (70%). Hydroxyl radicals (OH) have been detected in the catalytic ozonation process, which has been confirmed to determine the catalytic performance of NOx removal. Compared to CuO and Fe2O3, CuFe2O4 exhibits more surface hydroxyl groups and oxygen vacancies, indicating that the synergetic effect of the surface hydroxyl groups and oxygen vacancies plays an important role in the enhancement of the generation of hydroxyl radicals, thus the catalytic activity. A possible mechanism for the catalytic ozonation of NOx was proposed.

Nanostructured F doped cerium and titanium mixed oxide catalyst (CeTiF) and cerium and titanium mixed oxide catalyst (CeTi) were prepared by co-precipitation method. The F is for the first time to be doped into CeTi as the ozonation catalyst. Compared to CeTi, the catalyst of CeTiF exhibited a better catalytic activity, yielding 83% NOx (x = 1, 2) conversion at 40 °C. In order to investigate the effect of F on CeO2-TiO2 catalysts for the catalytic ozonation of NOx (x = 1, 2), the catalysts were characterized by XRD, PL spectra, Raman spectra, XPS, TGA, NH3-TPD and FTIR techniques. The CeTiF exhibits higher catalytic activity than CeTi, which is found that it presents linear relationship with the OH radical concentration. The doping of F does substitute the O in Ce O Ti, Ti O Ti or Ce O Ce linkage bonds to produce more oxygen vacancies, and slightly enhances the BET surface area and hydrophilicity, which promote the chemisorption of H2O to form surface OH, and benefiting the O3 adsorption on the surface OH, thus promoting the production of OH, further improving the catalytic performance. These oxygen vacancy and surface hydroxyl groups play a critical role in the OH production for NOx removal.

Water plays a crucial role in the synthesis mechanism of metal organic framework-5 (MOF-5). Synthesized MOF-5 with good phase structure and large specific surface area is largely determined by an important synthesis factor: the total water concentration of the initial synthesis solution (C tw ). An understanding of the effects of different and high C tw on the synthesis of MOF-5 and the investigation of the maximum C tw suitable for the synthesis of MOF-5 are important to guide the synthesis of MOF-5. Through the research of the maximum C tw , a favorable synthetic approach was established which could realize the synthesis of MOF-5 with fine performance on CO2 adsorption and separation. The research results show that the maximum C tw could be as high as 1,440mmol/L, and synthesized MOF-5 still has a good phase structure and a large specific surface area of 2,136m2/g (BET). Synthesized MOF-5 by the maximum C tw exhibits a high CO2 adsorption capacity of 2.5mmol/g and a low N2 adsorption capacity of 0.2mmol/g at 298 K and 100 kPa. More importantly, synthesized MOF-5 by the maximum C tw exhibits a high selectivity for CO2/N2 of 18-22 at 298 K and 20-130 kPa in simulated flue gas.

In this paper, CO atmosphere reduced cobalt manganate (CoMn2O4/CO), prepared by a hydrothermal method, was successfully utilized in catalytic ozonation for NOx removal. CoMn2O4/CO shows higher activity (84%) than CoMn2O4/air (82%), Co3O4 (76%) and Mn2O3 (76%). Hydroxyl radicals (·OH) have been detected in the catalytic ozonation process, which has been confirmed to determine the catalytic performance of NOx removal. Compared to Co3O4 and Mn2O3, CoMn2O4 exhibits more surface hydroxyl groups and oxygen vacancies, both of which are critical for the ·OH generation. More importantly, more oxygen vacancies are generated when the CoMn2O4 is calcined in the reduced atmosphere. These oxygen vacancies benefit the adsorption of sufficient H2O to yield active surface –OH on the catalyst surface, promoting the adsorption of O3 on the surface –OH and thus the production of ·OH radicals. A possible mechanism for the catalytic ozonation of NOx was proposed.

CeO2 grown on a reduced graphene oxide nanocomposite (RGO–CeO2) was successfully synthesized by a facile alkaline hydrothermal method with the addition of ethylene glycol. For the first time, it was utilized as an ozonation catalyst for denitrification at low temperatures. The RGO–CeO2 nanocomposite, in which the content of RGO was only 2.8 wt%, exhibited much higher catalytic activities (96.8% at 40 °C) than pure nano-CeO2 (78.2% at 40 °C), which was found to exhibit a positive relationship with the concentration of ˙OH radicals. There was no correlation between the surface hydroxyl densities and the catalytic activities of RGO–CeO2, RGO and CeO2, suggesting that not all surface hydroxyl groups exhibit the same high catalytic activity. The activity of surface hydroxyl groups becomes the dominant factor for determining catalytic performance. Compared with pure nano-CeO2, the surface hydroxyl activity was enhanced for RGO–CeO2 due to the generation of more oxygen vacancies from the reduction in crystallite size and better dispersion of CeO2. The surface –OH groups at the oxygen vacancy sites were more active than the intrinsic –OH of CeO2 at promoting the generation of ˙OH radicals and being conducive to denitrification.

Based on difference in work function, novel Au nanoparticle-decorated WO3@TiO2 ternary core–shell rod-like nanocomposites (Au-WO3@TiO2) are designed and constructed as solar-light-driven photocatalysts. The photocatalytic activities were evaluated by monitoring the concentration change of methylene blue (MB) under simulated solar light irradiation. The results show that the Au-WO3@TiO2 ternary core–shell nanocomposites exhibited higher photocatalytic performance than the pure WO3 nanorods, the Au decorated WO3 nanorods and the WO3@TiO2 core–shell nanorods. The highest photocatalytic activity was found in the 1 wt% Au-WO3@TiO2 ternary core–shell nanocomposites, whose degradation efficiency and apparent rate constant (k) are 94.5% in 240 min under simulated solar light irradiation and 0.0295 min−1, respectively. The high performance of the ternary composites can be attributed to high specific area by coating of TiO2, the high utilization of solar light achieved by the surface plasmon resonance (SPR) effect of Au nanoparticles, and the low recombination rate of electrons and holes caused by electron transfer from TiO2 to Au and WO3. This study may offer a demonstration to make use of WO3 based ternary structure to help suppress the recombination of photo-induced electrons and holes in TiO2 and ultimately improve the photocatalytic efficiencies for multiple energy and environmental application.

Asthma is a frequently diagnosed chronic pulmonary disease that is increasing in incidence. It is characterized by airway narrowing due to an immune response to allergens, infections, or air pollutants. Several types of cells participate in the initiation and development of asthma, including bronchial epithelial cells, smooth muscle cells, and immune cells (mast cells, T and B cells, and dendritic cells). Exosomes released in the asthmatic microenvironment exert a crucial function in intercellular signaling by transporting their contents, such as RNA, DNA, proteins, and lipid mediators, to recipient cells, which play key roles in the pathogenesis of asthma. In the present review, we summarize currently available information on the function of exosomes in the asthmatic microenvironment.

A vast amount of evidence indicates that long non-coding RNAs (lncRNAs) are involved in cancer. Previous studies have indicated that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) is aberrantly expressed in lung cancer, pancreatic ductal adenocarcinoma and hepatocellular carcinoma. However, the role of DGCR5 in papillary thyroid carcinoma (PTC) has remained elusive. In the present study, it was revealed that DGCR5 was significantly downregulated in PTC tissues compared with that in adjacent normal tissues. Through functional experiments, it was demonstrated that ectopic overexpression of DGCR5 markedly suppressed PTC cell growth and invasion. A bioinformatics analysis suggested that DGCR5 binds to microRNA (miR)-2861. A total of 5 putative binding sites for miR-2861 were identified in DGCR5, and a luciferase reporter assay confirmed the direct interaction between DGCR5 and miR-2861. Furthermore, reverse transcription-quantitative polymerase chain reaction analysis indicated that ectopic overexpression of DGCR5 led to a decreased expression of miR-2861 in PTC cells and miR-2861 mimic transfection caused a downregulation of DGCR5. miR-2861 level was upregulated in PTC tissues compared with adjacent tissues and negatively correlated with DGCR5 level. In addition, rescue experiments indicated that ectopic expression of miR-2861 reversed the effects of DGCR5 overexpression on PTC cell proliferation and invasion. Taken together, the present results demonstrated that DGCR5 inhibits PTC progression via sponging miR-2861, indicating DGCR5 may serve as a therapeutic target.

Objective: To identify the significantly altered circRNAs and mRNAs in thyroid cancer, investigate their target miRNAs and determine their biological functions. Methods: The differentially expressed circRNAs, mRNAs and pathways in thyroid cancer were identified by microarray analysis and gene set enrichment analysis (GSEA). The correlative circRNAs and mRNAs were found out through Pearson correlative analysis. The common target miRNAs of circNEK6 and FZD8 related to thyroid cancer was screened out through Targetscan, miRanda and HMDD analysis. The mRNA and protein expressions in thyroid cancer tissues and cells were detected by qRT-PCR and western blot. CircRNA was confirmed by the RNase R digestion and nucleic acid electrophoresis. The target relationships were verified by the dual luciferase reporter assay. Cell viability, invasion and apoptosis were determined by MTT assay, Transwell assay and flow cytometry, respectively. Results: CircNEK6 and FZD8 were significantly up-regulated in thyroid cancer, with strong correlations. The Wnt signaling pathway was activated in thyroid cancer. MiR-370-3p was the common target miRNA of circNEK6 and FZD8, and it was down-regulated in thyroid cancer. Overexpression of circNEK6 and FZD8 could promote the growth and invasion of thyroid cancer cells, while up-regulation of miR-370-3p could suppress thyroid cancer progression and inhibit the Wnt signaling pathway. MiR-370-3p’s effect on thyroid cancer cells could be rescued by circNEK6 or FZD8. Conclusion: CircNEK6 promoted the progression of thyroid cancer through up-regulating FZD8 and activating Wnt signaling pathway by targeting miR-370-3p.

Ginsenoside-Rg1 (G-Rg1) is an agent isolated from Panax ginseng that exerts anti-fibrotic effects; however, the mechanism is still unclear. Herein, we investigated whether G-Rg1 administration can mitigate or reverse unilateral ureteral obstruction (UUO)-induced renal fibrosis by regulating the Klotho/transforming growth factor (TGF)-β1/Smad signaling pathway in rats. Sprague-Dawley male rats were subjected to UUO, and rats in the treatment group were administered G-Rg1 or G-Rg1 plus Klotho short hairpin RNA interference (shRNA), while rats in the control and model groups were administered vehicle for 14 d. Epithelial-mesenchymal transition (EMT) biomarkers and Klotho/TGF-β1 signaling molecules were examined by immunohistochemistry, quantitative real-time PCR and Western blotting. Immunohistochemistry showed that UUO induced increased pro-fibrotic TGF-β1 expression, overexpression of the mesenchymal marker, α-smooth muscle actin (α-SMA), and suppression of the epithelial marker, E-cadherin. Moreover, Western blotting analysis indicated that UUO promoted TGF-β1 and phosphorylated Smad3 (p-Smad3) expression (p

Objectives The intention of our study was to investigate the relationship between miR‐144‐3p and EZH2 as well as the effects of their interaction on cell propagation and invasiveness in lung adenocarcinoma (LUAD). Methods The expression levels of miR‐144‐3p and EZH2 in LUAD tissues and normal tissues were determined by qRT‐PCR. The dual‐luciferase reporter assay was utilized to validate the targeting relationship between miR‐144‐3p and EZH2. MTT assay and colony formation assay were performed to evaluate the viability and propagation of LUAD cells, while the effects of miR‐144‐3p and EZH2 on LUAD cell invasiveness were confirmed by transwell assay. Protein expression levels of VEGFA, MMP2, and MMP9 were measured by Western blot. Furthermore, xenograft tumor models were established to verify the effects of miR‐144‐3p on tumor formation and EZH2, VEGFA, MMP2 and MMP9 expressions in vivo. Results miR‐144‐3P was downregulated in LUAD tissues, and overexpression of miR‐144‐3p inhibited propagation and invasiveness of LUAD cells. EZH2 was a target of miR‐144‐3p and was highly expressed in LUAD cells. Knockdown of EZH2 could suppress the propagation and invasion of LUAD cells. Increased miR‐144‐3p expression exerted an inhibitory effect on LUAD tumor formation in vivo. Conclusion Overexpression of miR‐144‐3p impeded the propagation and invasiveness of LUAD cells by targeting EZH2.

Multidrug resistance (MDR) is an obstacle for cancer chemotherapy. It was reported that 20(S)-ginsenoside Rg3 (hereafter Rg3) was able to regulate MDR in mouse leukemia cells. The present study investigated the effect of Rg3 on the MDR of A549 lung cancer cells. A cell viability assay revealed that Rg3 treatment increased cisplatin (DDP) cytotoxicity in DDP resistant A549 cells (A549/DDP). Furthermore, Rg3 increases the antitumor effect of DDP on A549/DDP xenograft mice. The expression of MDR-mediated proteins, including P-glycoprotein (P-gp), multidrug resistance-associated protein (MPR1) and lung resistance protein 1 (LPR1), was detected in tumor tissue of A549/DDP xenograft mice. The results revealed that Rg3 treatment inhibited the expression of these MDR-associated proteins. Additionally, technetium-99m labeled hexakis-2-methoxyisobutylisonitrile (99mTc-MIBI) single-photon emission computed tomography was used to monitor the effect of Rg3 on cisplatin sensitivity of A549/DDP xenograft tumors. It was observed that uptake of 99mTc-MIBI was increased by Rg3 treatment, which indicated that Rg3 is able to effectively enhance chemotherapy sensitivity of A549/DDP xenograft tumors. Taken together, these results revealed that Rg3 may be able to reverse MDR of lung cancer via the downregulation of P-gp, MPR1 and LPR1.