Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway.

Triple-negative breast cancer (TNBC) is a pathological subtype of breast cancer (BC) with high malignancy, strong invasiveness and poor prognosis. Long non-coding RNA (LncRNA) plays an important role during tumorigenesis. We identified that Linc00707 was upregulated in TNBC tissues by TCGA database and RT-qPCR assay, compared with normal breast tissues and other subtypes of BC. Linc00707 promoted TNBC cells proliferation, migration and invasion. Furthermore, we found that knockdown of Linc00707 influenced autophagy via PI3K/AKT/mTOR signaling pathway in TNBC cells. Linc00707 affected the progress of TNBC cells through affecting autophagy. Further mechanistic experiments confirmed that Linc00707 could competitively bind with miR-423-5p to up-regulate MARCH2 expression, ultimately promoting TNBC progression and autophagy through PI3K/AKT/mTOR pathway. In conclusion, we demonstrate that Linc00707 is a key molecule in tumor progression and may be an effective target for patients with TNBC.

Inhibition of FNDC1 suppresses gastric cancer progression by interfering with Gßγ-VEGFR2 complex formation.

Gastric cancer (GC) is a prevalent digestive tract malignant tumor characterized by an insidious onset, ease of metastasis, rapid growth, and poor prognosis. Here, we report that fibronectin type III domain containing 1 (FNDC1) has high expression in GC and indicates poor outcomes in patients with GC. FNDC1 over-expression or knockdown promotes or inhibits tumorigenesis and metastasis, respectively. The expression of FNDC1 is upregulated by TWIST1, strengthening its interaction with Gßγ and VEGFR2. The formation of the trimers, TWIST1 plus Gßγ and VEGFR2, increases VEGFR2 phosphorylation and Gßγ trafficking, which activates RAS-MAPK and PI3K-AKT signaling, benefiting GC progression. In this study, we demonstrated that arsenite can efficiently suppress FNDC1 expression, attenuating the formation of the trimers and downstream pathways. Altogether, our results indicate that FNDC1 might be a promising target for clinical treatment and prognostic judgment, while FNDC1 inhibition by arsenite provides a new opportunity for overcoming this fatal disease.

Associations between maternal exposure to ambient air pollution and very low birth weight: A birth cohort study in Chongqing, China.

Introduction: There have been many researches done on the association between maternal exposure to ambient air pollution and adverse pregnancy outcomes, but few studies related to very low birth weight (VLBW). This study thus explores the association between maternal exposure to ambient air pollutants and the risk of VLBW, and estimates the sensitive exposure time window. Methods: A retrospective cohort study analyzed in Chongqing, China, during 2015-2020. The Generalized Additive Model were applied to estimate exposures for each participant during each trimester and the entire pregnancy period. Results: For each 10 µg/m3 increase in PM2.5 during pregnancy, the relative risk of VLBW increased on the first trimester, with RR = 1.100 (95% CI: 1.012, 1.195) in the single-pollutant model. Similarly, for each 10 µg/m3 increase in PM10, there was a 12.9% (RR = 1.129, 95% CI: 1.055, 1.209) increase for VLBW on the first trimester in the single-pollutant model, and an 11.5% (RR = 1.115, 95% CI: 1.024, 1.213) increase in the multi-pollutant model, respectively. The first and second trimester exposures of NO2 were found to have statistically significant RR values for VLBW. The RR values on the first trimester were 1.131 (95% CI: 1.037, 1.233) and 1.112 (95% CI: 1.015, 1.218) in the single-pollutant model and multi-pollutant model, respectively; The RR values on the second trimester were 1.129 (95% CI: 1.027, 1.241) and 1.146 (95% CI: 1.038, 1.265) in the single-pollutant model and multi-pollutant model, respectively. The RR of O3 exposure for VLBW on the entire trimester was 1.076 (95% CI: 1.010-1.146), and on the second trimester was 1.078 (95% CI: 1:016, 1.144) in the single-pollutant model. Conclusion: This study indicates that maternal exposure to high levels of PM2.5, PM10, NO2, and O3 during pregnancy may increase the risk of very low birth weight, especially for exposure on the first and second trimester. Reducing the risk of early maternal exposure to ambient air pollution is thus necessary for pregnant women.

The short-term effects of air pollution exposure on preterm births in Chongqing, China: 2015-2020.

Accumulating evidence suggested that the risk of preterm births (PTBs) following prenatal exposure to air pollution was inconclusive. The aim of this study is to investigate the relationship between air pollution exposure in the days before delivery and PTB and assess the threshold effect of short-term prenatal exposure to air pollution on PTB. This study collected data including meteorological factors, air pollutants, and information in Birth Certificate System from 9 districts during 2015-2020 in Chongqing, China. Generalized additive models (GAMs) with the distributed lag non-linear models were conducted to assess the acute impact of air pollutants on the daily counts of PTB, after controlling for potential confounding factors. We observed that PM2.5 was related to increased occurrence of PTB on lag 0-3 and lag 10-21 days, with the strongest on the first day (RR = 1.017, 95%CI: 1.000-1.034) and then decreasing. The thresholds of PM2.5 for lag 1-7 and 1-30 days were 100 µg/m3 and 50 µg/m3, respectively. The lag effect of PM10 on PTB was very similar to that of PM2.5. In addition, the lagged and cumulative exposure of SO2 and NO2 was also associated with the increased risk of PTB. The lag relative risk and cumulative relative risk of CO exposure were the strongest, with a maximum RR at lag 0 (RR = 1.044, 95%CI: 1.018, 1.069). Importantly, the exposure-response curve of CO showed that RR increased rapidly when the concentration exceeded 1000 µg/m3. This study indicated significant associations between air pollution and PTB. The relative risk decreases with day lag, while the cumulative effect increases. Thus, pregnant women should understand the risk of air pollution and try to avoid high concentration exposure.

Chronic exposure to yttrium induced cell apoptosis in the testis by mediating Ca2+/IP3R1/CaMKII signaling.

Introduction: Environmental pollutants, such as rare earth elements, affect human health and particularly induce reproductive system injury. Yttrium (Y), one of the most widely used heavy rare earth elements, has been reported the cytotoxicity. However, the biological effects of Y3+ in the human body are largely unknown. Methods: To further investigate the effects of Y on the reproductive system, in vivo (rat models) and in vitro studies were performed. Histopathological and immunohistochemical examination were conducted, and western blotting assays were performed to detect the protein expression. TUNEL/DAPI staining were used to detect cell apoptosis, and the intracellular calcium concentrations were also determined. Results: Long-term exposure to YCl3 in rats produced significant pathological changes. YCl3 treatment could induce cell apoptosis in vivo and in vitro. In addition, YCl3 enhanced the concentration of cytosolic Ca2+ and up regulated the expression of IP3R1/CaMKII axis in Leydig cells. However, inhibition of IP3R1 and CaMKII with 2-APB and KN93, respectively, could reverse these effects. Conclusion: Long-term exposure to yttrium could induce testicular injury by stimulating cell apoptosis, which might be associated with activation of Ca2+/IP3R1/CaMKII axis in Leydig cells.

Association of Folic Acid Supplementation in Early Pregnancy with Risk of Gestational Diabetes Mellitus: A Longitudinal Study.

BACKGROUND: Gestational diabetes mellitus (GDM) may lead to many adverse effects on women and their offspring. METHOD: 24,429 pregnant women were enrolled during early pregnancy from January 2018 to December 2021. The self-reported intake of folic acid supplements was assessed via a questionnaire. Oral glucose tolerance tests were used for the diagnosis of GDM. The association between intake or not, dose, and duration of folic acid and GDM risk was assessed. RESULTS: 6396 (26.18%) women were diagnosed with GDM. In the univariate models, folic acid was found to be correlated with total GDM risk (OR = 0.82, 95% CI: 0.70~0.95, p = 0.009). After adjusting for potential confounders, the association with total GDM risk was not significant, but the association of folic acid with 2-h PBG diagnosed GDM risk was consistently significant (OR = 0.75, 95% CI: 0.63~0.90, p = 0.002). No significant association between the dose and duration of folic acid supplementation and GDM risk was observed in the analyses. CONCLUSION: Folic acid supplementation might be a protective factor for the risk of GDM caused by the high level of postprandial blood glucose, but the dose or duration-related association between folic acid supplementation and GDM risk is not clear.

LncRNA-AC009948.5 promotes invasion and metastasis of lung adenocarcinoma by binding to miR-186-5p.

Background: Long non-coding RNAs (LncRNAs) has been confirmed to play a crucial role in the development and progression of various cancer types. Here we evaluated the expression profiles of LncRNAs in Lung adenocarcinoma (LUAD) tissues and identified a novel LncRNA, termed LncRNA-AC009948.5. However, the role and potential molecular mechanisms of this novel LncRNA in LUAD carcinogenesis is unknown. Methods: Regarding the public databases and based on integrating bioinformatics analyses, we determined whether LncRNA-AC009948.5 exerts its oncogenic functions via sponging miR-186-5p in LUAD. Furthermore, we determined whether NCAPG2 was a downstream target of miR-186-5p. Moreover, the expression level and biological function of LncRNA-AC009948.5 in LUAD were determined by qRT-PCR, cell apoptosis, Edu, transwell, wound healing and western blot assays. Besides, xenograft mice were established for validation. We explored the expression of LncRNA-AC009948.5 and its roles in the prognosis of LUAD. Results: LncRNA expression microarray data indicate that LncRNA-AC009948.5 is upregulated in LUAD samples. The present study confirmed the upregulation of LncRNA-AC009948.5 in LUAD tissues and cells. Encreased expression of LncRNA-AC009948.5 was correlated with tumor size, lymph nodes, distant metastasis and histological grade, and poor prognosis.LncRNA-AC009948.5 knockdown significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, LncRNA-AC009948.5 upregulated had opposite effects. Mechanistically, we elucidated that LncRNA-AC009948.5 could directly bind to miR-186-5p and subsequently suppress expression of the target gene of NCAPG2. Conclusions: LncRNA-AC009948.5 promotes lung adenocarcinoma cells metastasis via the miR-186-5p/NCAPG2 axis and activation of the EMT process. Which may serve as potential targets for the treatment of LUAD in the future.

The miR-4732-5p/XPR1 axis suppresses the invasion, metastasis, and epithelial-mesenchymal transition of lung adenocarcinoma via the PI3K/Akt/GSK3ß/Snail pathway.

The roles of microRNAs (miRNAs) in the occurrence, metastasis, and prognosis of lung adenocarcinoma (LUAD) have been drawing extensive attention from researchers. The aim of this study is to identify the effects of miR-4732-5p on the migration, invasion, and metastasis of LUAD. In this study, we found that the expression of miR-4732-5p was decreased in LUAD based on the data derived from The Cancer Genome Atlas (TCGA) database, tissues, and cell lines. LUAD patients with a low expression of miR-4732-5p exhibited a lower survival rate. Meanwhile, miR-4732-5p could directly target xenotropic and polytropic retrovirus receptor 1 (XPR1), and elevated XPR1 was observed in LUAD mRNA microarrays, Gene Expression Omnibus (GEO), and The Human Protein Atlas (HPA) database. Overexpression of miR-4732-5p significantly inhibits the migration, invasion, and metastasis of LUAD in vitro and in vivo, which can be reversed by overexpression of XPR1. We also found that the PI3K/Akt/GSK3ß/Snail pathway induced by EGF induced EMT could be inhibited by miR-4732-5p overexpression and XPR1 knockdown. The migration and invasion of LUAD could be converted by cytoskeletal rearrangements, and the polymerization of EGF induced F-actin in A549 cells could be inhibited by elevated miR-4732-5p. Our results suggest that miR-4732-5p exerts anti-tumor effects on the invasion and metastasis of LUAD by regulating XPR1 in vivo and in vitro, indicating that the miR-4732-5p/XPR1 axis may be a potential target for LUAD therapeutic intervention.

Association between Maternal Exposure to Ambient Air Pollution and the Risk of Preterm Birth: A Birth Cohort Study in Chongqing, China, 2015-2020.

Recent study results on the association between maternal exposure to ambient air pollution with preterm birth have been inconsistent. The sensitive window of exposure and influence level of air pollutants varied greatly. We aimed to explore the association between maternal exposure to ambient air pollutants and the risk of preterm birth, and to estimate the sensitive exposure time window. A total of 572,116 mother-newborn pairs, daily concentrations of air pollutants from nearest monitoring stations were used to estimate exposures for each participant during 2015-2020 in Chongqing, China. We applied a generalized additive model and estimated RRs and 95% CIs for preterm birth in each trimester and the entire pregnancy period. In the single-pollutant model, we observed that each 10 µg/m3 increase in PM2.5 had a statistically significant effect on the third trimester and entire pregnancy, with RR = 1.036 (95% CI: 1.021, 1.051) and RR = 1.101 (95% CI: 1.075, 1.128), respectively. Similarly, for each 10 µg/m3 increase in PM10, there were 2.7% (RR = 1.027, 95% CI: 1.016, 1.038) increase for PTB on the third trimester, and 3.8% (RR = 1.038, 95% CI: 1.020, 1.057) increase during the whole pregnancy. We found that for each 10 mg/m3 CO increases, the relative risk of PTB increased on the first trimester (RR = 1.081, 95% CI: 1.007, 1.162), second trimester (RR = 1.116, 95% CI: 1.035, 1.204), third trimester (RR = 1.167, 95% CI: 1.090, 1.250) and whole pregnancy (RR = 1.098, 95% CI: 1.011, 1.192). No statistically significant RR was found for SO2 and NO2 on each trimester of pregnancy. Our study indicates that maternal exposure to high levels of PM2.5 and PM10 during pregnancy may increase the risk for preterm birth, especially for women at the late stage of pregnancy. Statistically increased risks of preterm birth were associated with CO exposure during each trimester and entire pregnancy. Reducing exposure to ambient air pollutants for pregnant women is clearly necessary to improve the health of infants.

Chondrocyte-derived Exosomal miR-195 Inhibits Osteosarcoma Cell Proliferation and Anti-Apoptotic by Targeting KIF4A in vitro and in vivo.

BACKGROUND: Osteosarcoma (OS) is a primary malignant tumor of the bone that occurs in adolescents and is characterized by a young age at onset, high malignancy, high rate of metastasis, and poor prognosis. However, the factors influencing disease progression and prognosis remain unclear. METHODS: In this study, we aimed to investigate the role of chondrocyte-derived exosomal miR-195 in OS. We used normal human chondrocytes to form miR-195-carrying exosomes to deliver miR-195 into OS cells. Xenograft tumor experiments were performed in mice intratumorally injected with exosomal miR-195. We found that kinesin superfamily protein 4A (KIF4A) promoted OS tumor progression and anti-apoptotic. RESULES: We demonstrated that miR-195 inhibited the expression of KIF4A by directly targeting its 3'-untranslated region. Moreover, we observed that exosomal miR-195 successfully inhibited OS cell tumor growth and antiapoptotic in vitro and suppressed tumor growth in vivo. CONCLUSION: Collectively, these results demonstrate that normal human chondrocyte-derived exosomal miR-195 can be internalized by OS cells and inhibit tumor growth and antiapoptotic by targeting KIF4A, providing a new direction for clarifying the molecular mechanism underlying OS development.

[miR-144-3p Inhibits the Invasion and Metastasis of Lung Adenocarcinoma Cells 
by Targeting IRS1].

BACKGROUND: MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression, influence cellular processes, and promote disease development. Variations in miRNA expression have been observed in many diseases, including hepatitis, cardiovascular disease, and cancer. The aim of this study is to investigate the effect of miR-144-3p on the invasion and metastasis of lung adenocarcinoma by targeting recombinant insulin receptor substrate 1 (IRS1). METHODS: The expression of miR-144-3p in patients with lung adenocarcinoma was queried through bioinformatics database. MirTarPathway was used to analyze the KEGG enrichment pathway of miRNA. The expression and plasmid transfection efficiency of miR-144-3p in lung adenocarcinoma cell lines were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Transwell assay was used to detect the changes of cell invasion and migration ability in different groups. Bioinformatics determined the key genes (Hub genes) of miR-144-3p; Double luciferase target assay was used to detect the mutual binding of miR-144 and IRS1. Western blot assay was used to detect the expression of IRS1 in different cell lines and the expression of after overexpression of miR-144. RESULTS: The expression of miR-144-3p in lung adenocarcinoma tissues was decreased, qRT-PCR results indicated that the expression of miR-144-3p in lung adenocarcinoma cell A549 was significantly decreased (P<0.05), and the overexpressed plasmid was successfully transfected (P<0.05). Overexpression of miR-144 decreased the ability of cell migration and invasion (P<0.05). The expression of IRS1 was up-regulated in lung adenocarcinoma tissues. Survival analysis showed that patients with lung adenocarcinoma with high IRS1 expression had a poor prognosis (P<0.05). Double luciferase assay results showed that miR-144 could specifically identify 3'-UTR of IRS1 and inhibit reporter enzyme expression (P<0.05). Western blot indicated that the expression of IRS1 was increased in A549 cells (P<0.05). After overexpression of miR-144, the expression level of IRS1 protein was decreased (P<0.05). Transwell experiment proved that miR-144-3p could inhibit invasion and metastasis of lung adenocarcinoma cells by targeting IRS1 (P<0.05). CONCLUSIONS: MiR-144-3p inhibits the invasion and migration of A549 cells through targeted regulation of IRS1, thus playing an anticancer role in tumors.

Quantitative visual pathway abnormalities predict visual field defects in patients with pituitary adenomas: a diffusion spectrum imaging study.

OBJECTIVES: This study was to investigate clinical applicability of diffusion spectrum imaging (DSI) for quantitative detection of visual pathway abnormalities to predict the degree of visual field defects (VFD) in patients with pituitary adenomas. METHODS: Sixty-five patients with pituitary adenomas and 33 healthy controls underwent conventional MRI and DSI scanning that allowed high-angular-resolution fiber tracking. Optic chiasmal compression and VFD were confirmed in all patients via radiological and neuro-ophthalmological examinations. Quantitative assessments of chiasmal lift, VFD, and DSI parameters from the optic nerve, optic tract, and optic radiation were performed. Group comparisons and correlation analyses were conducted in patients and controls. Using the 5-fold cross-validation method, the support vector machine classifiers were constructed to predict the degree of visual defects. RESULTS: The mean values of quantitative anisotropy and generalized fractional anisotropy in optic nerve and optic tract showed significant differences between patients and controls (p < 0.05). These parameters were also significantly correlated with the chiasmal lift distance and degree of visual defects (p < 0.05). All patients were divided into mild (n = 42) and severe (n = 23) VFD groups, using the mean deviation value of -8 dB as the threshold. The classifiers achieved an accuracy of 0.83, sensitivity of 0.78, and specificity of 0.86 to discriminate patients with mild and severe visual defects. CONCLUSIONS: Using high-angular-resolution fiber tracking, DSI may provide quantitative information to detect visual pathway abnormalities and be a potential diagnostic tool for determining the degree of visual field defects in pituitary adenomas. KEY POINTS: • Abnormal QA and GFA values of optic nerve and optic tract in adenoma patients • Close relationship between DSI parameters and VFD degree in adenoma patients • The classifiers achieved an accuracy of 0.83, sensitivity of 0.78, and specificity of 0.86 to discriminate patients with mild and severe VFD.

miR-193a-3p Promotes the Invasion, Migration, and Mesenchymal Transition in Glioma through Regulating BTRC.

BACKGROUND: The present study is aimed at exploring the specific expression of miR-193a-3p and the mechanism underlying miR-193a-3p-mediated mesenchymal transition (MT), invasion, and migration in glioma. METHODS: The gene expression profile datasets of GSE39486 and GSE25676 were downloaded from the National Center for Biotechnology (NCBI). Data regarding the expression of miR-193a-3p and survival curves were derived from Chinese Glioma Genome Atlas (CGGA). Online websites including miRWalk, DIANA, and starbase were employed to predict the target genes for miR-193a-3p. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed by the Omicsbean online software. Module analysis of the protein-protein interaction (PPI) networks was performed by the plug-in Molecular Complex Detection (MCODE), and the degrees of genes were calculated by CytoHubba plug-in of Cytoscape. Survival curves were based on the Gene Expression Profile Interaction Analysis (GEPIA). Transwell, wound healing, and Western blot experiments were performed to investigate the effects of miR-193a-3p and beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) on the invasion, migration, and MT of glioma. RESULTS: miR-193a-3p was highly expressed in glioma tissues and significantly correlated with poor survival in patients with glioma. The target genes for miR-193a-3p were involved in many cancer-related signaling pathways. The PPI showed 11 genes with both high degrees and MCODE scores in the network. Survival analysis demonstrated that the expression of BTRC was significantly correlated with the prognosis of patients with glioma. The results from the transwell, wound healing, and Western blot analyses suggested that miR-193a-3p promoted the invasion, migration, and MT of glioma cells, which could be reversed by BTRC. CONCLUSIONS: miR-193a-3p was upregulated in patients with glioma and could affect the invasion, migration, and MT of glioma by regulating BTRC.

[MiR-204 inhibits invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1].

OBJECTIVE: To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1. METHODS: The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability. RESULTS: The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells (P < 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients (P < 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells (P < 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients (P < 0.05) in association with a poorer prognosis of the patients (P < 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 (P < 0.05). CONCLUSIONS: miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.

[miR-93-5p promotes invasion and migration of triple negative breast cancer cells by targeting FGD5].

Objective To investigate the molecular mechanism by which miR-93-5p promotes the invasion and migration of triple negative breast cancer (TNBC) cells. Methods The miR-93-5p and faciogenital dysplasia-5 (FGD5) were screened out by Gene Expression Omnibus (GEO). Bioinformatics software was used to predict the candidate target genes for miR-93-5p. The relative expression of miR-93-5p in cells was detected by real-time quantitative PCR. Western blot was used to detect the relative expression of FGD5. TranswellTM assay was performed to detect the effects of miR-93-5p on the invasion and migration of MDA-MB-231 cells. The expression of FGD5 and survival curve in breast cancer and the correlation between miR-93-5p and FGD5 were analyzed by bioinformatics database. Dual luciferase reporter gene experiment was employed to verify the targeting relationship between miR-93-5p and FGD5. Results The miR-93-5p was highly expressed in TNBC tissues and cell lines. The higher the expression of miR-93-5p was, the worse the prognosis of breast cancer patients were. Knockdown of miR-93-5p inhibited the invasion and migration ability of MDA-MB-231 cells. Bioinformatics analysis showed that there were complementary sequences between miR-93-5p and FGD5. FGD5 presented low expression in breast cancer tissues and lower FGD5 expression in breast cancer patients corresponded to poorer prognosis. The expression levels between miR-93-5p and FGD5 were negatively correlated. Transfection of miR-93-5p inhibitor plasmid up-regulated the expression of FGD5 in TNBC cells. Dual luciferase reporter gene experiments confirmed that miR-93-5p could down-regulate the luciferase activity of wild-type FGD5. Conclusion The miR-93-5p can promote the invasion and migration of TNBC cells by targeting FGD5.

[Mechanism of DERL3 Affecting the Proliferation, Invasion and Metastasis of Lung Adenocarcinoma A549 Cells].

BACKGROUND: Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma. METHODS: Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin. RESULTS: The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05). CONCLUSIONS: Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

Corona Virus International Public Health Emergencies: Implications for Radiology Management.

The outbreak of 2019 novel coronavirus (2019-nCoV) pneumonia was reported in Wuhan, Hubei Province, China in December 2019 and has spread internationally. This article discusses how radiology departments can most effectively respond to this public health emergency.

[Moderate Angiogenic Effect of Xuefu Zhuyu Capsule by Regulating EphB4/EphrinB2].

Objective To observe moderate angiogenic effect of Xuefu Zhuyu Capsule (XFZYC) on human microvascular endothelial cell line 1 ( HMEC-1) , and its regulation effect on expression of EphB4/EphrinB2. Methods The moderate angiogenic effect of XFZYC was clarified by detecting XFZYC containing serum on cell viability, cell cycle, migration, adhesion and in vitro angiogenesis. Its effects on expressions of EphB4/EphrinB2 were detected by Real-time quantitative PCR and Western blot. Results XFZYC containing serum (XFZYC-CS) had no effect on the cell viability or cell ratio in phase S endothelial cells. Cell migration was significantly improved by 1.25% XFZYC-CS after 24, 48, and 72 h of action 2. 50% XFZYC-CS inhibited cell migration at the primary 24 h, but it significantly promoted cell migration at 48 and 72 h afterwards. It showed just an opposite tendency to 5. 00% XFZYC-CS. Cellular adhesion number was significantly reduced by 1. 25% XFZYC-CS at 72 h. Cellular adhesion number was significant- ly increased by 2. 50% XFZYC-CS at 24 and 48 h, but inhibited at 72 h 5. 00% XFZYC-CS showed inhibition at 24 h, but turned to promotion, and disappeared afterwards. In vessel formation aspect, only 2.50% XFZYC-CS showed vessel formation promotion 5. 00% XFZYC-CS showed inhibition on vessel formation at 48 and 72 h. Results of Real-time quantitative PCR and Western blot in 2. 50% XFZYC-CS showed EphB4 expression was up-regulated at 12 h; EphB4 expression was down-regulated while EphrinB2 expression was up-regulated at 24 h. Conclusions Only 2. 50% XFZYC-CS at 48 h had promotion of migration, adhe- sion, and in vitro angiogenesis of HMEC-1 , which was the optimal condition for vessel growth. These re- sults suggested XFZYC promoted angiogenesis in certain conditional limitations. But it regulated the ex- pression of EphB4/EphrinB2, which might be one of important factors.

Effect of EphB4/EphrinB2 reverse signal on angiogenesis induced by Xuefu Zhuyu Capsule () containing serum in human microvascular endothelial cell 1.

OBJECTIVE: To evaluate the effect of Xuefu Zhuyu Capsule ()-containing serum (XFZY-CS) on EphB4/ephrinB2 and its reverse signal in human microvascular endothelial cell-1 (HMEC-1). METHODS: XFZY-CS and the blank control serum were collected. HMEC-1 cells were randomly assigned to 6 groups including the concentration 1.25%, 2.5%, and 5% XFZY-CS groups and their blank serum control ones. The angiogenesis effect of XFZY-CS was tested with an in vitro tube formation assay and the best condition of pro-angiogenesis was determined. The effect of XFZY-CS on EphB4/ephrinB2 and the reverse signal were determined by Western blot and real-time quantitative polymerase chain reaction, respectively; we also confifirmed the results through activating and inhibiting the reverse signal by EphB4/fc and pyrophosphatase/ phosphodiesterase2 (PP2). RESULTS: XFZY-CS promoted angiogenesis at the concentration of 2.5% corresponding serum after being cultured for 48 h, while inhibited angiogenesis at the concentration of 5% after culturing for 48 and 72 h. Under the 2.5% serum concentration, XFZY up-regulated the expression of EphB4-mRNA at 12 h (P<0.05), and down-regulates its expression at 24 h (P<0.01). Protein expression of EphB4 was apparently up-regulated at 12 h and down-regulated at 24 h. The phosphorylation of ephrinB2 increased at 9 h (P<0.05). In addition, 2.5% XFZY-CS played a similar role as the reverse signaling activator EphB4/Fc ranging from 0.5 to 5 µg/mL (P>0.05). XFZY-CS also reduced the inhibitive effect of PP2 in limited periods. CONCLUSIONS: EphB4/ephrinB2 was the upstream signal in the process of angiogenesis and its reverse signaling was responsible for XFZY's effect on promoting angiogenesis.

Fabrication and characterization of antioxidant pickering emulsions stabilized by zein/chitosan complex particles (ZCPs).

Lipid peroxidation in oil-in-water (o/w) emulsions leads to rancidity and carcinogen formation. This work attempted to protect lipid droplets of emulsions from peroxidation via manipulation of the emulsions' interface framework using dual-function zein/CH complex particles (ZCPs). ZCP with intermediate wettability was fabricated via a simple antisolvent approach. Pickering emulsions were produced via a simple and inexpensive shear-induced emulsification technique. ZCP was irreversibly anchored at the oil-water interface to form particle-based network architecture therein, producing ultrastable o/w Pickering emulsions (ZCPEs). ZCPE was not labile to lipid oxidation, evidenced by low lipid hydroperoxides and malondialdehyde levels in the emulsions after thermally accelerated storage. The targeted accumulation of curcumin, a model antioxidant, at the interface was achieved using the ZCP as interfacial vehicle, forming antioxidant shells around dispersed droplets. The oxidative stability of ZCPEs was further improved. Interestingly, no detectable hexanal peak appeared in headspace gas chromatography of the Pickering emulsions. The novel interfacial architecture via the combination of steric hindrance from ZCP-based membrane and interfacial cargo of curcumin endowed the emulsions with favorable oxidative stability. This study opens a promising pathway for producing antioxidant emulsions via the combination of Pickering stabilization mechanism and interfacial delivery of antioxidant.