Fisetin Protects against Intracerebral Hemorrhage-Induced Neuroinflammation in Aged Mice

2018 ◽  
Vol 45 (3-4) ◽  
pp. 154-161 ◽  
Author(s):  
Cheng Chen ◽  
Li Yao ◽  
Jing Cui ◽  
Bao Liu
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Western Blot ◽  
Proinflammatory Cytokines ◽  
Cell Apoptosis ◽  
Calcium Binding ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Severity Scores ◽  
Cytokine Levels

Background: Fisetin is commonly used as an anti-inflammatory and neuroprotective drug. In this study, we aimed to investigate the efficacy of fisetin in alleviating intracerebral hemorrhage (ICH)-induced brain injury. Methods: Mouse ICH models were constructed using the collagenase-induction method. ICH mice received fisetin treatment at the dose of 10–90 mg/kg, followed by the evaluation of neurological deficit through neurologic severity scores (mNSS), brain water content and terminal deoxynucleotidyl transferase dUTP nick end labeling analysis of cell apoptosis. Cytokine levels were also assessed with enzyme-linked immunosorbent assay. The activation of astrocytes and microglia was evaluated through S100 staining and Western blot analysis of ionized calcium-binding adaptor molecule 1 respectively. Nuclear factor kappa-B (NF-κB) signaling was also evaluated by Western blot. Results: ICH mice demonstrated dramatic increase in mNSS, brain edema and cell apoptosis, indicating severe brain deficit. Fisetin treatment lowered these parameters, suggesting the alleviation of brain injury. Levels of proinflammatory cytokines were reduced, accompanied by a prominent decrease in activated astrocytes and microglia. NF-κB signaling was also attenuated by fisetin treatment. Conclusion: Fisetin effectively alleviates ICH by downregulating proinflammatory cytokines and attenuating NF-κB signaling. These data suggest fisetin as a valuable natural flavonol for clinical management of ICH-induced brain injury.

scholarly journals Can quantifying morphology and TMEM119 expression distinguish between microglia and infiltrating macrophages after ischemic stroke and reperfusion in male and female mice?

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Kimberly F. Young ◽  
Rebeca Gardner ◽  
Victoria Sariana ◽  
Susan A. Whitman ◽  
Mitchell J. Bartlett ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Western Blot ◽  
Calcium Binding ◽  
Transmembrane Protein ◽  
Brain Regions ◽  
Morphological Data ◽  
Cell Populations ◽  
Male And Female ◽  
Female Mice

AbstractBackgroundIschemic stroke is an acquired brain injury with gender-dependent outcomes. A persistent obstacle in understanding the sex-specific neuroinflammatory contributions to ischemic brain injury is distinguishing between resident microglia and infiltrating macrophages—both phagocytes—and determining cell population-specific contributions to injury evolution and recovery processes. Our purpose was to identify microglial and macrophage populations regulated by ischemic stroke using morphology analysis and the presence of microglia transmembrane protein 119 (TMEM119). Second, we examined sex and menopause differences in microglia/macrophage cell populations after an ischemic stroke.MethodsMale and female, premenopausal and postmenopausal, mice underwent either 60 min of middle cerebral artery occlusion and 24 h of reperfusion or sham surgery. The accelerated ovarian failure model was used to model postmenopause. Brain tissue was collected to quantify the infarct area and for immunohistochemistry and western blot methods. Ionized calcium-binding adapter molecule, TMEM119, and confocal microscopy were used to analyze the microglia morphology and TMEM119 area in the ipsilateral brain regions. Western blot was used to quantify protein quantity.ResultsPost-stroke injury is increased in male and postmenopause female mice vs. premenopause female mice (p< 0.05) with differences primarily occurring in the caudal sections. After stroke, the microglia underwent a region, but not sex group, dependent transformation into less ramified cells (p< 0.0001). However, the number of phagocytic microglia was increased in distal ipsilateral regions of postmenopausal mice vs. the other sex groups (p< 0.05). The number of TMEM119-positive cells was decreased in proximity to the infarct (p< 0.0001) but without a sex group effect. Two key findings prevented distinguishing microglia from systemic macrophages. First, morphological data were not congruent with TMEM119 immunofluorescence data. Cells with severely decreased TMEM119 immunofluorescence were ramified, a distinguishing microglia characteristic. Second, whereas the TMEM119 immunofluorescence area decreased in proximity to the infarcted area, the TMEM119 protein quantity was unchanged in the ipsilateral hemisphere regions using western blot methods.ConclusionsOur findings suggest that TMEM119 is not a stable microglia marker in male and female mice in the context of ischemic stroke. Until TMEM119 function in the brain is elucidated, its use to distinguish between cell populations following brain injury with cell infiltration is cautioned.

scholarly journals NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 333-342
Author(s):  
Yawei Feng ◽  
Jun Liu ◽  
Ranliang Wu ◽  
Peng Yang ◽  
Zhiqiang Ye ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Injury ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Western Blot Assay

AbstractBackground and aimAcute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI.Materials and methodsA septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay.ResultsNEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p.ConclusionDepletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.

scholarly journals Emodin protects against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Jingli Qian ◽  
Guoping Li ◽  
Xiaosheng Jin ◽  
Chunfang Ma ◽  
Wanru Cai ◽  
...  
Keyword(s):  
Lung Injury ◽  
Western Blot ◽  
Molecular Mechanisms ◽  
Mrna Level ◽  
Intestinal Injury ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Group Model ◽  
Expression Levels

Abstract Objective: Our aim was to investigate the effect of emodin on intestinal and lung injury induced by acute intestinal injury in rats and explore potential molecular mechanisms. Methods: Healthy male Sprague–Dawley (SD) rats were randomly divided into five groups (n=10, each group): normal group; saline group; acute intestinal injury model group; model + emodin group; model+NF-κB inhibitor pynolidine dithiocarbamate (PDTC) group. Histopathological changes in intestine/lung tissues were observed by Hematoxylin and Eosin (H&E) and terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling (TUNEL) staining. Serum IKBα, p-IKBα, surfactant protein-A (SP-A) and toll-like receptor 4 (TLR4) levels were examined using enzyme-linked immunosorbent assay (ELISA). RT-qPCR was performed to detect the mRNA expression levels of IKBα, SP-A and TLR4 in intestine/lung tissues. Furthermore, the protein expression levels of IKBα, p-IKBα, SP-A and TLR4 were detected by Western blot. Results: The pathological injury of intestinal/lung tissues was remarkedly ameliorated in models treated with emodin and PDTC. Furthermore, the intestinal/lung injury scores were significantly decreased after emodin or PDTC treatment. TUNEL results showed that both emodin and PDTC treatment distinctly attenuated the apoptosis of intestine/lung tissues induced by acute intestinal injury. At the mRNA level, emodin significantly increased the expression levels of SP-A and decreased the expression levels of IKBα and TLR4 in intestine/lung tissues. According to ELISA and Western blot, emodin remarkedly inhibited the expression of p-IKBα protein and elevated the expression of SP-A and TLR4 in serum and intestine/lung tissues induced by acute intestinal injury. Conclusion: Our findings suggested that emodin could protect against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway.

scholarly journals Correlation of Proinflammatory and Anti-Inflammatory Cytokine Levels with Histopathological Changes in an Adult Mouse Lung Model of Campylobacter jejuni Infection

2008 ◽  
Vol 15 (12) ◽  
pp. 1780-1787 ◽  
Author(s):  
Nadia Al-Banna ◽  
Raj Raghupathy ◽  
M. John Albert
Keyword(s):  
Campylobacter Jejuni ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Cytokine Production ◽  
Bacterial Load ◽  
Lung Model ◽  
Mouse Lung ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cytokine Levels ◽  
Anti Inflammatory

ABSTRACT Campylobacter jejuni is a major cause of diarrhea in humans. A mouse lung model of infection was previously established for C. jejuni. We used this model to study cytokine production in the lungs and correlated it with pathological changes. C. jejuni strain 81-176 or sterile phosphate-buffered saline was intranasally inoculated into adult BALB/c mice. The levels of proinflammatory cytokines (gamma interferon, tumor necrosis factor alpha, interleukin-1β [IL-1β], IL-2) and anti-inflammatory cytokines (IL-4, IL-10), in addition to those of IL-6, were assessed on days 1, 3, and 5 postinfection by enzyme-linked immunosorbent assay, and the ratios of proinflammatory cytokines to anti-inflammatory cytokines were calculated. Since IL-6 is unique in that it is both a proinflammatory cytokine and a TH2 cytokine, it was considered to be both in the determination of these ratios. The significance of the cytokine levels and ratios were determined by the Mann-Whitney U test (P ≤ 0.05). The induction of proinflammatory cytokines in the lungs of infected mice, as indicated by the cytokine levels and ratios, coincided with the accumulation of neutrophils and activated macrophages, in addition to the clearance of the bacterial load and bacteriumlike structures that we have previously shown in the same groups of mice. This was followed by increased levels of anti-inflammatory cytokines and the resolution of inflammation and pathology in the lungs. This study demonstrates the dynamics of cytokine production and their correlation with tissue inflammation and the resolution of infection. This model is useful for further studies of the pathogenesis of C. jejuni infection and vaccine evaluation.

scholarly journals Role of flunarizine hydrochloride in secondary brain injury following intracerebral hemorrhage in rats

2017 ◽  
Vol 30 (4) ◽  
pp. 413-419 ◽  
Author(s):  
Jianping Niu ◽  
Rui Hu
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Water Content ◽  
Cell Apoptosis ◽  
Akt Pathway ◽  
Secondary Brain Injury ◽  
Brain Water Content ◽  
Hematoma Volume ◽  
Brain Water

This study aimed to explore the role and mechanism(s) of flunarizine hydrochloride in the intracerebral hemorrhage (ICH) rats. The 32 adult male Sprague Dawley (SD) rats were randomly assigned into four groups: control group, sham group, ICH group, and FLU + ICH group. The effects of flunarizine hydrochloride were assessed on the basis of hematoma volume, blood–brain barrier (BBB) integrity, and brain water content in the ICH rat models. The role of flunarizine hydrochloride in cell recovery was assessed by behavioral scores, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot assay. Involvement of PI3K/AKT pathway in exerting the effect of flunarizine hydrochloride was also determined. Results showed that the hematoma volume, BBB integrity, and brain water content were significantly decreased in the FLU + ICH group. Cell apoptosis significantly increased in the ICH model group, while flunarizine hydrochloride decreased this increase. The expressions of glial cell line-derived neurotrophic factor (GDNF), neuroglobin (NGB), and p-AKT were increased after flunarizine hydrochloride treatment in ICH rats. In conclusion, flunarizine hydrochloride has protective effects against ICH by reducing brain injury, cell apoptosis, and the activation of P13K/AKT pathway. These findings provide a theoretical basis for the treatment of flunarizine hydrochloride in ICH.

Protective effects of quercetin on traumatic brain injury induced inflammation and oxidative stress in cortex through activating Nrf2/HO-1 pathway

2021 ◽  
Vol 39 (1) ◽  
pp. 73-84
Author(s):  
Jianqiang Song ◽  
Guoliang Du ◽  
Haiyun Wu ◽  
Xiangliang Gao ◽  
Zhen Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Inflammatory Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
The Brain ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Traumatic brain injury (TBI) has been a serious public health issue. Clinically, there is an urgent need for agents to ameliorate the neuroinflammation and oxidative stress induced by TBI. Our previous research has demonstrated that quercetin could protect the neurological function. However, the detailed mechanism underlying this process remains poorly understood. Objective: This research was designed to investigate the mechanisms of quercetin to protect the cortical neurons. Methods: A modified weight-drop device was used for the TBI model. 5, 20 or 50 mg/kg quercetin was injected intraperitoneally to rats at 0.5, 12 and 24 h post TBI. Rats were sacrificed three days post injury and their cerebral cortex was obtained from the injured side. The rats were randomly assigned into three groups of equal number: TBI and quercetin group, TBI group, and Sham group. The brain water content was calculated to estimate the brain damage induced by TBI. Immunohistochemical and Western blot assays were utilized to investigate the neurobehavioral status. Enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction were performed to evaluate the inflammatory responses. The cortical oxidative stress was measured by estimating the activities of malondialdehyde, superoxide dismutase, catalase and glutathione-Px. Western blot was utilized to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). Results: Quercetin attenuated the brain edema and microgliosis in TBI rats. Quercetin treatment attenuated cortical inflammatory responses and oxidative stress induced by TBI insults. Quercetin treatment activated the cortical Nrf2/HO-1 pathway in TBI rats. Conclusions: Quercetin ameliorated the TBI-induced neuroinflammation and oxidative stress in the cortex through activating the Nrf2/HO-1 pathway.

scholarly journals lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-κB Pathway

2022 ◽  
Vol 2022 ◽  
pp. 1-7
Author(s):  
Shuaidong Mao ◽  
Huan Huang ◽  
Xianzheng Chen
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Western Blot ◽  
Water Content ◽  
Brain Tissue ◽  
Sham Group ◽  
Neuron Specific Enolase ◽  
Neurological Function ◽  
And Oxidative Stress

Objective. To explore the effect of long noncoding RNA H19 (lncRNA H19) on brain injury in rats following experimental intracerebral hemorrhage (ICH). Methods. Rat ICH model was established with type IV collagenase. The neurological function scores were evaluated, and the water content in brain tissue was measured. The nerve injury indexes, inflammatory factors, and oxidative stress indexes were also measured. Moreover, the expression of lncRNA H19 was determined by qRT-PCR, and Western blot detected NF-κB pathway-related protein expression. Results. Compared with the sham group, the neurological function scores, the water content in brain tissue, and levels of injury indicators myelin basic protein (MBP), S-100B, and neuron-specific enolase (NSE) in the ICH rats were significantly increased. Meanwhile, the levels of TNF-α, IL-6, IL-1β, ROS, and MDA were significantly increased, but the levels of SOD were significantly decreased. In addition, the expression of lncRNA H19 in the brain tissue in the ICH group was significantly higher than that in the sham group. After further interference with lncRNA H19 expression (sh-H19 group), the levels of all the above indicators were reversed and the neurological damage was improved. Western blot results showed that the expression of NF-κBp65 and IKKβ was significantly higher, and IκBα expression was lower in the perivascular hematoma tissue in the ICH group compared with the sham group. Compared with the sh-NC group, NF-κBp65 and IKKβ expression were significantly lower and IκBα was significantly higher in the sh-H19 group. Conclusion. lncRNA H19 exacerbated brain injury in rats with ICH by promoting neurological impairment, brain edema, and releasing inflammatory responses and oxidative stress. This may be related to the activation of NF-κB signaling pathway.

scholarly journals CENP-U function on TNBC.

2019 ◽  
Vol 5 (suppl) ◽  
pp. 31-31
Author(s):  
Jin Zhang
Keyword(s):  
Breast Cancer ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Annexin V ◽  
Normal Breast ◽  
Breast Cancer Cell Lines ◽  
Enzyme Linked Immunosorbent Assay ◽  
Specific Antibodies ◽  
Signaling Activation

31 Background: Centromere protein (CENP-U) gene, as an important constitutive kinetochorecomponent, plays significant roles in cell caryomitosis. Our previous research found that about 25% of transgenic mice with CENP-U amplified had suffered breast cancer in body surface. Also, in highly aggressive breast cancer cell lines, CENP-U presented the highest expression. Furthermore, the CENP-U protein expression obviously increased in human invasive breast carcinoma compared with the normal gland and intra-ductal tissue.Here we aimed to investigate the biological functions and potential molecular mechanism of CENP-U in breast cancer tumorigenesis. Methods: Gene knockdown was accomplished by transient transfection. In addition, cell proliferation was analyzed with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay while cell apoptosis was measured by flow cytometry using an annexin V-FITC apoptosis detection kit. Then, VEGF secretion in the supernatant was detected with an enzyme-linked immunosorbent assay (ELISA). Furthermore,Vascular endothelial markers of nude mouse were discovered by immunohistochemistry. And the signaling activation in the breast cancer cells was accessed by western blot using specific antibodies. Results: We observed higher CENP-U expression in breast cancer compared to adjacent normal breast tissue, especially in TNBC.The MTT and EdU assay showed that CENP-U promoted the proliferation of the triple negative breast cancer (TNBC) cells while CENP-U downregulated promoted cell apoptosis. Furthermore, the ELISA results revealed that CENP-U significantly promoted the production and secretion of VEGF in TNBC cells. In addition, CENP-U downregulated inhibits tumor growth and angiogenesis in vivo. Importantly, CENP-U targeted HIF-1α,VEGFA and COX-2, which were shown by the specific antibodies in the western blot. Conclusions: The results showed that CENP-U influence the proliferation, apoptosis and angiogenesis especially of TNBC cells. But the affected signaling pathways require further study.

scholarly journals Can brain natriuretic peptide, S100b, and interleukin-6 prognosticate the neurological consequences in Egyptian patients presented with supratentorial intracerebral hemorrhage?

2020 ◽  
Vol 11 ◽  
pp. 460
Author(s):  
Hany A. Fikry Eldawoody ◽  
Mohammed Abdel Bari Mattar ◽  
Abeer Mesbah ◽  
Ashraf Zaher ◽  
Mohammed Elsherif
Keyword(s):  
Intracerebral Hemorrhage ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Interleukin 6 ◽  
Calcium Binding ◽  
Length Of Hospital Stay ◽  
Serum Levels ◽  
Severity Scores ◽  
Egyptian Patients ◽  
Ich Score

Background: Biomarkers in supratentorial intracerebral hemorrhage (SICH) enhance the prognosis of the disease. This study aimed to assess the prognosticative grade of S100 calcium-binding protein B (S100B), interleukin-6 (IL-6), and the pro-brain natriuretic peptide (pro-BNP) in SICH outcome prediction. Methods: Blood samples of 50 SICH patients were analyzed for the biomarkers. The patients were classified into two groups with and without intraventricular hemorrhage (IVH). The following scales including Glasgow Coma Score (GCS), the Barthel index (BI), intracerebral hemorrhage (ICH) score, ICH volume, National Institutes of Health Stroke Scale (NIHSS), Modified Rankin Score (mRS), and length of stay were used to evaluate the severity. Results: The severity scores (NIHSS, GCS, BI, mRI) were significantly higher in SICH patients with IVH versus SICH patients without IVH (P = 0.002, 0.008, 0.001, and 0.03, respectively). Serum levels for a pro-BNP and S100b are significantly higher in SICH patients with IVH versus SICH patients without IVH (P = 0.02 and 0.027, respectively). Multivariate correlations between demographic (age), biomarkers panel (IL-6, S100b, and proBNP), and clinical and severity scores (ICH score, ICH volume, length of hospital stay [LOS], BI, mRS, GCS, and NIHSSS) in all studied patients showed a highly significant correlation between ICH score and pro-BNP (P = 0.04). There was a highly significant correlation between LOS and IL-6 (P = 0.003). Conclusion: Pro-BNP, IL-6, and S100b are greatly associated with the presence of IVH that, in turn, correlated well with poor clinical outcome measures.

CENP-U function on TNBC.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e12546-e12546
Author(s):  
Jin Zhang
Keyword(s):  
Breast Cancer ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Annexin V ◽  
Breast Cancer Cell Lines ◽  
Enzyme Linked Immunosorbent Assay ◽  
Specific Antibodies ◽  
Apoptosis Detection ◽  
Signaling Activation

e12546 Background: Centromere protein (CENP-U) gene, as an important constitutive kinetochore component, plays significant roles in cell caryomitosis. Our previous research found that about 25 % of transgenic mice with CENP-U amplified had suffered breast cancer in body surface. Also, in highly aggressive breast cancer cell lines, CENP-U presented the highest expression. Furthermore, the CENP-U protein expression obviously increased in human invasive breast carcinoma compared with the normal gland and intra-ductal tissue. Methods: Gene knockdown was accomplished by transient transfection. In addition, cell proliferation was analyzed with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay while cell apoptosis was measured by flow cytometry using an annexin V-FITC apoptosis detection kit. Then, VEGF secretion in the supernatant was detected with an enzyme-linked immunosorbent assay (ELISA). Furthermore,Vascular endothelial markers of nude mouse were discovered by immunohistochemistry. And the signaling activation in the breast cancer cells was accessed by western blot using specific antibodies. Results: The MTT and EdU assay showed that CENP-U promoted the proliferation of the triple negative breast cancer (TNBC) cells while CENP-U downregulated promoted cell apoptosis. Furthermore, the ELISA results revealed that CENP-U significantly promoted the production and secretion of VEGF in TNBC cells. In addition, CENP-U downregulated inhibits tumor growth and angiogenesis in vivo. Importantly, CENP-U targeted HIF-1α,VEGFA, p-AKT and stat3, which were shown by the specific antibodies in the western blot. Conclusions: The results showed that CENP-U influence the proliferation, apoptosis and angiogenesis especially of TNBC cells. But the affected signaling pathways require further study.

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