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Search results for: ATF3

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#33647349   2021/02/26 To Up

Integrated miRNA and mRNA omics reveal the anti-cancerous mechanism of Licochalcone B on Human Hepatoma Cell HepG2.

To unravel the potential of Licochalcone B as an anti-tumour phytochemical agent and evaluate its underlying mechanisms, we analyzed the mRNAs and miRNAs expression profiles of HepG2 cells in response to Licochalcone B (120 μM). mRNA and miRNA expression libraries were conducted and functional analysis for differential expression mRNAs was carried out utilizing Clue GO. We found 763 Licochalcone B -responsive differently expressed genes, among them, 572 mRNAs were up-regulated and 191 mRNAs were down-regulated, many of which were related to the MAPK signaling pathway. A protein-protein interaction network was constructed to discover the hub genes, and IL6, FOS, JUN, NOTCH1, UBC, UBB, CXCL8, CDKN1A, IL1B, ATF3, and GATA3 genes were screened out. Additionally, miRNAs engaged in Licochalcone B -mediated regulation on HepG2 cells were also studied. 85 differential expression miRNAs were identified, including 39 up-regulated miRNAs and 46 down-regulated miRNAs. Co-expression of miRNA-mRNA network was created and two key miRNAs (hsa-miR-29b-3p and hsa-miR-96-5p) were identified. These recognized key genes, miRNA, and the miRNA-mRNA regulatory network may provide clues to understand the molecular mechanism of Licochalcone B as an apoptotic inducer which may offer hint for its application as a functional food component.
Jun Wang, Chu-Yan Wang

1005 related Products with: Integrated miRNA and mRNA omics reveal the anti-cancerous mechanism of Licochalcone B on Human Hepatoma Cell HepG2.

100 50 mg0.1ml (1mg/ml)1mg0.1 mg500100ug100μl100μl100μl0.1 mg100ug Lyophilized

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#33640762   2021/02/25 To Up

Activating transcription factor 3 involved in Pseudomonas aeruginosa PAO1-induced macrophage senescence.

Pseudomonas aeruginosa (PA) is one of the most prevalent pathogens that cause nosocomial infection in critical patients. Previously, we reported PA induced macrophage to senescence under the circumstance of infection. As an oxidative stress responsiveness element, activating transcription factor 3 (ATF3) might be involved in the macrophage senescence process. To test this presumption, we manipulated the expression of ATF3 in macrophage by using a PAO1 infection system. In the present study, ATF3 expression in macrophage was increased, following the duration and colony counts of PAO1 infection. Knockdown of ATF3 in macrophage resulted in increased percentage of senescent macrophage under PAO1 infection, while overexpressing ATF3 partly blocked PAO1-induced macrophage senescence. In accordance with the senescent phenotype, elevated reactive oxygen species (ROS) production was shown in ATF3 knockdown macrophages. Also, capacity of phagocytosis was also affected by manipulation of ATF3 expression in macrophages, and increased phagocytosed fluorescent beads was found in ATF3 knockdown macrophage. ATF3 might regulate the senescence process through influence on NF-κB translocation. During infection, the overexpression or downregulation of ATF3 in macrophage negatively modulated the translocation of NF-κB p65 and its phosphorylation at Ser-536. As a result, IL-6 and TNFα was elevated, while IL-10 decreased in case of ATF3 knockdown. In conclusion, ATF3 negatively regulates NF-κB translocation and activation, and participates in PA-induced macrophage senescence. As oxidative stress and inflammation induced element, ATF3 may modulate macrophage-related host defense.
Qi Zhao, Yi-Feng Luo, Mi Tian, Yong-Long Xiao, Hou-Rong Cai, Hui Li

1845 related Products with: Activating transcription factor 3 involved in Pseudomonas aeruginosa PAO1-induced macrophage senescence.

200ug0.1ml10 ug0.1ml 100ul0.1ml200ug200ug1 mg200ug100 ul10ug

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#33628043   2021/02/17 To Up

Comprehensive Analysis of LncRNA-mRNA Expression Profiles and the ceRNA Network Associated with Pyroptosis in LPS-Induced Acute Lung Injury.

To explore the molecular mechanism and search for candidate lncRNA and mRNA associated with pyroptosis in the gene expression profile of LPS-induced acute lung injury (ALI).
Deqiang Luo, Fen Liu, Jianguo Zhang, Qiang Shao, Wenqiang Tao, Rui Xiao, Wei Dai, Chengzhi Ding, Kejian Qian

2939 related Products with: Comprehensive Analysis of LncRNA-mRNA Expression Profiles and the ceRNA Network Associated with Pyroptosis in LPS-Induced Acute Lung Injury.

1 mg 100ul

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#33626541   2021/02/24 To Up

Genetic Polymorphisms in Activating Transcription Factor 3 Binding Site and the Prognosis of Early-Stage Non-Small Cell Lung Cancer.

Activating transcription factor 3 (ATF3) plays a significant role in cancer development and progression. We investigated the association between variants in expression quantitative trait loci (eQTLs) within ATF3 binding regions and the prognosis of non-small cell lung cancer (NSCLC) after surgery.
Hyo-Gyoung Kang, Ji Eun Park, Shin Yup Lee, Jin Eun Choi, Sook Kyung Do, Mi Jeong Hong, Jang Hyuck Lee, Ji Yun Jeong, Young Woo Do, Eung Bae Lee, Kyung Min Shin, Won Ki Lee, Sun Ha Choi, Yong Hoon Lee, Hye Won Seo, Seung Soo Yoo, Jaehee Lee, Seung Ick Cha, Chang Ho Kim, Sukki Cho, Sanghoon Jheon, Jae Yong Park

1517 related Products with: Genetic Polymorphisms in Activating Transcription Factor 3 Binding Site and the Prognosis of Early-Stage Non-Small Cell Lung Cancer.



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#33615312   // To Up

Mitochondria Autoimmunity and MNRR1 in Breast Carcinogenesis: A Review.

We review here the evidence for participation of mitochondrial autoimmunity in BC inception and progression and propose a new paradigm that may challenge the prevailing thinking in oncogenesis by suggesting that mitochondrial autoimmunity is a major contributor to breast carcinogenesis and probably to the inception and progression of other solid tumors. It has been shown that MNRR1 mediated mitochondrial-nuclear function promotes BC cell growth and migration and the development of metastasis and constitutes a proof of concept supporting the participation of mitochondrial autoimmunity in breast carcinogenesis. The resemblance of the autoantibody profile in BC detected by IFA with that in the rheumatic autoimmune diseases suggested that studies on the autoantibody response to tumor associated antigens and the characterization of the mtDNA- and nDNA-encoded antigens may provide functional data on breast carcinogenesis. We also review the studies supporting the view that a panel of autoreactive nDNA-encoded mitochondrial antigens in addition to MNRR1 may be involved in breast carcinogenesis. These include GAPDH, PKM2, GSTP1, SPATA5, MFF, ncRNA PINK1-AS/DDOST as probably contributing to BC progression and metastases and the evidence suggesting that DDX21 orchestrates a complex signaling network with participation of JUND and ATF3 driving chronic inflammation and breast tumorigenesis. We suggest that the widespread autoreactivity of mtDNA- and nDNA-encoded mitochondrial proteins found in BC sera may be the reflection of autoimmunity triggered by mitochondrial and non-mitochondrial tumor associated antigens involved in multiple tumorigenic pathways. Furthermore, we suggest that mitochondrial proteins may contribute to mitochondrial dysfunction in BC even if mitochondrial respiration is found to be within normal limits. However, although the studies show that mitochondrial autoimmunity is a major factor in breast cancer inception and progression, it is not the only factor since there is a multiplex autoantibody profile targeting centrosome and stem cell antigens as well as anti-idiotypic antibodies, revealing the complex signaling network involved in breast carcinogenesis. In summary, the studies reviewed here open new, unexpected therapeutic avenues for cancer prevention and treatment of patients with cancer derived from an entirely new perspective of breast carcinogenesis.
Félix Fernández Madrid, Lawrence I Grossman, Siddhesh Aras

2322 related Products with: Mitochondria Autoimmunity and MNRR1 in Breast Carcinogenesis: A Review.



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#33614628   2021/01/26 To Up

A Comparative Analysis of Reactive Müller Glia Gene Expression After Light Damage and microRNA-Depleted Müller Glia-Focus on microRNAs.

Müller glia (MG) are the predominant glia in the neural retina and become reactive after injury or in disease. microRNAs (miRNAs) are translational repressors that regulate a variety of processes during development and are required for MG function. However, no data is available about the MG miRNAs in reactive gliosis. Therefore, in this study, we aimed to profile miRNAs and mRNAs in reactive MG 7 days after light damage. Light damage was performed for 8 h at 10,000 lux; this leads to rapid neuronal loss and strong MG reactivity. miRNAs were profiled using the Nanostring platform, gene expression analysis was conducted via microarray. We compared the light damage dataset with the dataset of Dicer deleted MG in order to find similarities and differences. We found: (1) The vast majority of MG miRNAs declined in reactive MG 7 days after light damage. (2) Only four miRNAs increased after light damage, which included miR-124. (3) The top 10 genes found upregulated in reactive MG after light damage include and . (4) The miRNA decrease in reactive MG 7 days after injury resembles the profile of Dicer-depleted MG after one month. (5) The comparison of both mRNA expression datasets (light damage and Dicer-cKO) showed 1,502 genes were expressed under both conditions, with , , and as top upregulated candidates. (6) The DIANA-TarBase v.8 miRNA:RNA interaction tool showed that three miRNAs were found to be present in all networks, i.e., after light damage, and in the combined data set; these were miR-125b-5p, let-7b and let-7c. Taken together, results show there is an overlap of gene regulatory events that occur in reactive MG after light damage (direct damage of neurons) and miRNA-depleted MG (Dicer-cKO), two very different paradigms. This suggests that MG miRNAs play an important role in a ubiquitous MG stress response and manipulating these miRNAs could be a first step to attenuate gliosis.
Seoyoung Kang, Daniel Larbi, Monica Andrade, Sara Reardon, Thomas A Reh, Stefanie G Wohl

1865 related Products with: A Comparative Analysis of Reactive Müller Glia Gene Expression After Light Damage and microRNA-Depleted Müller Glia-Focus on microRNAs.

300 units496T450 ug50 ug100.00 ug

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#33610681   2021/02/18 To Up

FOXI1 inhibits gastric cancer cell proliferation by activating miR-590/ATF3 axis via integrating ChIP-seq and RNA-seq data.

FOXI1 plays a key role in the development of gastric cancer. However, the whole genome FOXI1 binding sites and its target genes are unclear. In the present study, we used ChIP-seq and RNA-seq technologies to identify the target gene of FOXI1. Firstly, ChIP-seq data showed that, 4476 unique peaks in the genome region were captured. Most of these binding peaks are located in introns or intergenic regions. We annotated all the peaks to the nearest gene and identified 404 genes as FOXI1 binding genes. KEGG and GO analysis showed that FOXI1 binding gene to be correlated with the cellular process, cell part, cell, binding, single-organism process. Further, we performed FOXI1-overexpressed RNA-seq experiment. We comprehensively analyzed the ChIP-seq and RNA-seq data and take the intersection of two databases, several genes were identified. ATF3 was selected from the intersection since ATF3 was the most enriched mRNA after FOXI1 overexpressed. ChIP-qPCR and luciferase report gene were used to validate that ATF3 was target gene of FOXI1. Intriguely, ATF3 protein was significantly downregulated after FOXI1 overexpressed. We found FOXI1 can also bind to the promoter of miR-590 and active it which directly target ATF3. The binding site between FOXI1 and miR-590 was verified by ChIP-qPCR and luciferase report gene, and the target relationship between miR-590 and ATF3 was confirmed by dual-luciferase reporter gene. In conclusion, our data identified the genome binding sites of FOXI1, and provide evidence that FOXI1 inhibits gastric cancer cell proliferation by activating miR-590/ATF3 axis.
Ruifang Sun, Weidong Lü, Zhigang Liu, Yang Yang, Xiaofei Wang, Xinliang Zhao, Shufeng Fu, Wei Dai, Chen Huang, Dongmei Diao

1320 related Products with: FOXI1 inhibits gastric cancer cell proliferation by activating miR-590/ATF3 axis via integrating ChIP-seq and RNA-seq data.

96T24 reactions100ul2500 assays5 x 2 ml

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#33608508   2021/02/19 To Up

Zinc transporter ZIP7 is a novel determinant of ferroptosis.

Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical features. Here, we reported that zinc is also essential for ferroptosis in breast and renal cancer cells. Zinc chelator suppressed ferroptosis, and zinc addition promoted ferroptosis, even during iron chelation. By interrogating zinc-related genes in a genome-wide RNAi screen of ferroptosis, we identified SLC39A7, encoding ZIP7 that controls zinc transport from endoplasmic reticulum (ER) to cytosol, as a novel genetic determinant of ferroptosis. Genetic and chemical inhibition of the ZIP7 protected cells against ferroptosis, and the ferroptosis protection upon ZIP7 knockdown can be abolished by zinc supplementation. We found that the genetic and chemical inhibition of ZIP7 triggered ER stresses, including the induction of the expression of HERPUD1 and ATF3. Importantly, the knockdown of HERPUD1 abolished the ferroptosis protection phenotypes of ZIP7 inhibition. Together, we have uncovered an unexpected role of ZIP7 in ferroptosis by maintaining ER homeostasis. These findings may have therapeutic implications for human diseases involving ferroptosis and zinc dysregulations.
Po-Han Chen, Jianli Wu, Yitong Xu, Chien-Kuang Cornelia Ding, Alexander A Mestre, Chao-Chieh Lin, Wen-Hsuan Yang, Jen-Tsan Chi

1420 related Products with: Zinc transporter ZIP7 is a novel determinant of ferroptosis.

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#33608016   2021/02/19 To Up

Inhibitory role of ATF3 in gastric cancer progression through regulating cell EMT and stemness.

Gastric cancer (GC) is one of the most common cancers and the third leading cause of cancer related mortality worldwide. The 5-year survival rate is rather low owing to advanced unresectable and distant metastasis. The EMT has been widely implicated in the stemness, metastatic dormancy, and chemoresistance of different solid tumors. Given the fact that activating transcription factor-3 (ATF3) is a member of the ATF/CREB family of transcription factors and its role in regulation of GC recurrence and metastasis remain poorly understood, the aim of the present study was to investigate its potential impact in epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties and GC aggression.
Chuanqian Huang, Renli Chen, Fangjing Zheng, Yirong Tang, Xiukang Wang, Zichun Chen, Xiaolan Lai

1907 related Products with: Inhibitory role of ATF3 in gastric cancer progression through regulating cell EMT and stemness.



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#33603714   2021/02/02 To Up

Integrated Analysis of Key Genes and Pathways Involved in Nonalcoholic Steatohepatitis Improvement After Roux-en-Y Gastric Bypass Surgery.

As the incidence of nonalcoholic fatty liver disease (NAFLD) increases globally, nonalcoholic steatohepatitis (NASH) has become the second common cause of liver transplantation for liver diseases. Recent evidence shows that Roux-en-Y gastric bypass (RYGB) surgery obviously alleviates NASH. However, the mechanism underlying RYGB induced NASH improvement is still elusive.
Fu Chen, Yong Zhou, Zhiyuan Wu, Yunze Li, Wenlong Zhou, Yong Wang

1111 related Products with: Integrated Analysis of Key Genes and Pathways Involved in Nonalcoholic Steatohepatitis Improvement After Roux-en-Y Gastric Bypass Surgery.

1 mg10 mg100 0.1 mg20 µl100 μg2 mg10 mg100 100 0.1 mg

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