The role of miRNA-571 and miRNA-559 in lung cancer by affecting the expression of genes associated with the ErbB signaling pathway

Gene Reports ◽  
2021 ◽  
pp. 101436
Author(s):  
Saade Abdalkareem Jasim ◽  
Abdulhadi Omear ◽  
Ali H. Al-Marzoqi
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Expression Of Genes ◽  
Erbb Signaling ◽  
Erbb Signaling Pathway

scholarly journals The role of miRNA-377 as a tumor suppressor in lung cancer by negative regulation of genes belonging to ErbB signaling pathway

2021 ◽  
Author(s):  
Saba Hashemi ◽  
Naghmeh Yari ◽  
Fatemeh Rahimi Jamnani ◽  
Reza Mahdian ◽  
Morteza Karimi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Signaling Pathway ◽  
Negative Regulation ◽  
Erbb Signaling ◽  
Erbb Signaling Pathway

scholarly journals The Role of miRNA-377 as a Tumor Suppressor in Lung Cancer by Negative Regulation of Genes Belonging to ErbB Signaling Pathway

2021 ◽  
Author(s):  
Saba Hashemi ◽  
Naghmeh Yari ◽  
Fatemeh Rahimi Jamnani ◽  
Reza Mahdian ◽  
Morteza Karimipoor ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Luciferase Reporter ◽  
Mrna Levels ◽  
Erbb Signaling ◽  
Erbb Signaling Pathway ◽  
Human Nsclc

Abstract The ErbB signaling pathway plays important role in the pathogenesis of lung cancer. We explored the role of miRNA-377 as a tumor suppressor in NSCLC through silencing of some genes in the ErbB pathway.Targeting the effect of miRNA-377 on EGFR, MAPK1, ABL2, and PAK2 was evaluated. The expression levels of these genes and miRNA-377 were surveyed in NSCLC and normal human tissues, Calu-6, and A549 cells. Real-time PCR was used to figure out whether miRNA-377 could decrease the target genes mRNAs in transfected lung cancer cell lines. The effects of miRNA-377 on apoptosis cell and proliferation were analyzed. We showed that miRNA-377 targets EGFR, MAPK1, and PAK2 mRNAs in in-silico and luciferase reporter assay. The expression of miRNA-377 was significantly downregulated in human NSCLC tissues, Calu-6 and A549 cells compared to their controls. We observed a negative correlation between EGFR, MAPK1, PAK2, and miRNA-377 expression in human NSCLC tissues. A significant reduction in EGFR, MAPK1, and PAK2 mRNA levels was detected, following miRNA-377 transfection in Calu-6 and A549 cells. The higher levels of miRNA-377 in Calu-6, and A549 cells induced apoptosis and reduced proliferation, significantly. All these data reveal that miRNA-377 functions as a tumor suppressor in NSCLC and may serve as a potential therapeutic target for the treatment of NSCLC.

scholarly journals Genetic and Epigenetic Analysis of erbB Signaling Pathway Genes in Lung Cancer

2010 ◽  
Vol 5 (12) ◽  
pp. 1887-1893 ◽  
Author(s):  
Mohammad Obaidul Hoque ◽  
Mariana Brait ◽  
Eli Rosenbaum ◽  
Maria Luana Poeta ◽  
Prodipto Pal ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Erbb Signaling ◽  
Epigenetic Analysis ◽  
Erbb Signaling Pathway

scholarly journals Role of the Wnt Signaling Pathway and Lung Cancer

2007 ◽  
Vol 2 (10) ◽  
pp. 889-892 ◽  
Author(s):  
Meredith Tennis ◽  
Michelle Van Scoyk ◽  
Robert A. Winn
Keyword(s):  
Lung Cancer ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway

scholarly journals The Role of PKR/eIF2α Signaling Pathway in Prognosis of Non-Small Cell Lung Cancer

PLoS ONE ◽  
2011 ◽  
Vol 6 (11) ◽  
pp. e24855 ◽  
Author(s):  
Yong He ◽  
Arlene M. Correa ◽  
Maria Gabriela Raso ◽  
Wayne L. Hofstetter ◽  
Bingliang Fang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Dysregulation in EGF/ERBB signaling pathway may explain abnormalities in cellular migration in bipolar disorder in patient-derived neural precursors

2021 ◽  
Author(s):  
Salil.K. Sukumaran ◽  
Pradip Paul ◽  
Vishweshwa Guttal ◽  
Alekhya Vemula ◽  
Harsimar Bhatt ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Signaling Pathway ◽  
Structural Changes ◽  
Time Lapse ◽  
Cellular Migration ◽  
Control Line ◽  
Post Mortem ◽  
Post Mortem Brain ◽  
Erbb Signaling ◽  
Erbb Signaling Pathway

ABSTRACTCellular migration is a ubiquitous feature of development that brings brain cells into appropriate spatial relationships. Cortical thinning has been reported in post-mortem brain samples of patients with bipolar disorder (BD). It could be that defective cellular migration during brain development is one of the contributing mechanisms in BD pathogenesis, leading to abnormalities reported at post-mortem, and during brain imaging. To probe the role of cellular migration in BD, we conducted time-lapse analysis of migration of neural precursor cells (NPCs) previously generated in our laboratory. Two NPC lines (B1 and B2) and one control line (C1) were used for the cell migration experiments. Time-lapse images were recorded every 15 min, for 15 hours, and analysed for speed and direction of cellular migration. Abnormalities in cellular migration was a common feature observed in both patient-derived NPCs. Consequently, we investigated underlying mechanistic irregularities in B1 and B2 lines that may contribute to the observed phenotype. To this end, transcriptional changes were compared between the patient-derived cells with the control line. Additionally, we examined exonic variations in genes related to cellular migration or motility. Our analysis showed downregulation of multiple genes that are all part of the EGF/ERBB signaling pathway. Collective dysregulation may be producing the defective cellular phenotype. These cellular migration abnormalities may be linked to structural changes in the brain reported in bipolar disorder.

scholarly journals CIRP Promotes the Progression of Non-small Cell Lung Cancer Through Activation of Wnt/β-catenin Signaling via CTNNB1

2021 ◽  
Author(s):  
Yi Liao ◽  
Jianguo Feng ◽  
Weichao Sun ◽  
Chao Wu ◽  
Jingyao Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

Abstract Background: Cold-inducible RNA binding protein (CIRP) is a newly discovered proto-oncogene. In this study, we investigated the role of CIRP in the progression of non-small cell lung cancer (NSCLC) using clinic samples, cultured cell lines and animal lung cancer models. Methods: Tissue arrays, IHC and HE staining, immunoblotting, and qRT-PCR were used to detect the indicated gene expression; Plasmid and siRNA transfections as well as viral infection were used to manipulate gene expression; Cell proliferation assay, cell cycle analysis, cell migration and invasion analysis, soft agar colony formation assay, tail intravenous injecting and subcutaneously inoculating of animal models were performed to study the role of CIRP in NSCLC cells; Gene expression microarray was used to select the underlying pathways; RNA immunoprecipitation assay, biotin pull-down assay, immuno-purification assay, mRNA decay analyses and luciferase reporter assay were performed to elucidate the mechanisms. The log-rank (Mantel-Cox) test, independent sample T test, the nonparametric Mann-Whitney test, spearman rank test and two-tailed independent sample T-test were used accordingly in our study. Results: Our data showed that CIRP was highly expressed in NSCLC tissue, and its level was negatively correlated with the prognosis of NSCLC patients. By manipulating CIRP expression in A549, H460, H1299, and H1650 cell lines, we demonstrated that CIRP overexpression promoted the transition of G1/G0 phase to S phase and the formation of enhanced malignant phenotype of NSCLC, reflected by increased proliferation, enhanced invasion/metastasis and greater tumorigenic capabilities both in vitro and in vivo. Transcriptome sequencing further demonstrated that CIRP acted on cell cycle, DNA replication and Wnt signaling pathway to exert its pro-oncogenic action. Mechanistically, CIRP directly bound to the 3’- and 5'-UTR of CTNNB1 mRNA, leading to enhanced stability and translation of CTNNB1 mRNA and promote IRES-mediated protein synthesis, respectively. Eventually, the increased CTNNB1 protein levels mediated excessive activation of the Wnt/β-Catenin signaling pathway and its downstream C-myc, COX-2, CCND1, MMP7, VEGFA and CD44. Conclusion: Our results support CIRP as a candidate oncogene in NSCLC and a potential target for NSCLC therapy.

scholarly journals miR-429 Suppresses Proliferation and Migration in Glioblastoma Cells and Induces Cell-cycle Arrest via Modulating Several Target Genes of ERBB Signaling Pathway

2021 ◽  
Author(s):  
Fatemeh Gheidari ◽  
Ehsan Arefian ◽  
Mahboubeh Kabiri ◽  
Ehsan Seyedjafari ◽  
Ladan Teimoori-Toolabi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Target Genes ◽  
Cycle Arrest ◽  
Cell Proliferation And Migration ◽  
Erbb Signaling ◽  
And Migration ◽  
Erbb Signaling Pathway ◽  
Proliferation And Migration

Abstract Glioblastoma is aggressive and lethal brain cancer, which is incurable by cancer standard treatments. miRNAs have great potential to be used for gene therapy due to their ability to modulate several target genes simultaneously. We found miR-429 is downregulated in glioblastoma and has several predicted target genes from the ERBB signaling pathway using bioinformatics tools. ERBB is the most over-activated genetic pathway in glioblastoma patients, which is responsible for augmented cell proliferation and migration in glioblastoma multiforme (GBM). Here we overexpressed miR-429 using lentiviral vectors in GBM U-251 cells and observed that the expression level of several oncogenes of the ERBB pathway, EGFR, PIK3CA, PIK3CB, KRAS, and MYC significantly decreased; as shown by real-time PCR and western blotting. Using the luciferase assay, we showed that miR-429 directly targets MYC, BCL2, and EGFR. In comparison to scrambled control, miR-429 had a significant inhibitory effect on cell proliferation and migration as deduced from MTT and scratch wound assays and induced cell-cycle arrest in flow cytometry. Altogether miR-429 seems to be an efficient suppressor of the ERBB genetic signaling pathway and a potential therapeutic for glioblastoma.

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