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

Author(s):  
Saba Hashemi ◽  
Naghmeh Yari ◽  
Fatemeh Rahimi Jamnani ◽  
Reza Mahdian ◽  
Morteza Karimi ◽  
...  
2021 ◽  
Author(s):  
Saba Hashemi ◽  
Naghmeh Yari ◽  
Fatemeh Rahimi Jamnani ◽  
Reza Mahdian ◽  
Morteza Karimipoor ◽  
...  

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.


2010 ◽  
Vol 5 (12) ◽  
pp. 1887-1893 ◽  
Author(s):  
Mohammad Obaidul Hoque ◽  
Mariana Brait ◽  
Eli Rosenbaum ◽  
Maria Luana Poeta ◽  
Prodipto Pal ◽  
...  

2007 ◽  
Vol 2 (10) ◽  
pp. 889-892 ◽  
Author(s):  
Meredith Tennis ◽  
Michelle Van Scoyk ◽  
Robert A. Winn

2009 ◽  
Vol 206 (5) ◽  
pp. 977-980 ◽  
Author(s):  
Barbara A. Malynn ◽  
Averil Ma

Many B cell cancers are characterized in part by the dysregulation of the NF-κB signaling pathway. A new study identifies somatic mutations in TNFAIP3, the gene encoding the NF-κB inhibitor A20, in Hodgkin lymphomas and primary mediastinal lymphomas. These data reveal the role of A20 as a tumor suppressor protein.


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

2021 ◽  
Author(s):  
Salil.K. Sukumaran ◽  
Pradip Paul ◽  
Vishweshwa Guttal ◽  
Alekhya Vemula ◽  
Harsimar Bhatt ◽  
...  

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.


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