scholarly journals Erratum: Corrigendum: Down-regulation of miR-206 is associated with Hirschsprung disease and suppresses cell migration and proliferation in cell models

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Ankur Sharan ◽  
Hairong Zhu ◽  
Hua Xie ◽  
Hongxing Li ◽  
Junwei Tang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Hirschsprung Disease ◽  
Cell Models ◽  
Down Regulation ◽  
Cell Migration And Proliferation

scholarly journals Down-regulation of miR-206 is associated with Hirschsprung disease and suppresses cell migration and proliferation in cell models

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Ankur Sharan ◽  
Hairong Zhu ◽  
Hua Xie ◽  
Hongxing Li ◽  
Junwei Tang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Hirschsprung Disease ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Down Regulation ◽  
Tissue Samples ◽  
Qrt Pcr ◽  
Cell Migration And Proliferation ◽  
Dual Luciferase Reporter Assay

Abstract Hirschsprung disease (HSCR) is a well-known congenital digestive disease that originates due to the developmental disorder of neural crest cells. MiR-206 is kown to have a relationship with digestive malfunctions. Therefore, we investigated whether or not miR-206 was involved in the pathogenesis of HSCR. qRT-PCR and Western blot assays were used to detect the expression levels of miRNA and mRNAs and proteins in case and control tissue samples and two cell lines (293T and SH-SY5Y). The functions of miR-206 in vitro were measured by transwell assay, CCK8 assay and flow cytometry. Finally, we conducted dual-luciferase reporter assay to verify the connections between miR-206 and the target mRNA SDPR. Down-regulation of miR-206 was found in HSCR case tissue samples compared with controls, which was validated to be connected with the increased level of mRNA and protein of SDPR by qRT-PCR and dual-luciferase reporter assay. Moreover, miR-206 suppressed the cell migration and proliferation and silencing of SDPR could rescue the extent of the suppressing effects by miR-206 inhibitor. The findings suggest that miR-206 may play a significant role in the pathogenesis of HSCR, as well as inhibiting the cell migration and proliferation by targeting SDPR in disease models.

scholarly journals Increased miR-214 expression suppresses cell migration and proliferation in Hirschsprung disease by interacting with PLAGL2

2019 ◽  
Vol 86 (4) ◽  
pp. 460-470 ◽  
Author(s):  
Liang Wu ◽  
Wenzheng Yuan ◽  
Jinhuang Chen ◽  
Zili Zhou ◽  
Yan Shu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Hirschsprung Disease ◽  
Cell Migration And Proliferation

scholarly journals HHV-8 reduces dendritic cell migration through down-regulation of cell-surface CCR6 and CCR7 and cytoskeleton reorganization

2012 ◽  
Vol 9 (1) ◽  
Author(s):  
Mara Cirone ◽  
Valeria Conte ◽  
Antonella Farina ◽  
Sandro Valia ◽  
Pankaj Trivedi ◽  
...  
Keyword(s):  
Cell Migration ◽  
Dendritic Cell ◽  
Cell Surface ◽  
Down Regulation ◽  
Cytoskeleton Reorganization ◽  
Dendritic Cell Migration

scholarly journals Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase Cδ

2010 ◽  
Vol 17 (2) ◽  
pp. 335-349 ◽  
Author(s):  
Inga Mertens-Walker ◽  
Christine Bolitho ◽  
Robert C Baxter ◽  
Deborah J Marsh
Keyword(s):  
Ovarian Cancer ◽  
Cell Migration ◽  
Protein Kinase ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Migration ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Gf 109203X ◽  
Cell Migration And Proliferation

The gonadotropin hypothesis proposes that elevated serum gonadotropin levels may increase the risk of epithelial ovarian cancer (EOC). We have studied the effect of treating EOC cell lines (OV207 and OVCAR-3) with FSH or LH. Both gonadotropins activated the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) pathway and increased cell migration that was inhibited by the MAPK 1 inhibitor PD98059. Both extra- and intracellular calcium ion signalling were implicated in gonadotropin-induced ERK1/2 activation as treatment with either the calcium chelator EGTA or an inhibitor of intracellular calcium release, dantrolene, inhibited gonadotropin-induced ERK1/2 activation. Verapamil was also inhibitory, indicating that gonadotropins activate calcium influx via L-type voltage-dependent calcium channels. The cAMP/protein kinase A (PKA) pathway was not involved in the mediation of gonadotropin action in these cells as gonadotropins did not increase intracellular cAMP formation and inhibition of PKA did not affect gonadotropin-induced phosphorylation of ERK1/2. Activation of ERK1/2 was inhibited by the protein kinase C (PKC) inhibitor GF 109203X as well as by the PKCδ inhibitor rottlerin, and downregulation of PKCδ was inhibited by small interfering RNA (siRNA), highlighting the importance of PKCδ in the gonadotropin signalling cascade. Furthermore, in addition to inhibition by PD98059, gonadotropin-induced ovarian cancer cell migration was also inhibited by verapamil, GF 109203X and rottlerin. Similarly, gonadotropin-induced proliferation was inhibited by PD98059, verapamil, GF 109203X and PKCδ siRNA. Taken together, these results demonstrate that gonadotropins induce both ovarian cancer cell migration and proliferation by activation of ERK1/2 signalling in a calcium- and PKCδ-dependent manner.

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