KIAA1199: A novel regulator of MEK/ERK‐induced Schwann cell dedifferentiation

Boerboom, Angélique; Reusch, Céline; Pieltain, Alexandra; Chariot, Alain; Franzen, Rachelle

doi:10.1002/glia.23188

Cited by 19 publications

(13 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…KIAA1199, also defined as cell migration inducing protein (CEMIP), has been reported to be overexpressed in many cancers and promoted cancer metastasis through different signaling pathways, such as Wnt signaling and MEK1/ERK1/2 signalling [ 26 , 27 ]. Evensen et al found KIAA1199 was upregulated in breast cancer metastatic tissues, and resulted in EMT in breast cancer cells, inhibited cell migration in vitro and decreased metastasis in vivo [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer

Sun

Wang

et al. 2018

J Exp Clin Cancer Res

View full text Add to dashboard Cite

BackgroundLncRNA TUG1 has been reported to be highly expressed in CRC samples and cells and promoted metastasis by affecting EMT, indicating a poor prognosis for colorectal cancer (CRC). In this study, we determined the underlying mechanism for tumor oncogenesis of lncRNA TUG1 in CRC metastasis.MethodsThe expressions of miR-600 and KIAA1199 in 76 CRC patients and CRC cells and CRC metastatic tissues were determined using qRT-PCR. Epithelial-mesenchymal transition (EMT)-related proteins were determined using western blot. CRC cell metastasis was assessed by colony formation, wound healing and transwell assay. Luciferase reporter gene assay was used to confirm miR-600 binding to KIAA1199 3’UTR.ResultsOur data showed that lncRNA TUG1 was upregulated in CRC cells, miR-600 was downregulated in CRC tissues, cell lines and CRC metastatic tissues, and low miR-600 expression predicted a poor clinical prognosis. Overexpression of miR-600 suppressed CRC cell migration/invasion and EMT-related proteins in vitro, inhibited tumor volume and weight, and decreased the number of CRC liver metastasis in vivo. KIAA1199 was upregulated in CRC tissues, and was negatively regulated by miR-600. KIAA1199 overexpression promoted CRC cell migration and invasion, which reversed the inhibition effect of miR-600 mimic on migration and invasion of CRC cells. Moreover, TUG1 negatively regulated miR-600, and inhibition of TUG1 suppressed CRC cell migration and invasion and EMT-related proteins via regulating miR-600.ConclusionOur study proved that TUG1 promoted KIAA1199 expression to accelerate EMT and metastasis of CRC cell through inhibition of miR-600 expression.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer

Sun

Wang

et al. 2018

J Exp Clin Cancer Res

View full text Add to dashboard Cite

show abstract

“…The rationale for investigating PKA and PKC is further supported by the evidence that the modulatory effects of PKA and PKC are involved in the activation of ERK pathway and transcription factors that regulate receptors (Cornelison et al, ; Liu, Chen, Liedtke, & Simon, ; Seybold, ; Wang, Cao, Liu, & Liu, ). Our findings were in agreement with other studies showing that elevated levels of ERK, PKA and PKC in TGs contribute to peripheral sensitivity (Boerboom, Reusch, Pieltain, Chariot, & Franzen, ; Cornelison et al, ; Wang et al, ; Yuan et al, ). We also confirmed that SP upregulated p‐ERK1/2, RAS, B‐Raf, PKA and PKC pathways under inflammatory conditions.…”

Section: Discussionsupporting

confidence: 93%

Activation of the RAS/B‐RAF‐MEK‐ERK pathway in satellite glial cells contributes to substance p‐mediated orofacial pain

Zhang

Song

Liu

et al. 2019

Eur J of Neuroscience

View full text Add to dashboard Cite

The cross talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs) is crucial for the regulation of inflammatory orofacial pain. Substance P (SP) plays an important role by activating neurokinin (NK)‐I receptors in this cross talk. The activation of extracellular signal‐regulated kinase (ERK) 1/2, protein kinase A (PKA) and protein kinase C (PKC) in neurons and SGCs of peripheral ganglions by peripheral inflammation is associated with inflammatory hypersensitivity. This study tested the hypothesis that SP evoked SP‐NK‐I receptor positive feedback via the Renin–Angiotensin System/B‐Protein Kinase A‐Rapidly Accelerates Fibrosarcoma‐MEK‐Extracellular Signal‐Regulated Kinase (RAS/PKA‐RAF‐MEK‐ERK) pathway, which is involved in pain hypersensitivity. Inflammatory models were induced in vivo by injecting Complete Freund's adjuvant (CFA) into the whisker pad of rats. SP was administrated to SGCs in vitro for investigating, whether SP regulates the expression of NK‐I receptor in the SGC nucleus. The effects of RAS‐RAF‐MEK, PKA and PKC pathways in this process were measured by co‐incubating SGCs with respective Raf, PKA, PKC and MEK inhibitors in vitro and by pre‐injecting these inhibitors into the TG in vivo. SP significantly upregulated NK‐I receptor, p‐ERK1/2, Ras, B‐Raf, PKA and PKC in SGCs under inflammatory conditions. In addition, L703,606 (NK‐I receptor antagonist), U0126 (MEK inhibitor), Sorafenib (Raf inhibitor) and H892HCL (PKA inhibitor) but not chelerythrine chloride (PKC inhibitor) significantly decreased NK‐I mRNA and protein levels induced by SP. The allodynia‐related behavior evoked by CFA was inhibited by pre‐injection of L703,606, U0126, Sorafenib and H892HCL into the TG. Overall, SP upregulates NK‐I receptor in TG SGCs via PKA/RAS‐RAF‐MEK‐ERK pathway activation, contributing to a positive feedback of SP‐NK‐I receptor in inflammatory orofacial pain.

show abstract

“…IL27RA might participate in immune regulation in CNS (Iwasaki et al, 2015;Yoshida and Hunter, 2015). CEMIP may be related to brain function and development (Yoshino et al, 2017(Yoshino et al, , 2018, MEK/ERK-induced Schwann-cell dedifferentiation (Boerboom et al, 2017), immune response in glioblastoma (Motaln et al, 2012), and WNT signaling (Li et al, 2017;Duong et al, 2018;Liang et al, 2018). It was frequently reported in colorectal cancers as well (Fink et al, 2015;Zhang et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Construction and Validation of a 13-Gene Signature for Prognosis Prediction in Medulloblastoma

et al. 2020

View full text Add to dashboard Cite

Background: Recent studies have identified several molecular subgroups of medulloblastoma associated with distinct clinical outcomes; however, no robust gene signature has been established for prognosis prediction. Our objective was to construct a robust gene signature-based model to predict the prognosis of patients with medulloblastoma. Methods: Expression data of medulloblastomas were acquired from the Gene Expression Omnibus (GSE85217, n = 763; GSE37418, n = 76). To identify genes associated with overall survival (OS), we performed univariate survival analysis and least absolute shrinkage and selection operator (LASSO) Cox regression. A risk score model was constructed based on selected genes and was validated using multiple datasets. Differentially expressed genes (DEGs) between the risk groups were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and protein-protein interaction (PPI) analyses were performed. Network modules and hub genes were identified using Cytoscape. Furthermore, tumor microenvironment (TME) was evaluated using ESTIMATE algorithm. Tumor-infiltrating immune cells (TIICs) were inferred using CIBERSORTx. Results: A 13-gene model was constructed and validated. Patients classified as high-risk group had significantly worse OS than those as low-risk group (Training set: p < 0.0001; Validation set 1: p < 0.0001; Validation set 2: p = 0.00052). The area under the curve (AUC) of the receiver operating characteristic (ROC) analysis indicated a good performance in predicting 1-, 3-, and 5-year OS in all datasets. Multivariate analysis integrating clinical factors demonstrated that the risk score was an independent predictor for the OS (validation set 1: p = 0.001, validation set 2: p = 0.004). We then identified 265 DEGs between risk groups and PPI analysis predicted modules that were highly related to central nervous system and embryonic development. The risk score was significantly correlated with programmed deathligand 1 (PD-L1) expression (p < 0.001), as well as immune score (p = 0.035), stromal score (p = 0.010), and tumor purity (p = 0.010) in Group 4 medulloblastomas. Correlations between the 13-gene signature and the TIICs in Sonic hedgehog and Group 4 medulloblastomas were revealed.

show abstract

KIAA1199: A novel regulator of MEK/ERK‐induced Schwann cell dedifferentiation

Cited by 19 publications

References 57 publications

RETRACTED ARTICLE: LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer

RETRACTED ARTICLE: LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer

Activation of the RAS/B‐RAF‐MEK‐ERK pathway in satellite glial cells contributes to substance p‐mediated orofacial pain

Construction and Validation of a 13-Gene Signature for Prognosis Prediction in Medulloblastoma

Contact Info

Product

Resources

About