Targeting YOD1 by RNA Interference Inhibits Proliferation and Migration of Human Oral Keratinocytes through Transforming Growth Factor-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>β</mml:mi></mml:mrow></mml:math>3 Signaling Pathway

Zhou, Xuechou; Chen, Gang; Li, Meng-Xue; Wang, Heng-Xue; Hong, Jia-Wei; Shen, Jun-Yu; Wang, Qi; Ge, Xing; Zhang, Ding; Xu, Li‐Chun

doi:10.1155/2018/6254308

Cited by 9 publications

(8 citation statements)

References 39 publications

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“…Previous studies suggested that YOD1 correlated with another congenital malformed disease: nonsyndromic cleft lip, with or without cleft palate (NSCL/P). RNA interference and overexpression experiments indicated that YOD1 could enhance cell migration during lip and palate formation through the transforming growth factor (TGF)-β3 signaling pathway ( Zhou et al, 2018 ). A mutation of YOD1 may lead to impeded cell migration resulting in NSCL/P ( Ju et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Key Modules and Hub Genes Identified by Coexpression Network Analysis for Revealing Novel Biomarkers for Spina Bifida

Feng

Yuan

2020

Front. Genet.

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Spina bifida is a common neural tube defect (NTD) accounting for 5–10% of perinatal mortalities. As a polygenic disease, spina bifida is caused by a combination of genetic and environmental factors, for which the precise molecular pathogenesis is still not systemically understood. In the present study, we aimed to identify the related gene module that might play a vital role in the occurrence and development of spina bifida by using weighted gene co-expression network analysis (WGCNA). Transcription profiling according to an array of human amniocytes from patients with spina bifida and healthy controls was downloaded from the Gene Expression Omnibus database. First, outliers were identified and removed by principal component analysis (PCA) and sample clustering. Then, genes in the top 25% of variance in the GSE4182 dataset were then determined in order to explore candidate genes in potential hub modules using WGCNA. After data preprocessing, 5407 genes were obtained for further WGCNA. Highly correlated genes were divided into nineteen modules. Combined with a co-expression network and significant differentially expressed genes, 967 candidate genes were identified that may be involved in the pathological processes of spina bifida. Combined with our previous microRNA (miRNA) microarray results, we constructed an miRNA–mRNA network including four miRNAs and 39 mRNA among which three key genes were, respectively, linked to two miRNA-associated gene networks. Following the verification of qRT-PCR and KCND3 was upregulated in the spina bifida. KCND3 and its related miR-765 and miR-142-3p are worthy of further study. These findings may be conducive for early detection and intervention in spina bifida, as well as be of great significance to pregnant women and clinical staff.

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Section: Discussionmentioning

confidence: 99%

Key Modules and Hub Genes Identified by Coexpression Network Analysis for Revealing Novel Biomarkers for Spina Bifida

Feng

Yuan

2020

Front. Genet.

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“…Due to the balance change between the above, TGF-β often changes from tumor suppression factor to tumor promotion factor during cancer progression [ 32 ]. Studies have reported that YOD1 RNAi in Human Oral Keratinocytes can inhibit cell proliferation and migration related to the pathogenesis of nonsyndromic cleft lip with or without cleft palate (NSCL/P) through TGF-β 3 signaling [ 33 ], which suggested that the targeted inhibition of YOD1 in the advanced stage of cancer may also play a role in inhibiting cell proliferation and migration. The above may be the key pathways that YOD1 promotes the occurrence and development of pancreatic cancer and affect the prognosis.…”

Section: Discussionmentioning

confidence: 99%

YOD1 serves as a potential prognostic biomarker for pancreatic cancer

Zhang

Zhao

et al. 2022

Cancer Cell Int

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Background Ubiquitination is a basic post-translational modification of intracellular proteins and can be reversed enzymatically by DUBs (deubiquitinating enzymes). More than 90 DUBs have been identified. Among them, the deubiquitinating enzyme YOD1, a member of the ovarian tumor domain protease (OTUs) subfamily, is involved in the regulation of endoplasmic reticulum (ER)-related degradation pathways. In fact, it is reported that YOD1 is an important proliferation and metastasis-inducing gene, which can stimulate the characteristics of cancer stem cells and maintain circulating tumor cells (CTC). However, the expression level, prognostic effect and biological functional mechanism of YOD1 in pancreatic cancer are still unclear. Results In the GEO and TCGA databases, YOD1 mRNA expression is significantly up regulated in a variety of human pancreatic cancer tissues. Survival analysis showed that the up regulation of YOD1 can predict poor prognosis of pancreatic cancer. Cox analysis showed that high YOD1 expression is an independent prognostic factor of pancreatic cancer. ROC analysis shows that YOD1 has significant diagnostic value. The immunohistochemistry (IHC) results showed that the protein expression level of YOD1 in pancreatic cancer tissue was higher than that in neighboring non-pancreatic cancer tissues (P < 0.001). In addition, we found that YOD1 expression is negatively correlated with the infiltration level of CD8 + T cells, macrophages, neutrophils and dendritic cells (DC) in pancreatic cancer. The expression of YOD1 has a strong correlation with the different immune marker sets in PAAD. Co-expression network and functional enrichment analysis indicate that YOD1 may participate in the development of pancreatic cancer through cell adhesion molecules, p53, Hippo, TGF-β and other pathways. The experimental results of EDU, Transwell, Immunohistochemistry (IHC), Western blot and Flow Cytometry indicate that YOD1 is highly expressed in pancreatic cancer cells and pancreatic cancer tissues, and its overexpression can promote the proliferation and metastasis of pancreatic cancer cells and affect the immune microenvironment. Conclusion Our results indicate that YOD1 may be a useful biomarker for the prognosis of human pancreatic cancer, and it may also be a potential molecular target for the diagnosis and treatment of pancreatic cancer.

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“…One precursor cell was HUC-MSCs, which can differentiate into chondrocytes ( Brown et al, 2019 ). Another mature cell line was HOK cells from oral mucosa, which was used to study the pathogenesis of NSCLP in previous studies ( Zhou et al, 2018 ; Li et al, 2020 ). The zebrafish palate consists of cells derived from the frontonasal and maxillary domain, which is similar to the palatogenesis of mammals ( Duncan et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

SP1-Mediated Upregulation of Long Noncoding RNA ZFAS1 Involved in Non-syndromic Cleft Lip and Palate via Inactivating WNT/β-Catenin Signaling Pathway

Chen

Jia

Cai

et al. 2021

Front. Cell Dev. Biol.

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Non-syndromic cleft lip and palate (NSCLP) is one of the most common congenital malformations with multifactorial etiology. Although long non-coding RNAs (lncRNAs) have been implicated in the development of lip and palate, their roles in NSCLP are not fully elucidated. This study aimed to investigate how dysregulated lncRNAs contribute to NSCLP. Using lncRNA sequencing, bioinformatics analysis, and clinical tissue sample detection, we identified that lncRNA ZFAS1 was significantly upregulated in NSCLP. The upregulation of ZFAS1 mediated by SP1 transcription factor (SP1) inhibited expression levels of Wnt family member 4 (WNT4) through the binding with CCCTC-binding factor (CTCF), subsequently inactivating the WNT/β-catenin signaling pathway, which has been reported to play a significant role on the development of lip and palate. Moreover, in vitro, the overexpression of ZFAS1 inhibited cell proliferation and migration in human oral keratinocytes and human umbilical cord mesenchymal stem cells (HUC-MSCs) and also repressed chondrogenic differentiation of HUC-MSCs. In vivo, ZFAS1 suppressed cell proliferation and numbers of chondrocyte in the zebrafish ethmoid plate. In summary, these results indicated that ZFAS1 may be involved in NSCLP by affecting cell proliferation, migration, and chondrogenic differentiation through inactivating the WNT/β-catenin signaling pathway.

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Targeting YOD1 by RNA Interference Inhibits Proliferation and Migration of Human Oral Keratinocytes through Transforming Growth Factor-β3 Signaling Pathway

Cited by 9 publications

References 39 publications

Key Modules and Hub Genes Identified by Coexpression Network Analysis for Revealing Novel Biomarkers for Spina Bifida

Key Modules and Hub Genes Identified by Coexpression Network Analysis for Revealing Novel Biomarkers for Spina Bifida

YOD1 serves as a potential prognostic biomarker for pancreatic cancer

SP1-Mediated Upregulation of Long Noncoding RNA ZFAS1 Involved in Non-syndromic Cleft Lip and Palate via Inactivating WNT/β-Catenin Signaling Pathway

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