<i>MiR-638</i>
            suppresses the progression of oral squamous cell carcinoma through wnt/β-catenin pathway by targeting phospholipase D1

Tang, Kailiang; Han-Ying, Tang; Du, Yi; Tian, Tian; Xiong, Sheng

doi:10.1080/21691401.2019.1647222

Cited by 22 publications

(14 citation statements)

References 29 publications

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“…Similarly deregulation of miR-572 and upregulation of miR-638 was exclusively associated with MM 16,48 . In contrast, downregulated expression of miR-638 was observed in our datasets as reported in other cancers including breast cancers 49 and oral squamous cell carcinoma 50 .…”

Section: Discussionsupporting

confidence: 55%

Genome-Wide Identification of Potential Biomarkers in Multiple Myeloma Using Meta-Analysis of mRNA and miRNA Expression Data

Katiyar

Kaur

Rani

et al. 2021

Preprint

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Multiple myeloma (MM) is a plasma cell malignancy with diverse clinical phenotypes and molecular heterogeneity that is not completely understood. Recent studies have identified differentially expressed patterns of genes (DEGs) or miRNAs (DEMs) in MM. But these signatures overlap partially, plausibly due to complexity of myeloma genome, diversity in cell lines studied, molecular technologies and analytical tools utilized in these studies. This warrants further investigations since DEGs/DEMs can impact clinical outcomes and guide personalized therapy. We conducted the genome-wide meta-analysis of expression datasets on DEGs/DEMs in MM and derive net putative signatures and potential biomarkers for MM. A set of 110 DEMs and 3,817 DEGs were identified to be differentially expressed. Among these, 86 DEMs (60 downregulated; 26 upregulated) correlated with 1,970 target DEGs (1373 downregulated; 597 upregulated). Signatures of 23 DEMs (‘Union 23’) and 196 DEGs (‘Union 196’) were deduced that shared 10 DEMs and 13 DEGs with published signatures, respectively. The study has identified five topmost nodal genes (APP, KIAA0101, CDK2, ESR1 and FN1) derived from functional modules in PPI networks and has paved the way for further studies to establish their prognostic potential and role in therapeutics for MM. The integrated bioinformatics methods and expression profiling techniques may lead to the identification of putative hub genes and expression signatures that can serve as predictive biomarkers of MM progression.

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Section: Discussionsupporting

confidence: 55%

Genome-Wide Identification of Potential Biomarkers in Multiple Myeloma Using Meta-Analysis of mRNA and miRNA Expression Data

Katiyar

Kaur

Rani

et al. 2021

Preprint

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“…Some studies have suggested that miR-638 and miR-182 may also target PLD1. 32,33 However, no changes in miR-638 were found in our microRNA microarray assay after cadmium exposure for 6 weeks.…”

Section: Discussionmentioning

confidence: 68%

MiR‐122‐5p and miR‐326‐3p promote cadmium‐induced NRK‐52E cell apoptosis by downregulating PLD1

Wang

Liang

Deng

et al. 2020

Environmental Toxicology

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Cadmium is a toxic heavy metal distributed broadly in the environment and manufactory industry. Long‐term exposure to cadmium, considered as a risk for kidney injury, leads to chronic kidney disease eventually. Phospholipase D1 (PLD1) promotes cell proliferation and inhibits apoptosis, and might be involved in cadmium‐induced kidney injury. In this study, we used miRNA microarray assays and bioinformatics analysis to identify miRNAs, which may regulate PLD1 expression and exert an impact on cadmium‐induced kidney injury. MiR‐122‐5p and miR‐326‐3p，selected as candidates, were explored for their regulatory functions in kidney injury, using NRK‐52E cells. Both of these two miRNAs exhibited higher expression in kidneys of SD rats after exposure to cadmium for 6 weeks. Cadmium treatment also increased miR‐122‐5p and miR‐326‐3p and decreased PLD1 in NRK‐52E cells. Both of miR‐122‐5p and miR‐326‐3p could downregulate PLD1 expression through targeting its 3′UTR and enhance cadmium‐induced apoptosis, while inhibiting either of these two miRNAs could reverse such effects. In conclusion, our results suggest that miR‐122‐5p and miR‐326‐3p might enhance cadmium‐induced NRK‐52E cell apoptosis through downregulating PLD1 expression.

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“…Among these, miR‐638 is reported to function as a tumor suppressor and inhibits cell migration in HCC 33 . It also influences cancer cell progression through the Wnt/β‐catenin pathway and affects the cell cycle by suppressing cyclin D1 expression 34,35 . Another candidate, miR‐663a, also has a tumor suppressor function, showing anti‐proliferative effects and suppression of invasiveness and tumor growth in HCC 36 .…”

Section: Discussionmentioning

confidence: 99%

“…13 33 It also influences cancer cell progression through the Wnt/β-catenin pathway and affects the cell cycle by suppressing cyclin D1 expression. 34,35 Another candidate, miR-663a, also has a tumor suppressor function, showing anti-proliferative effects and suppression of invasiveness and tumor growth in HCC. 36 Conversely, miR-3648 is reported to promote cell invasion and migration in bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

Serum exosomal miR‐638 is a prognostic marker of HCC via downregulation of VE‐cadherin and ZO‐1 of endothelial cells

et al. 2021

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer‐related death. High recurrence rates after curative resection and the lack of specific biomarkers for intrahepatic metastases are major clinical problems. Recently, exosomal microRNAs (miRNAs) have been reported to have a role in the formation of the pre‐metastatic niche and as promising biomarkers in patients with malignancy. Here we aimed to clarify the molecular mechanisms of intrahepatic metastasis and to identify a novel biomarker miRNA in patients with HCC. A highly intrahepatic metastatic cell line (HuH‐7M) was established by in vivo selection. HuH‐7M showed increased proliferative ability and suppression of apoptosis and anoikis. HuH‐7M and the parental cell (HuH‐7P) showed the similar expression of epithelial‐mesenchymal transition markers and cancer stem cell markers. In vivo, mice treated with exosomes derived from HuH‐7M showed increased tumorigenesis of liver metastases. Exosomes from HuH‐7M downregulated endothelial cell expression of vascular endothelial‐cadherin (VE‐cadherin) and zonula occludens‐1 (ZO‐1) in non‐cancerous regions of liver and increased the permeability of FITC‐dextran through the monolayer of endothelial cells. The miRNAs (miR‐638, miR‐663a, miR‐3648, and miR‐4258) could attenuate endothelial junction integrity by inhibiting VE‐cadherin and ZO‐1 expression. In patients with HCC, higher serum exosomal miR‐638 expression was associated with tumor recurrence. In conclusion, the miRNAs secreted from a highly metastatic cancer cell can promote vascular permeability via downregulation of endothelial expression of VE‐cadherin and ZO‐1. Serum exosomal miR‐638 expression holds potential for serving as a significant and independent prognostic marker in HCC.

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MiR-638 suppresses the progression of oral squamous cell carcinoma through wnt/β-catenin pathway by targeting phospholipase D1

Abstract: View related articles View Crossmark data Citing articles: 5 View citing articles MiR-638 suppresses the progression of oral squamous cell carcinoma through wnt/b-catenin pathway by targeting phospholipase D1

Cited by 22 publications

References 29 publications

Genome-Wide Identification of Potential Biomarkers in Multiple Myeloma Using Meta-Analysis of mRNA and miRNA Expression Data

Genome-Wide Identification of Potential Biomarkers in Multiple Myeloma Using Meta-Analysis of mRNA and miRNA Expression Data

MiR‐122‐5p and miR‐326‐3p promote cadmium‐induced NRK‐52E cell apoptosis by downregulating PLD1

Serum exosomal miR‐638 is a prognostic marker of HCC via downregulation of VE‐cadherin and ZO‐1 of endothelial cells

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