miR‐133a‐3p suppresses cell proliferation, migration, and invasion and promotes apoptosis in esophageal squamous cell carcinoma

Yin, Yue; Du, Lei; Li, Xuezhen; Zhang, Xiaoyan; Gao, Yongli

doi:10.1002/jcp.27896

Cited by 45 publications

(48 citation statements)

References 19 publications

(41 reference statements)

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“…5 Accumulating studies have indicated that miR-133a-3p serves in a tumor suppressive role in cancers. [6][7][8] For instance, Zhang et al 6 found forced miR-133a-3p expression inhibits autophagy to hinder gastric cancer metastasis via blocking GABARAPL1 and ATG13 expression. 6 In addition, Yin et al 7 showed miR-133a-3p expression level was decreased in esophageal squamous cell carcinoma, and it could negatively regulate COL1A1 expression.…”

Section: Introductionmentioning

confidence: 99%

“…[6][7][8] For instance, Zhang et al 6 found forced miR-133a-3p expression inhibits autophagy to hinder gastric cancer metastasis via blocking GABARAPL1 and ATG13 expression. 6 In addition, Yin et al 7 showed miR-133a-3p expression level was decreased in esophageal squamous cell carcinoma, and it could negatively regulate COL1A1 expression. 7 Functional assays indicated miR-133a-3p was able to inhibit cell growth by inhibiting apoptosis via affecting COL1A1.…”

Section: Introductionmentioning

confidence: 99%

“…6 In addition, Yin et al 7 showed miR-133a-3p expression level was decreased in esophageal squamous cell carcinoma, and it could negatively regulate COL1A1 expression. 7 Functional assays indicated miR-133a-3p was able to inhibit cell growth by inhibiting apoptosis via affecting COL1A1. 7 Furthermore, Tang et al revealed miR-133a-3p expression was lower in prostate cancer tissues than in normal tissues.…”

Section: Introductionmentioning

confidence: 99%

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<p>miR-133a-3p Regulates Hepatocellular Carcinoma Progression Through Targeting CORO1C</p>

Han¹,

Ding²,

Wang³

et al. 2020

CMAR

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Introduction: MicroRNAs (miRNAs) are key modulators for gene expression via inducing translational repression or target gene degradation. miR-133a-3p was reported to stimulate or inhibit cancer progression but its role in hepatocellular carcinoma (HCC) remains to be explored. Methods: Quantitative real-time PCR (RT-qPCR) was utilized to explore miR-133a-3p expression level in HCC cells. Dual-luciferase activity reporter assay was used to validate the direct interaction between miR-133a-3p and coronin-like actin-binding protein 1C (CORO1C). In addition, we analyzed the expression levels of miR-133a-3p and CORO1C in HCC tissues and normal tissues on the UCALAN website. Functional assays including cell counting kit-8 assay, colony formation assay, flow cytometry analysis and transwell invasion assay were conducted to explore the biological functions of miR-133a-3p in HCC. Results: miR-133a-3p was found to have downregulated expression in HCC tissues and cells. Meanwhile, we showed that low miR-133a-3p levels were correlated with poorer overall survival of HCC patients. Overexpression of miR-133a-3p suppressed HCC cell growth and invasion but promoted cell apoptosis via targeting CORO1C. Discussion: Our results revealed a novel mechanism of miR-133a-3p in regulating HCC progression and provided evidence that miR-133a-3p functions as a tumor suppressor in HCC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

<p>miR-133a-3p Regulates Hepatocellular Carcinoma Progression Through Targeting CORO1C</p>

Han¹,

Ding²,

Wang³

et al. 2020

CMAR

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“…[ 39 ] Previous studies have demonstrated ESCC cells could produce COL1A1 endogenously, [ 40 ] and miR-133a-3p could inhibit the ESCC cell proliferation, invasion, and migration by targeting COL1A1. [ 41 ] However, the specific roles of COL1A2 in various tumors remain controversial. In bladder and colorectal cancer, COL1A2 was significantly downregulated and mainly plays an anticarcinogenic role in tumor development.…”

Section: Discussionmentioning

confidence: 99%

Common gene signatures and key pathways in hypopharyngeal and esophageal squamous cell carcinoma

Zhou¹,

Liu

Zhu³

et al. 2020

Medicine

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Background: Hypopharyngeal and esophageal squamous cell carcinoma (ESCC) are the most common double primary tumors with poor prognosis. Intensive work has been made to illuminate the etiology, but the common carcinogenic mechanism remains unclear. Thus, we conducted the study to seek to find the common gene signatures and key functional pathways associated with oncogenesis and treatment in hypopharyngeal squamous cell carcinoma (HSCC) and ESCC by bioinformatic analysis. Methods: Three independent datasets (GSE2379, GSE20347, and GSE75241) were screened out from the Gene Expression Omnibus (GEO) database and the overlapping differentially expressed genes (DEGs) were identified using GEO2R online platform. Subsequently, the Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis of DEGs were conducted using database for annotation, visualization and integrated discovery (DAVID). Meanwhile, the protein–protein interaction network (PPI) constructed by search tool for the retrieval of interacting genes (STRING) was visualized using Cytoscape. Afterwards, the most key module and hub genes were extracted from the PPI network using the Molecular Complex Detection plugin. Moreover, the gene expression profiling interactive analysis (GEPIA) was applied to verify the expression differences and conduct the survival analyses of hub genes. Finally, the interaction network of miRNAs and hub genes constructed by encyclopedia of RNA interactomes (ENCORI) was visualized using Cytoscape. Results: A total of 43 DEGs were identified, comprising 25 upregulated genes and 18 downregulated genes, which were mainly involved in the extracellular matrix-receptor interaction, collagen metabolic, epidermis development, cell adhesion, and PI3K/Akt signaling pathways. Subsequently, 12 hub genes were obtained and survival analysis demonstrated SERPINE1 and SPP1 were closely related to poor prognosis of patients with HSCC and ESCC. Finally, hsa-miR-29c-3p, hsa-miR-29a-3p, and hsa-miR-29b-3p were confirmed as the top 3 interactive miRNAs that target the most hub genes according to the interaction network of miRNAs and hub genes. Conclusion: The common gene signatures and functional pathways identified in the study may contribute to understanding the molecular mechanisms involved in the carcinogenesis and progression of HSCC and ESCC, and provide potential diagnostic and therapeutic targets.

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“…COL1A1 and bronectin 1 (FN1) are highly expressed in esophageal squamous cell carcinoma (ESCC) tissues. Both COL1A1 and FN1 can promote ESCC cell proliferation and invasion [32,33]. COL1A2 is signi cantly down-regulated in colorectal cancer (CRC) tissues, and COL1A2 mRNA expression levels are related to tumor differentiation, invasion, and lymph node metastasis in CRC patients.…”

Section: Expression Of Lgals1 and Its Diagnostic Value In Escamentioning

confidence: 99%

The Diagnostic Value of LGALS1 in Esophageal Cancer and its Potential Molecular Pathways via Bioinformatic Analysis

Yang

Yue

et al. 2020

Preprint

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Background: Esophageal cancer is one of the most common malignant tumors. The purpose of this study was to reveal the expression of LGALS1 in esophagus cancer (ESCA) and its clinical value, and to explore the mechanism of LGALS1 in the occurrence and development of ESCA.Methods: Oncomine, Tumor Immune Estimation Resource (Timer) and The Cancer Genome Atlas (TCGA) database were used to analyze the expression of LGALS1 in ESCA and its value in the diagnosis of ESCA. The correlation between LGALS1 and the clinicopathological characteristics of ESCA patients was analyzed in the Ualcan database. In TCGA database, we performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) to elucidate the potential mechanism underlying the role of LGALS1 in ESAC. LGALS1 co-expressed genes were imported into the String database to build a protein-protein interaction (PPI) network. The CytoHubba plug-in in Cytoscape was used to screen the hub gene and was verified in Gene Expression Profiling Interactive Analysis (GEPIA) and TCGA database.Results: LGALS1 was highly expressed in ESCA tissues. Increasing the expression level of LGALS1 was related to age, ethnicity, clinical stage, tumor grade, and histological subtype of ESCA patients, and receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) was 0.8511 (P <0.001). There are 482 LGALS1 co-expressed genes. GO and KEGG show that LGALS1 co-expressed genes are mainly involved in endothelial cell differentiation, transforming growth factor receptor signaling pathway, epithelial cell proliferation, ECM receptor interactions, leukocyte migration, transcriptional disorders during cancer, PI3K/AKT signaling pathway and other processes. GSEA showed that elevated LGALS1 was mainly enriched for ECM receptor interactions, cancer pathways, and TGF BETA signaling pathways. The Hub genes COL1A1, FN1, COL1A2, COL3A1, COL5A1, COL5A2, COL4A2, COL18A1, and COL6A1 are higher expressed in ESCA tissues and have diagnostic significance in ESCA.Conclusion: LGALS1 expression is elevated in ESCA patients and may be a potential diagnostic marker for ESCA patients. PI3K/AKT signaling pathway, TGF BETA signaling pathway, cancer pathway, cytokine and cytokine interaction may be an important pathway for regulation in occurrence and development of ESCA.

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miR‐133a‐3p suppresses cell proliferation, migration, and invasion and promotes apoptosis in esophageal squamous cell carcinoma

Cited by 45 publications

References 19 publications

<p>miR-133a-3p Regulates Hepatocellular Carcinoma Progression Through Targeting CORO1C</p>

<p>miR-133a-3p Regulates Hepatocellular Carcinoma Progression Through Targeting CORO1C</p>

Common gene signatures and key pathways in hypopharyngeal and esophageal squamous cell carcinoma

The Diagnostic Value of LGALS1 in Esophageal Cancer and its Potential Molecular Pathways via Bioinformatic Analysis

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