miR-1266-3p Suppresses Epithelial-Mesenchymal Transition in Colon Cancer by Targeting P4HA3

Zhou, Hailang; Huang, Shu; Shao, Chang-Jiang; Zou, Junwei; Zhou, Anni; Yu, Jiufeng; Xu, Chunfang

doi:10.1155/2022/1542117

Cited by 6 publications

(4 citation statements)

References 42 publications

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“…Many previous studies have shown that P4HA3 promotes tumor cell growth, proliferation, and metastasis in HNSC by activating the EMT process ( Wang et al, 2020 ). Targeting P4HA3 inhibits EMT in colon cancer ( Zhou et al, 2022a ). TGF-β enables cancer cell invasion and metastasis and inhibits the anti-tumor activity of immune cells ( Derynck et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…P4HA3 (prolyl 4-hydroxylase subunit alpha 3) is a protein-coding gene that belongs to the prolyl 4-hydroxylase family members. A study found that P4HA3 expression is upregulated in patients with renal cell carcinoma (RCC), promoting cancer growth, invasion, and metastasis ( Zhou et al, 2022a ). It has been reported that in gastric cancer (GC), P4HA3 is significantly upregulated compared to normal tissue and is associated with unfavorable overall survival (OS) ( Song et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

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Systematic pan-cancer analysis of the potential tumor diagnosis and prognosis biomarker P4HA3

Zhang

Nong

et al. 2023

Front. Genet.

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Purpose: Prolyl 4-hydroxylase subunit alpha 3 (P4HA3) is implicated in several cancers’ development. However, P4HA3 has not been reported in other cancers, and the exact mechanism of action is currently unknown.Materials and methods: First, the expression profile of P4HA3 was analyzed using a combination of the University of California Santa Cruz (UCSC) database, Cancer Cell Line Encyclopedia (CCLE) database, and Genotype-Tissue Expression (GTEx) database. UniCox and Kaplan-Meier were used to analyze the predictive value of P4HA3. The expression of P4HA3 was analyzed in clinical staging, immune subtypes, and Molecular subtypes. Secondly, the correlation of P4HA3 with immunomodulatory genes, immune checkpoint genes, RNA modification genes, immune cell infiltration, cancer-related functional status, tumor stemness index, DNA mismatch repair (MMR) genes and DNA Methyltransferase was examined. The role of P4HA3 in DNA methylation, copy number variation (CNV), mutational status, tumor mutational burden (TMB), and microsatellite instability (MSI) was also analyzed. In addition, gene set enrichment analysis (GSEA) was used to explore the potential functional mechanisms of P4HA3 in pan-cancer. Finally, P4HA3-related drugs were searched in CellMiner, Genomics of Drug Sensitivity in Cancer (GDSC), and Cancer Therapeutics Response Portal (CTRP) databases.Results: P4HA3 is significantly overexpressed in most cancers and is associated with poor prognosis. P4HA3 is strongly associated with clinical cancer stage, immune subtypes, molecular subtypes, immune regulatory genes, immune checkpoint genes, RNA modifier genes, immune cell infiltration, cancer-related functional status, tumor stemness index, MMR Gene, DNA Methyltransferase, DNA methylation, CNV, mutational status, TMB, and MSI are closely related. Available enrichment analysis revealed that P4HA3 is associated with the epithelial-mesenchymal transition and immune-related pathways. There are currently 20 drugs associated with P4HA3.Conclusion: In human pan-cancer, P4HA3 is associated with poor patient prognosis and multiple immune cells and may be a novel immunotherapeutic target. It may act on tumor progression through the epithelial-mesenchymal transition (EMT) pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Systematic pan-cancer analysis of the potential tumor diagnosis and prognosis biomarker P4HA3

Zhang

Nong

et al. 2023

Front. Genet.

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“…MiRNA is a small, non-coding, single-stranded RNA molecule consisting of about 19-23 nucleotides (37). MiRNA regulates gene expression mainly by degrading mRNA or inhibiting its translation (38).…”

Section: Organ/tissue Genesmentioning

confidence: 99%

Biomarker identification of chronic atrophic gastritis and its potential drug analysis

Song¹,

Cao²,

Li³

et al. 2022

Front. Gastroenterol.

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BackgroundChronic atrophic gastritis (CAG) is the first step of gastric precancerous lesions, and the study of the pathogenesis of CAG is helpful for the prevention and treatment of gastric cancer(GC). The purpose of this study is to explore the potential biomarkers and therapeutic drugs of CAG through bioinformatics analysis.MethodsThe GSE11632 dataset was downloaded from Gene Expression Omnibus (GEO) database and the differentially expressed genes (DEGs) were obtained by using GEO2R online tool. We searched GeneCard and DisGeNET databases for genes related to CAG and used the overlapping genes as final DEGs for further functional enrichment analysis and Protein-protein Interaction (PPI) network analysis. Tissue-specific expressed genes were identified by BioGPS database. Cytoscape software was used to identify key hub genes and validated them in GSE27411 data sets. The upstream miRNAs of hub gene was predicted by TargetScan, miRDB and miRWalk. Finally, run the Connectivity Map (CMap) to identify new potential drugs for the treatment of CAG.ResultsA total of 430 differentially expressed mRNA were identified in this study, including 315 up-regulated genes and 115 down-regulated genes. After intersecting with CAG-related genes in GeneCard and DisGeNET databases, 42 DEGs were obtained. 24 DEGs were identified as tissue-specific expressed genes, most of which were expressed in stomach. GO and KEGG pathway analysis showed that DGEs was mainly enriched in digestion, IL-1 production, gastric acid secretion and so on. A total of 6 hub genes were generated by cytoHubba plug-in, among which ATP4A, CFTR and EPCAM had high diagnostic value. A total of 13 overlapping miRNA were predicted by 6 hub genes.ConclusionATP4A, CFTR and EPCAM may be potential biomarkers of CAG. hsa-miR-185-5p-CFTR, hsa-miR-4644-CFTR and hsa-miR-4505-CFTR are potential RNA regulatory pathways to control the progression of CAG disease. Finally, amonafide, etoposide, mycophenolate-mofetil, cycloheximide and Emetine may be potential therapeutic drugs for CAG.

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“…Certain miRNAs bind to the 3′-UTRs of target mRNAs to inhibit gene expression [ 7 ]. For example, miR-1266-3p can inhibit the development of colon cancer by targeting the 3′-UTR of P4HA3 and inhibiting its expression [ 8 ]. Studies showed differential miRNA expression is involved in the ongoing pathophysiology of OA [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR‐182‐5p Targets FGF9 to Alleviate Osteoarthritis

Sun

et al. 2023

Analytical Cellular Pathology

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Background. The pathogenesis of osteoarthritis (OA) is complex and there is no specific drug for treatment. The aim of this study was to identify the molecular targets of OA therapy, focusing on the expression and biological functions of miR-182-5p and its target genes in OA. Methods. miR-182-5p and fibroblast growth factor 9 (FGF9) were overexpressed or knocked down in IL-1β-induced chondrocytes. An OA knee model was performed by surgically destroying the medial meniscus. The gene expression of miR-182-5p and FGF9 was calculated. The protein FGF9 was tested by western blotting. Cell counting kit-8 (CCK8), plate cloning assay, and flow cytometry were conducted to evaluate cell proliferation and apoptosis. The expression of inflammatory factors, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and interleukin (IL)-8, was evaluated using enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter assays validated the targeting relationship between miR-182-5p and FGF9. Hematoxylin–eosin (HE) and safranin O-fast Green (S–O) staining were utilized to access cartilage damage. Ki67 expression in cartilage was detected using immunohistochemistry (IHC). TdT-mediated dUTP nick-end labeling (TUNEL) assays were used to calculate the apoptosis rate of cartilage. Results. The expression of miR-182-5p was upregulated, and FGF9 was downregulated in the IL-1β-induced chondrocytes. OA chondrocytes proliferation ability in the miR-182-5p mimics group was decreased, and the apoptosis rate and inflammatory factor were increased. Transfection with miR-182-5p inhibitor increased the proliferative ability and decreased the apoptosis rate in the IL-1β-induced chondrocytes. Transfection with miR-182-5p inhibitor reversed IL-1β-induced inflammatory factor release in chondrocytes. Targeted binding sites existed between miR-182-5p and FGF9. After overexpression of FGF9, the miR-182-5p effect on OA chondrocytes was reversed. The hyaline cartilage thickness and proteoglycan content decreased in OA rats, and this was reversed by miR-182-5p inhibitor treatment. Conclusions. miR-182-5p expression levels were increased in OA chondrocytes and regulated chondrocyte proliferation, apoptosis, and inflammation by targeting FGF9. miR-182-5p is a potential gene for OA treatment.

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miR-1266-3p Suppresses Epithelial-Mesenchymal Transition in Colon Cancer by Targeting P4HA3

Cited by 6 publications

References 42 publications

Systematic pan-cancer analysis of the potential tumor diagnosis and prognosis biomarker P4HA3

Systematic pan-cancer analysis of the potential tumor diagnosis and prognosis biomarker P4HA3

Biomarker identification of chronic atrophic gastritis and its potential drug analysis

Inhibition of miR‐182‐5p Targets FGF9 to Alleviate Osteoarthritis

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