<scp>MiR</scp>‐770 promotes oral squamous cell carcinoma migration and invasion by regulating the Sirt7/Smad4 pathway

Jia, Bin; Zhang, Sanke; Wu, Shuang; Zhu, Qinglin; Li, Wenlu

doi:10.1002/iub.2426

Cited by 22 publications

(12 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that dysregulation of miRNAs often leads to cancer occurrence ( Geng et al, 2018 ; Park et al, 2018 ). MiR-770 is known to have important biological functions in cancer tumorigenesis and metastasis ( Feng et al, 2019 ; Jia et al, 2020 ). Our current study found that miR-770 was significantly downregulated in exosomes, and it could suppress the migration and invasion of NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage Polarization via Targeting MAP3K1 to Inhibit the Invasion of Non-small Cell Lung Cancer Cells

Liu

Luo

Wang

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

BackgroundNon-small cell lung carcinoma (NSCLC) is a type lung cancer with high malignant behaviors. MicroRNAs (miRNAs) are known to be involved in progression of NSCLC. In order to explore potential targets for the treatment of NSCLC, bioinformatics tool was used to analyze differential expressed miRNAs between NSCLC and adjacent normal tissues.MethodsBioinformatics tool was used to find potential targets for NSCLC. Cell proliferation was investigated by Ki67 staining. Cell apoptosis was measured by flow cytometry. mRNA and protein expression in NSCLC cells were detected by RT-qPCR and Western-blot, respectively. Transwell assay was performed to test the cell migration and invasion. In order to investigate the function of exosomal miRNA in NSCLC, in vivo model of NSCLC was constructed.ResultsMiR-770 was identified to be downregulated in NSCLC, and miR-770 agomir could significantly inhibit NSCLC cell proliferation through inducing the apoptosis. Additionally, the metastasis of NSCLC cells was decreased by miR-770 agomir. MAP3K1 was identified to be the target mRNA of miR-770. Meanwhile, tumor cell-derived exosomal miR-770 inhibited M2 macrophage polarization via downregulation of MAP3K1, which in turn suppressed NSCLC cell invasion. Besides, tumor cell-derived exosomal miR-770 markedly decreased NSCLC tumor growth in vivo through suppressing M2 macrophage polarization.ConclusionTumor cell-derived exosomal miR-770 inhibits M2 macrophage polarization to inhibit the invasion of NSCLC cells via targeting MAP3K1. Thus, this study provided a new strategy for the treatment of NSCLC.

show abstract

Section: Discussionmentioning

confidence: 99%

Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage Polarization via Targeting MAP3K1 to Inhibit the Invasion of Non-small Cell Lung Cancer Cells

Liu

Luo

Wang

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…Oral cancer represents a relatively non frequent disease, largely preventable but burdened by a high mortality rate [ 74 ]. SIRT7 antagonizes oral cancer metastasis through the deacetylation of small mother against decapentaplegic 4 (Smad4) and can be found frequently downregulated in vivo because of miR-770 expression, whose expression represents a negative prognostic factor [ 75 ]. In oral squamous carcinoma cells Cal27, SIRT1 determines cell apoptosis affecting procaspase-3 and cyclin B1, ultimately exercising an anticancer effect [ 76 ]; additively, SIRT1 has been demonstrated to induce E-cadherin expression and to repress transforming growth factor-beta (TGF-β) interfering with the acquisition of the metastatic phenotype [ 77 ].…”

Section: Sirtuins and Cancermentioning

confidence: 99%

Mitochondrial Sirtuins in Chronic Degenerative Diseases: New Metabolic Targets in Colorectal Cancer

Colloca¹,

Balestrieri²,

Anastasio³

et al. 2022

IJMS

View full text Add to dashboard Cite

Sirtuins (SIRTs) are a family of class III histone deacetylases (HDACs) consisting of seven members, widely expressed in mammals. SIRTs mainly participate in metabolic homeostasis, DNA damage repair, cell survival, and differentiation, as well as other cancer-related biological processes. Growing evidence shows that SIRTs have pivotal roles in chronic degenerative diseases, including colorectal cancer (CRC), the third most frequent malignant disease worldwide. Metabolic alterations are gaining attention in the context of CRC development and progression, with mitochondrion representing a crucial point of complex and intricate molecular mechanisms. Mitochondrial SIRTs, SIRT2, SIRT3, SIRT4 and SIRT5, control mitochondrial homeostasis and dynamics. Here, we provide a comprehensive review on the latest advances on the role of mitochondrial SIRTs in the initiation, promotion and progression of CRC. A deeper understanding of the pathways by which mitochondrial SIRTs control CRC metabolism may provide new molecular targets for future innovative strategies for CRC prevention and therapy.

show abstract

“…The length of the microRNA (miRNA/miR) is about 20 to 25 nucleotides, which have key regulatory functions in the occurrence or development of cancer, and can be involved in the regulation of tumor immune microenvironment 6 , cell migration, invasion and epithelial interstitial transformation 7 . MiR-770 promoted the migration and invasion of OSCC by regulating the Sirt7/Smad4 pathway 8 . MiR-487a-3p was found to inhibit the growth and invasion of OSCC by regulating the expression of PPM1A, thereby playing a tumor suppressor effect 9 .…”

Section: Introductionmentioning

confidence: 98%

Construction of the miRNA-mRNA regulatory network and analysis of hub genes in oral squamous cell carcinoma

Cui¹,

Song²,

Chen³

et al. 2022

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

View full text Add to dashboard Cite

Background. Oral squamous cell carcinoma (OSCC) severely affects the quality of life and the 5-year survival rate is low. Exploring the potential miRNA-mRNA regulatory network and analyzing hub genes and clinical data can provide a theoretical basis for further elucidating the pathogenesis of OSCC. Methods. The miRNA expression datasets of GSE113956 and GSE124566 and mRNA expression datasets of GSE31056, GSE37991 and GSE13601 were obtained from the Gene Expression Omnibus databases. The differentially expressed miRNAs (DEMs) and mRNAs (DEGs) were screened using GEO2R. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by DAVID database. The PPI network was established through STRING database and the hub genes were preliminarily screened out by Cytoscape software. After identifying the hub genes in the TCGA database, we predicted the potential DEM transcription factors, constructed a miRNA-mRNA regulatory network, and analyzed the relationship between the hub genes and clinical data. Results. A total of 28 DEMs and 764 DEGs were screened out, which were composed of 285 up-regulated genes and 479 down-regulated genes. Enrichment analysis showed that up-regulation of DEGs were mainly enriched in extracellular matrix organization and cancer-related pathway, while down-regulation of DEGs were mainly enriched in muscular system process and adrenaline signal transduction. After preliminary screening by PPI network and identification in TCGA, the up-regulated FN1, COL1A1, COL1A2, AURKA, CCNB1, CCNA2, SPP1, CDC6, and down-regulated ACTN2, TTN, IGF1, CAV3, MYL2, DMD, LDB3, CSRP3, ACTA1, PPARG were identified as hub genes. The miRNA-mRNA regulation network showed that hsa-miR-513b was the DEM with the most regulation, and COL1A1 was the DEG with the most regulation. In addition, CDC6, AURKA, CCNB1 and CCNA2 were related to overall survival and tumor differentiation. Conclusions. The regulatory relationship of hsa-miR-513b/ CDC6, CCNB1, CCNA2 and the regulatory relationship of hsa-miR-342-5p /AURKA were not only verified in the miRNA-mRNA regulatory network but also related to overall survival and tumor differentiation. These results indicated that they participated in the cellular regulatory process, and provided a molecular mechanism model for the study of pathogenesis.

show abstract

MiR‐770 promotes oral squamous cell carcinoma migration and invasion by regulating the Sirt7/Smad4 pathway

Cited by 22 publications

References 22 publications

Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage Polarization via Targeting MAP3K1 to Inhibit the Invasion of Non-small Cell Lung Cancer Cells

Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage Polarization via Targeting MAP3K1 to Inhibit the Invasion of Non-small Cell Lung Cancer Cells

Mitochondrial Sirtuins in Chronic Degenerative Diseases: New Metabolic Targets in Colorectal Cancer

Construction of the miRNA-mRNA regulatory network and analysis of hub genes in oral squamous cell carcinoma

Contact Info

Product

Resources

About