Small nucleolar RNA host gene 22 (SNHG22) promotes the progression of esophageal squamous cell carcinoma by miR-429/SESN3 axis

Li, Zhongwen; Ting-you, Zhang; Yue, Guojun; Tian, Xin; Wu, Jinzhi; Feng, Guangyong; Wang, Yongsheng

doi:10.21037/atm-20-5332

Cited by 15 publications

(7 citation statements)

References 31 publications

(36 reference statements)

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“…The abnormal expression of COL1A1 has been reported in several cancers, including AD [31][32][33]. The miR-429 gene can bind to SNHG22 and SESN3 in the SC cells [34], and several reports have even proved that the expression of miR-205 can distinguish between squamous cell carcinoma and adenocarcinoma in lung cancer biopsies [35,36]. To summarize, the selected differentially expressed genes between the AD and SC, especially with statistically significant ROC curve and association with overall survival, may act as significant biomarkers to subclassify NSCLC or important targets helping in designing a precise therapy for lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of The Potential Signature Genes Between Lung Adenocarcinoma and Lung Squamous Cell Carcinoma

wang²,

Xie

et al. 2021

Preprint

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Objectives:The purpose of this study was to identify and compare the potential signature genes along with the key pathways related to the pathogenesis of lung adenocarcinoma and lung squamous cell carcinoma through bioinformatics analysis.Methods:The differential expressions of miRNAs (DEmiRNAs) and mRNAs (DEmRNAs) in lung adenocarcinoma (AD) and lung squamous cell carcinoma (SC) were identified using the microarray data of 2miRNA and 6 mRNA from the Gene Expression Omnibus (GEO) database. The interaction between the DEmiRNAs and DEmRNAs was explored, followed by the KEGG pathway enrichment, Gene Ontology annotation (GO) enrichment analysis, DEmiRNA-gene interactive network, and protein-protein interaction (PPI) network to predict the hub genes and identify the key pathways. The sequencing data was then downloaded from The Cancer Genome Atlas (TCGA) to validate the hub genes, perform survival analysis, construct the ROC curve along with identifying the regulatory networks of mRNA-miRNA-lncRNA. Finally, the resulting signature genes and significant regulatory networks in AD and SC were filtrated across these analyses.Results:The DEmiRNAs and DEmRNAs were found to be significantly enriched in the phagosomes, human T-cell leukemia virus 1 infection, and ECM-receptor interaction in the AD, whereas in SC, they were enriched in the cell cycle and p53 signaling pathways. Furthermore, we found that the hsa-miR-21-5p, hsa-miR-200a-5p, and COL1A1 may act as potential meaningful biomarkers for the AD while hsa-miR-141-3p, hsa-miR-429, hsa-miR-130b-3p, hsa-miR-205-5p, and FRMD6 may play an important role in SC. The HMGA1/hsa-miR-424-5p/PVT1 maybe a significant regulatory network of AD while KIF11/hsa-miR-30d-5p/DLEU2, CCNE2/hsa-miR-30d-5p/DLEU2, and SPTBN1/hsa-miR-218-5p/MAGI2-AS3 may be the useful networks in regulating the SC progression.Conclusion: This study provided the signature targets and theoretical basis for further research on the biomarkers and molecular mechanisms of the SC, AD, and NSCLC.

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Section: Discussionmentioning

confidence: 99%

Identification of The Potential Signature Genes Between Lung Adenocarcinoma and Lung Squamous Cell Carcinoma

wang²,

Xie

et al. 2021

Preprint

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“…Moreover, this gene was reported as an oncogene in esophageal squamous cell carcinoma cells 112 . Rakibul Islam et al 107 , 113 have done a survival analysis, and their results show a worse overall survival value for SFN , and Outcomes show that SFN may play a crucial role in the development of NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Drug repositioning in non-small cell lung cancer (NSCLC) using gene co-expression and drug–gene interaction networks analysis

MotieGhader

Tabrizi-Nezhadi

Paskeh

et al. 2022

Sci Rep

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Lung cancer is the most common cancer in men and women. This cancer is divided into two main types, namely non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Around 85 to 90 percent of lung cancers are NSCLC. Repositioning potent candidate drugs in NSCLC treatment is one of the important topics in cancer studies. Drug repositioning (DR) or drug repurposing is a method for identifying new therapeutic uses of existing drugs. The current study applies a computational drug repositioning method to identify candidate drugs to treat NSCLC patients. To this end, at first, the transcriptomics profile of NSCLC and healthy (control) samples was obtained from the GEO database with the accession number GSE21933. Then, the gene co-expression network was reconstructed for NSCLC samples using the WGCNA, and two significant purple and magenta gene modules were extracted. Next, a list of transcription factor genes that regulate purple and magenta modules' genes was extracted from the TRRUST V2.0 online database, and the TF–TG (transcription factors–target genes) network was drawn. Afterward, a list of drugs targeting TF–TG genes was obtained from the DGIdb V4.0 database, and two drug–gene interaction networks, including drug-TG and drug-TF, were drawn. After analyzing gene co-expression TF–TG, and drug–gene interaction networks, 16 drugs were selected as potent candidates for NSCLC treatment. Out of 16 selected drugs, nine drugs, namely Methotrexate, Olanzapine, Haloperidol, Fluorouracil, Nifedipine, Paclitaxel, Verapamil, Dexamethasone, and Docetaxel, were chosen from the drug-TG sub-network. In addition, nine drugs, including Cisplatin, Daunorubicin, Dexamethasone, Methotrexate, Hydrocortisone, Doxorubicin, Azacitidine, Vorinostat, and Doxorubicin Hydrochloride, were selected from the drug-TF sub-network. Methotrexate and Dexamethasone are common in drug-TG and drug-TF sub-networks. In conclusion, this study proposed 16 drugs as potent candidates for NSCLC treatment through analyzing gene co-expression, TF–TG, and drug–gene interaction networks.

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“…In addition, high expression of miR-675 was found in AFP-secreting HCC, which usually links to a significant rise in proliferative and growth capacity [ 38 ]. On the contrary, SESN3 has been suggested as a tumor-suppressor in HCC, since SESN3 deficiency promoted carcinogen-induced HCC via regulating the hedgehog pathway [ 39 ]. To validate the involvements of miR-675 and SESN3 in EGR1-mediated events.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic role of early growth response-1 in liver cancer through the regulation of the microRNA-675/sestrin 3 and the Wnt/β-catenin signaling pathway

et al. 2021

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Early growth response-1 (EGR1) is a multi-domain protein and an immediate early transcription factor that is induced during liver injury and controls the expression of a variety of genes implicated in metabolism, cell proliferation, and tumorigenesis. Liver cancer (LC) is a highly malignant disease with high mortality worldwide. This study focused on the function of EGR1 in LC development and the mechanism of action. Two LC-related datasets GSE101728 and GSE138178 downloaded from the Gene Expression Omnibus (GEO) database were used for identification of key genes involved in cancer progression. A microarray analysis was conducted to identify differentially expressed microRNAs (miRNAs) after EGR1 knockdown. The target gene of miR-675 was identified by integrated analysis. EGR1 and miR-675 were highly expressed, whereas sestrin 3 (SESN3) was poorly expressed in LC tissues and cells. High EGR1 expression was associated with poor liver function and disease severity in patients with LC. Knockdown of EGR1 weakened proliferation and invasiveness of LC cells. EGR1 bound to the miR-675 promoter and increased its transcription, and miR-675 bound to SESN3 mRNA to induce its downregulation. miR-675 upregulation promoted the malignance of LC cells, but further upregulation of SESN3 reduced invasiveness of cells. SESN3 was enriched in the Wnt/β-catenin signaling. EGR1 and miR-675 activated the Wnt/β-catenin through downregulating SESN3. This study demonstrated that EGR1 promotes the malignant behaviors of LC cells through mediating the miRNA-675/SESN3/ Wnt/β-catenin axis.

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Small nucleolar RNA host gene 22 (SNHG22) promotes the progression of esophageal squamous cell carcinoma by miR-429/SESN3 axis

Cited by 15 publications

References 31 publications

Identification of The Potential Signature Genes Between Lung Adenocarcinoma and Lung Squamous Cell Carcinoma

Identification of The Potential Signature Genes Between Lung Adenocarcinoma and Lung Squamous Cell Carcinoma

Drug repositioning in non-small cell lung cancer (NSCLC) using gene co-expression and drug–gene interaction networks analysis

Oncogenic role of early growth response-1 in liver cancer through the regulation of the microRNA-675/sestrin 3 and the Wnt/β-catenin signaling pathway

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