Oncogenic role of miR‑183‑5p in lung adenocarcinoma: A comprehensive study of qPCR, inï¿½vitro experiments and bioinformatic analysis

He, Rong‐Quan; Li, Gao; Ma, Jie; Li, Zu‐Yun; Hu, Xiaohua

doi:10.3892/or.2018.6429

Cited by 19 publications

(17 citation statements)

References 59 publications

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“…The cBioPortal database (http://www.cbioportal.org) was mined for mutation profiles of MIR22HG in HCC. 22 The alteration status of MIR22HG in 440 TCGA provisional HCC samples was queried from the OncoPrint module of cBioPortal.…”

Section: Potential Molecular Mechanism Of Mir22hg In Hccmentioning

confidence: 99%

<p>MIR22HG As A Tumor Suppressive lncRNA In HCC: A Comprehensive Analysis Integrating RT-qPCR, mRNA-Seq, And Microarrays</p>

Xiong

et al. 2019

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Introduction: MIR22HG has a reported involvement in the tumorigenesis of a variety of cancers, including hepatocellular carcinoma (HCC). However, the exact molecular mechanism of MIR22HG in HCC has not been clarified. Methods: In the present study, we integrated data from in-house RT-qPCR, RNA-sequencing, microarray, and literature studies to conduct a comprehensive evaluation of the clinicopathological and prognostic significance of MIR22HG in an extremely large group of HCC samples. We also explored the potential mechanism of MIR22HG in HCC by analyzing the alteration profiles of MIR22HG in HCC to predict transcription factors (TFs) that may interact with MIR22HG and to annotate the biological functions of genes co-expressed with MIR22HG. MIR22HG expression was also compared in HCC nude mice xenografts before and after a treatment with nitidine chloride. Results: We found that MIR22HG was downregulated in HCC and that this downregulation correlated with the malignant phenotype of HCC. Comprehensive analysis of the prognostic impact of MIR22HG in HCC revealed a beneficial effect of MIR22HG on the survival outcome of HCC patients. Seven cases of MIR22HG deep deletion occurred in 360 of the cancer genome atlas (TCGA) provisional HCC samples. A total of 22 MIR22HG-TF-mRNA triplets in HCC were predicted by the lncRNAmap. Co-expressed genes of MIR22HG, identified by weighted correlation network analysis (WGCNA), mainly participated in the pathways involving osteoclast differentiation, chemokine signaling pathways, and hematopoietic cell lineage. In vivo experiments demonstrated that nitidine chloride could stimulate MIR22HG expression in HCC xenografts. Conclusion: In summary, MIR22HG may play a tumor-suppressive role in HCC by coordinating with predicted TFs and co-expressed genes, such as NLRP3, CSF1R, SIGLEC10, and ZEB2, or by being controlled by nitidine chloride.

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Section: Potential Molecular Mechanism Of Mir22hg In Hccmentioning

confidence: 99%

<p>MIR22HG As A Tumor Suppressive lncRNA In HCC: A Comprehensive Analysis Integrating RT-qPCR, mRNA-Seq, And Microarrays</p>

Xiong

et al. 2019

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“…Studies using human-derived samples offering sufficient CASC9 expression data (where the numbers of LUSC and non-cancer cases exceeded 3) in LUSC and non-cancer samples for the calculation of a standardized mean difference (SMD) were included. Basic information, as well as expression and diagnostic data, including accession ID, first author, publication year, country, experiment type, sample type, platform, number of cases in the cancer or non-cancer groups, mean ± SD of CASC9 expression in the cancer or non-cancer groups, true positives, false positives, false negatives and true negatives, were extracted from the included studies according to methods described previously (23). An SMD with the 95% confidence interval (CI) and summarized receiver operating characteristic (SROC) curves were produced for the integrated meta-analysis, consisting of the in-house RT-qPCR data, TCGA data and microarray chip data from ArrayExpress, as described previously (23).…”

Section: Integrated Meta-analysis Of Casc9 Expression In Lusc and Nonmentioning

confidence: 99%

The expression, significance and function of cancer susceptibility candidate�9 in lung squamous cell carcinoma: A bioinformatics and in�vitro investigation

Guo

Zeng

et al. 2019

Int J Oncol

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The cancer susceptibility candidate 9 (CASC9) gene has been reported to exert an oncogenic effect in several types of cancer. However, its role in lung squamous cell carcinoma (LUSC) is unknown. Therefore, the present study examined the expression of CASC9 in LUSC and non-cancer tissues by reverse transcription-quantitative polymerase chain reaction assays and by data mining of high-throughput public databases, including The Cancer Genome Atlas, the Gene Expression Omnibus, ArrayExpress and the Cancer Cell Line Encyclopedia. In vitro experiments were conducted to investigate the effects of CASC9 on the viability and the proliferation of LUSC cells. Furthermore, consulting the alteration status of CASC9 in LUSC from cBioPortal, functional enrichment analysis of co-expressed genes, prediction of potential transcription factors, and inspection of adjacent protein-coding genes were conducted to explore the potential molecular mechanism of CASC9 in LUSC. The results revealed that CASC9 was overexpressed in LUSC tissue, and significantly associated with the malignant progression of LUSC. In vitro experiments demonstrated that CASC9 knockdown by RNA interference attenuated the viability and proliferation of LUSC cells. Multiple copies of CASC9 gene were detected in 4 of 179 available sequenced LUSC cases. A functional enrichment analysis of 200 co-expressed genes indicated that these genes were significantly associated with terms, including 'cell-cell junction organization', 'desmosome organization', 'epidermis development', 'Hippo signaling pathway', 'pathogenic Escherichia coli infection' and 'PID HIF1 TF pathway'. Three genes, Fos-related antigen 2 (FOSL2), SWI/SNF complex subunit SMARCC2, and transcription factor COE1 (EBF1), were predicted by lncRNAMap to be associated with CASC9. Among these, the expression of FOSL2 and EBF1 was positively and negatively correlated with the expression of CASC9, respectively. Two adjacent protein-coding genes, cysteine-rich secretory protein LCCL domain-containing 1 and hepatocyte nuclear factor 4-γ, were also positively correlated with CASC9 expression. In conclusion, the present data suggest that CASC9 serves as an oncogene in LUSC and may be a promising target for alternative therapeutic options for patients with this condition.

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“…The relative miR-182-5p expression level was computed using the method of 2 -Δcq . The statistical analysis for the RT-qPCR was as described previously [39].…”

Section: Methodsmentioning

confidence: 99%

“…Alterations in the expression of miR-182-5p in LUADs, non-LUADs, NSCLC, and non-NSCLC, in addition to the distribution of miR-182-5p in groups of different clinical variables, were calculated to determine the clinical significance of miR-182-5p. The statistical analysis of the miRNA-seq data has been described in detail elsewhere [39]. cases.…”

Section: Methodsmentioning

confidence: 99%

MiR-182-5p and its target HOXA9 in non-small cell lung cancer: a clinical and in-silico exploration with the combination of RT-qPCR, miRNA-seq and miRNA-chip

Yan

Yang

et al. 2020

BMC Med Genomics

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Background: MiR-182-5p, a cancer-related microRNA (miRNA), modulates tumorigenesis and patient outcomes in various human malignances. This study interroted the clinicopathological significance and molecular mechanisms of miR-182-5p in non-small cell lung cancer (NSCLC). Methods: The clinical significance of miR-182-5p in NSCLC subtypes was determined based on an analysis of 124 samples (lung adenocarcinomas [LUADs], n = 101; lung squamous cell carcinomas [LUSCs], n = 23) obtained from NSCLC patients and paired noncancer tissues and an analysis of data obtained from public miRNA-seq database, miRNA-chip database, and the scientific literature. The NSCLC samples (n = 124) were analyzed using the real-time quantitative polymerase chain reaction (RT-qPCR). Potential targets of miR-182-5p were identified using lists generated by miRWalk v.2.0, a comprehensive atlas of predicted and validated targets of miRNA-target interactions. Molecular events of miR-182-5p in NSCLC were unveiled based on a functional analysis of candidate targets. The association of miR-182-5p with one of the candidate target genes, homeobox A9 (HOXA9), was validated using inhouse RT-qPCR and dual-luciferase reporter assays. Results: The results of the in-house RT-qPCR assays analysis of data obtained from public miRNA-seq databases, miRNA-chip databases, and the scientific literature all supported upregulation of the expression level of miR-182-5p level in NSCLC. Moreover, the in-house RT-qPCR data supported the influence of upregulated miR-182-5p on malignant progression of NSCLC. In total, 774 prospective targets of miR-182-5p were identified. These targets were mainly clustered in pathways associated with biological processes, such as axonogenesis, axonal development, and Ras protein signal transduction, as well as pathways involved in axonal guidance, melanogenesis, and longevity regulation, in multiple species. Correlation analysis of the in-house RT-qPCR data and dual-luciferase reporter assays confirmed that HOXA9 was a direct target of miR-182-5p in NSCLC. Conclusions: The miR-182-5p expression level was upregulated in NSCLC tissues. MiR-182-5p may exert oncogenic influence on NSCLC through regulating target genes such as HOXA9.

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Oncogenic role of miR‑183‑5p in lung adenocarcinoma: A comprehensive study of qPCR, inï¿½vitro experiments and bioinformatic analysis

Cited by 19 publications

References 59 publications

<p>MIR22HG As A Tumor Suppressive lncRNA In HCC: A Comprehensive Analysis Integrating RT-qPCR, mRNA-Seq, And Microarrays</p>

<p>MIR22HG As A Tumor Suppressive lncRNA In HCC: A Comprehensive Analysis Integrating RT-qPCR, mRNA-Seq, And Microarrays</p>

The expression, significance and function of cancer susceptibility candidate�9 in lung squamous cell carcinoma: A bioinformatics and in�vitro investigation

MiR-182-5p and its target HOXA9 in non-small cell lung cancer: a clinical and in-silico exploration with the combination of RT-qPCR, miRNA-seq and miRNA-chip

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