LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells

Dong, Lemei; Hong, Huisuo; Chen, Xiaowei; Huang, Zhiming; Wu, Wei; Wu, Fang

doi:10.1080/21691401.2018.1464462

Cited by 28 publications

(15 citation statements)

References 29 publications

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“…Among these 26 HCC-related RNA editing sites, the top three affected miRNAs were miR-17-3p, miR-20b-3p, and miR-593-3p (with 11, 7, and 7 target regulation changes induced by HCC-related editing sites, respectively ( Supplementary Table S5). Notably, miR-17-3p, miR-20b-3p, and miR-593-3p are widely involved in caner initiation and progression, including HCC (42)(43)(44)(45)(46). We observed that the expression levels of 163 RNA editing sites were correlated with the editing degree of corresponding genes, of which 10 were HCC-related editing sites.…”

Section: The Functional Consequence Of Rna Editing Sitesmentioning

confidence: 79%

Genomic Identification of RNA Editing Through Integrating Omics Datasets and the Clinical Relevance in Hepatocellular Carcinoma

Chen

Wang

et al. 2020

Front. Oncol.

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RNA editing is a widespread post-transcriptional mechanism to introduce single nucleotide changes to RNA in human cancers. Here, we characterized the global RNA editing profiles of 373 hepatocellular carcinoma (HCC) and 50 adjacent normal liver samples from The Cancer Genome Atlas (TCGA) and revealed that most editing events tend to occur in minor percentage of samples with moderate editing degrees (20-30%). Moreover, these RNA editing prefer to be A-to-I RNA editing in protein coding genes, especially in 3 ′ UTR regions. Considering the association between DNA mutation and RNA editing, our analysis found that RNA editing maybe a complementary event for DNA mutation of HCC risk genes in HCC patients. We next identified 454 HCC-related editing sites, and many locate on the same genes with the same editing patterns. The functional consequences of editing revealed 2,086 functional editing sites and demonstrated that most editing in coding regions are non-synonymous variations. Furthermore, our results showed that editing in the 3 ′ UTR regions tend to influence miRNA-target binding, and the editing degree seems to be negatively correlated with gene expression. Finally, we found that 46 HCC-related editing sites with consequence are able to distinguish the prognosis differences of HCC patients, suggesting their clinical relevance. Together, our results highlight RNA editing as a valuable molecular resource for investigating HCC mechanisms and clinical treatments.

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Section: The Functional Consequence Of Rna Editing Sitesmentioning

confidence: 79%

Genomic Identification of RNA Editing Through Integrating Omics Datasets and the Clinical Relevance in Hepatocellular Carcinoma

Chen

Wang

et al. 2020

Front. Oncol.

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“…MiR-593-3p is a potential tumor suppressor in gastric cancer and lung cancer. Dong et al reported miR-593-3p inhibited proliferation and metastasis of gastric cancer cells [ 20 ]. Han et al showed that miR-593-3p represses lung cancer growth and migration [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of hsa_circ_0136666 predicts poor prognosis and initiates osteosarcoma tumorigenesis through miR-593-3p/ZEB2 pathway

Zhang

Zhou

Yuan

et al. 2020

Aging

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Background: Osteosarcoma (OS) is a type of malignant bone tumor with a growing incidence. Increasing studies indicate circular RNA (circRNA) has a vital function in tumorigenesis. Yet, how circRNA regulates OS development is not clear. In the present work, we aimed to investigate the roles of hsa_circ_0136666 in OS progression. Results: hsa_circ_0136666 was shown to be upregulated in OS and correlated with advanced stage and poor prognosis. Functional investigation using CCK8, colony formation assay and Transwell assay demonstrated that hsa_circ_0136666 promoted OS proliferation, migration and invasion, but inhibited cell death. Additionally, we identified hsa_circ_0136666 was a molecular sponge for miR-593-3p to facilitate ZEB2 expression. MiR-593-3p and ZEB2 were inversely expressed in OS tissues. And hsa_circ_0136666 exerts oncogenic roles in OS relying on miR-593-3p and ZEB2. Conclusion: Our results demonstrate the involvement of hsa_circ_0136666 in regulating OS tumorigenesis and it may be a therapeutic target. Methods: The expression of hsa_circ_0136666 was analyzed by qRT-PCR in OS tissues and cell lines. Proliferation was measured via CCK8 and colony formation assays. Migration and invasion were determined through Transwell assay. Luciferase reporter assay was utilized to determine the interaction between hsa_circ_0136666 and miR-593-3p or between miR-593-3p and ZEB2. Animal experiment was performed to investigate the role of hsa_circ_0136666 in vivo.

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Section: Discussionmentioning

confidence: 99%

“…LINC02163 is upregulated in gastric cancer, presenting a close relationship with tumor size, distant metastasis, and clinical stage 25 . In addition, patients with gastric cancer showing high LINC02163 expression exhibit shorter overall survival and lower disease-free survival rates than patients showing low LINC02163 expression 25 . Functionally, LINC02163 knockdown suppresses gastric cancer cell proliferation, colony formation, invasion, and epithelial–mesenchymal transition in vitro, promotes G 0 /G 1 cell cycle arrest, and decreases tumor growth in vivo 25 .…”

Section: Discussionmentioning

confidence: 99%

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Long Noncoding RNA LINC02163 Accelerates Malignant Tumor Behaviors in Breast Cancer by Regulating the MicroRNA-511-3p/HMGA2 Axis

Qin

Jin

et al. 2020

oncol res

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Long intergenic non-protein-coding RNA 02163 (LINC02163) has been reported to be upregulated and work as an oncogene in gastric cancer. The aims of the present study were to determine the expression profile and clinical value of LINC02163 in breast cancer. Additionally, the detailed functions of LINC02163 in breast cancer were explored and relevant molecular events were elucidated. In this study, LINC02163 was upregulated in breast cancer, and its expression level was closely associated with tumor size, lymph node metastasis, and TNM stage. Patients with breast cancer presenting high LINC02163 expression exhibited shorter overall survival than those presenting low LINC02163 expression. Knockdown of LINC02163 resulted in a decrease in breast cancer cell proliferation, migration, and invasion and an increase in cell apoptosis in vitro. In addition, silencing of LINC02163 impeded breast cancer tumor growth in vivo. Mechanistic investigation revealed that LINC02163 served as a competing endogenous RNA for microRNA-511-3p (miR-511-3p) and consequently upregulated the expression of highmobility group A2 (HMGA2), a downstream target of miR-511-3p. Intriguingly, miR-511-3p inhibition and HMGA2 restoration counteracted the effects of LINC02163 deficiency on the malignant properties of breast cancer cells. LINC02163 exerts cancer-promoting effects during the initiation and progression of breast cancer via regulation of the miR-511-3p/HMGA2 axis. Our findings add to our understanding of the roles of the LINC02163/miR-511-3p/HMGA2 pathway as a regulator of breast cancer pathogenesis and may be useful in the development of lncRNA-directed cancer diagnosis, prognosis, and therapy.

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LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells

Cited by 28 publications

References 29 publications

Genomic Identification of RNA Editing Through Integrating Omics Datasets and the Clinical Relevance in Hepatocellular Carcinoma

Genomic Identification of RNA Editing Through Integrating Omics Datasets and the Clinical Relevance in Hepatocellular Carcinoma

Overexpression of hsa_circ_0136666 predicts poor prognosis and initiates osteosarcoma tumorigenesis through miR-593-3p/ZEB2 pathway

Long Noncoding RNA LINC02163 Accelerates Malignant Tumor Behaviors in Breast Cancer by Regulating the MicroRNA-511-3p/HMGA2 Axis

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