High Expression of Long Noncoding RNA PCNA-AS1 Promotes Non-Small-Cell Lung Cancer Cell Proliferation and Oncogenic Activity via Upregulating CCND1

Wu, Chuanyong; Zhu, Xiaoting; Xia, L.; Wang, Lin; Yu, Wenjing; Guo, Qiaojuan; Zhao, Mingna; Lou, Jiatao

doi:10.7150/jca.39087

Cited by 12 publications

(9 citation statements)

References 35 publications

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“…Cell proliferation abilities were evaluated using Cell counting kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (EdU) incorporation assays as previously described ( Wu et al, 2020 ). Briefly, for CCK-8 assay, 3000 indicated LUAD cells were plated into 96-well plates per well.…”

Section: Methodsmentioning

confidence: 99%

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Chang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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Lung adenocarcinoma (LUAD) is the main histological type of lung cancer, which is the leading cause of cancer-related deaths. Long non-coding RNAs (lncRNAs) were recently revealed to be involved in various cancers. However, the clinical relevance and potential biological roles of most lncRNAs in LUAD remain unclear. Here, we identified a prognosis-related lncRNA ITGB1-DT in LUAD. ITGB1-DT was upregulated in LUAD and high expression of ITGB1-DT was correlated with advanced clinical stages and poor overall survival and disease-free survival. Enhanced expression of ITGB1-DT facilitated LUAD cellular proliferation, migration, and invasion, and also lung metastasis in vivo. Knockdown of ITGB1-DT repressed LUAD cellular proliferation, migration, and invasion. ITGB1-DT interacted with EZH2, repressed the binding of EZH2 to ITGB1 promoter, reduced H3K27me3 levels at ITGB1 promoter region, and therefore activated ITGB1 expression. Through upregulating ITGB1, ITGB1-DT activated Wnt/β-catenin pathway and its downstream target MYC in LUAD. The expressions of ITGB1-DT, ITGB1, and MYC were positively correlated with each other in LUAD tissues. Intriguingly, ITGB1-DT was found as a transcriptional target of MYC. MYC directly transcriptionally activated ITGB1-DT expression. Thus, ITGB1-DT formed a positive feedback loop with ITGB1/Wnt/β-catenin/MYC. The oncogenic roles of ITGB1-DT were reversed by depletion of ITGB1 or inhibition of Wnt/β-catenin pathway. In summary, these findings revealed ITGB1-DT as a prognosis-related and oncogenic lncRNA in LUAD via activating the ITGB1-DT/ITGB1/Wnt/β-catenin/MYC positive feedback loop. These results implicated ITGB1-DT as a potential prognostic biomarker and therapeutic target for LUAD.

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Section: Methodsmentioning

confidence: 99%

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Chang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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“…These studies all suggest the complicated role TIMP1 plays in cancer development. We also found out that the other up-regulated genes including CCNA2, CCNB1, CDC20, CDC6, CCND1, CDK4 and CDK1 are implicated with chemokine signaling pathway and also capable to regulate tumour angiogenesis [21] , and survival [22][23] .…”

Section: Discussionmentioning

confidence: 62%

Identification of Key Genes and Pathways in Colorectal Cancer by Integrated Bioinformatics Analysis

Wang

Zhang

2020

Preprint

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PurposeIn order to understand the mechanism of colorectal cancer occurrence and development, we screened related core genes and provided new targets for clinical diagnosis and treatment of colorectal cancer.MethodsWe downloaded CRC-associated gene expression profile of GSE110233 from Gene Expression Omnibus (GEO) dataset. There were 26 samples in this dataset, all the differentially expressed genes (DEGs) with p<0.05 and fold change ≥1 or ≤-1 were identified. Gene ontology (GO) and "Kyoto Encyclopedia of Genes and Genomes" (KEGG) were used to search for these DEG enrichment methods. In addition, the protein-protein interaction (PPI) network was also used to construct visual interactions between proteins. At last, we used GEPIA to conduct the survival analysis 4 down-regulation and 8 up-regulation genes for clarify the potential effects on CRC.ResultsA total of 866 differentially expressed genes were obtained, including 360 up-regulated genes and 506 down-regulated genes. These genes were involve in Cell proliferation; Extracellular exosome; Protein binding; Chemokine activity. Genes were mainly involved in the KEGG pathway termed Cell cycle; PI3K-Akt signaling pathway; Mineral absorption; MicroRNAs in cancer; Cytokine-cytokine receptor interaction. We finally found 12 hubgenes by PPI connective degree whom named PRKACB, FGFR2, FGFR3, CKB, TIMP1, CCNA2, CCNB1, CDC20, CDC6, CCND1, CDK4 and CDK1.ConclusionBioinformatics is helpful for comprehensive and in-depth study of the occurrence and development mechanism of diseases, to screen possible core targets, and to provide a reliable basis for clinical diagnosis and treatment of colorectal cancer.

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“…20 PCNA-AS1 facilitates oncogenic activity in NSCLC by targeting CCND1. 21 LncRNA SLCO4A1-AS1 was implicated in bladder cancer 11 and colorectal cancer, 10,12 but it has not been investigated in NSCLC till now. Presently, SLCO4A1-AS1 presented an enhanced expression in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA SLCO4A1-AS1 drives the progression of non-small-cell lung cancer by modulating miR-223-3p/IKKα/NF-κB signaling

Yang

Zhang

et al. 2020

Cancer Biology & Therapy

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Globally, lung cancer is known as a major cause of cancer-associated death and non-small-cell lung cancer (NSCLC) accounts for majority of all cases. Growing evidence has emerged that long non-coding RNAs (lncRNAs) act as vital regulatory molecules in various malignancies. Nevertheless, the function of SLCO4A1 antisense RNA 1(SLCO4A1-AS1) in NSCLC is vague. This study intended to investigate the biological role and probable regulatory mechanism of SLCO4A1-AS1 in NSCLC. qRT-PCR revealed that SLCO4A1-AS1 level was upregulated in NSCLC. Function assays manifested that silence of SLCO4A1-AS1 attenuated NSCLC cell proliferation, migration and invasion but promoted NSCLC cell apoptosis. Furthermore, we disclosed that SLCO4A1-AS1 activated NF-κB pathway in NSCLC, and that IKKα, an NF-κB pathway-related gene, possessed an enhanced level in NSCLC tissues and cells. Importantly, miR-223-3p bound with SLCO4A1-AS1 and IKKα. Further, SLCO4A1-AS1 competitively bound with miR-223-3p to increase IKKα expression, thereby activating NF-κB signaling pathway. In conclusion, SLCO4A1-AS1 drove NSCLC progression by activating NF-κB signaling pathway via sponging miR-223-3p to enhance IKKα expression. Thus, SLCO4A1-AS1 might be a promising biomarker for NSCLC treatment.

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High Expression of Long Noncoding RNA PCNA-AS1 Promotes Non-Small-Cell Lung Cancer Cell Proliferation and Oncogenic Activity via Upregulating CCND1

Cited by 12 publications

References 35 publications

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Identification of Key Genes and Pathways in Colorectal Cancer by Integrated Bioinformatics Analysis

Long non-coding RNA SLCO4A1-AS1 drives the progression of non-small-cell lung cancer by modulating miR-223-3p/IKKα/NF-κB signaling

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