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Your search keyword '"LINC00968"' showing total 3 results
Start Over Descriptor "LINC00968" Topic adenocarcinoma
3 results on '"LINC00968"'

1. Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA.

Author

Li, Dong-Yao, ChEN, WEN-Jie, Shang, Jun, ChEN, Gang, and Li, Shi-Kang

Subjects
*NON-small-cell lung carcinoma, *NON-coding RNA, *MICRORNA, *MICROARRAY technology, *ADENOCARCINOMA
Abstract

Long non‑coding RNAs (lncRNAs) have been demonstrated to mediate carcinogenesis in various types of cancer. However, the regulatory role of lncRNA LINC00968 in lung adenocarcinoma remains unclear. The microRNA (miRNA) expression in LINC00968‑overexpressing human lung adenocarcinoma A549 cells was detected using miRNA microarray analysis. miR‑9‑3p was selected for further analysis, and its expression was verified in the Gene Expression Omnibus (GEO) database. In addition, the regulatory axis of LINC00968 was validated using The Cancer Genome Atlas (TCGA) database. Results of the GEO database indicated miR‑9‑3p expression in lung adenocarcinoma was significantly higher compared with normal tissues. Functional enrichment analyses of the target genes of miR‑9‑3p indicated protein binding and the AMP‑activated protein kinase pathway were the most enriched Gene Ontology and KEGG terms, respectively. Combining target genes with the correlated genes of LINC00968 and miR‑9‑3p, 120 objective genes were obtained, which were used to construct a protein‑protein interaction (PPI) network. Cyclin A2 (CCNA2) was identified to have a vital role in the PPI network. Significant correlations were detected between LINC00968, miR‑9‑3p and CCNA2 in lung adenocarcinoma. The LINC00968/miR‑9‑3p/CCNA2 regulatory axis provides a new foundation for further evaluating the regulatory mechanisms of LINC00968 in lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Published
2018
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2. LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis

Author

Dong He, Ruhong Li, Zhizhao Chen, Xiaowei Xing, Hao Bo, Yuxing Zhu, Lian Gong, Ke Cao, Wei Xiong, Jianda Zhou, Yanhong Zhou, Long Jin, Jingjing Li, Liang Xiang, Ming Zhou, and Mengqing Xiao

Subjects
Male, Aging, Lung Neoplasms, Mice, Nude, Adenocarcinoma of Lung, In situ hybridization, Biology, Metastasis, Smad7 Protein, LINC00968, SMAD7, Cell Movement, Databases, Genetic, medicine, metastasis, Animals, Humans, Neoplasm Invasiveness, Cell Proliferation, Reporter gene, Hippo signaling pathway, Mice, Inbred BALB C, Competing endogenous RNA, Cell growth, Cell Biology, medicine.disease, Tumor Burden, Blot, Gene Expression Regulation, Neoplastic, MicroRNAs, A549 Cells, lung adenocarcinoma (LUAD), Cancer research, Disease Progression, Adenocarcinoma, RNA, Long Noncoding, prognosis, Research Paper, Signal Transduction
Abstract

Background: Long non-coding RNAs (LncRNAs) have been associated with several types of cancer. However, little is known about their role in lung adenocarcinoma (LUAD). Results: LINC00968 was significantly differentially expressed in LUAD tissues. Downregulated LINC00968 was associated with clinicopathological features of LUAD. LINC00968 inhibited cell growth and metastasis by regulating the Hippo signaling pathway We demonstrated that LINC00968 acts as a ceRNA to consume miR-21-5p, enhancing the accumulation of SMAD7, a miR-21-5p target. Conclusions: LINC00968 limits LUAD progression via the miR-21-5p/SMAD7 axis and may serve as a prognostic biomarker and therapeutic target for LUAD. Methods: We conducted comprehensive data mining on LINC00968 based on the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) database. The expression of LINC00968 in LUAD cells was determined using in situ hybridization. We detected LINC00968 function in LUAD cells using the MTT, clone formation, and transwell assays, and tumor xenografts. Label-free quantitative proteomics, western blotting, a dual-luciferase reporter assay, immunofluorescence, and RNA immunoprecipitation assays were used to determine the correlations among LINC00968, miR-21-5p, and SMAD7. Gain- and loss-function approaches were used to explore the effects of LINC00968, miR-21-5p, and SMAD7 on cell proliferation, migration, and invasion.

Published
2020

3. linc00968 inhibits the tumorigenesis and metastasis of lung adenocarcinoma via serving as a ceRNA against miR-9-5p and increasing CPEB3

Author

Huaping Tang, Yan Feng, Yueqin Hao, and Xiaolei Han

Subjects
LUAD, Aging, CPEB3, Cell, Adenocarcinoma of Lung, Biology, medicine.disease_cause, Metastasis, Downregulation and upregulation, Cell Line, Tumor, medicine, Gene silencing, Humans, Neoplasm Metastasis, Competing endogenous RNA, linc00968, RNA-Binding Proteins, Cell migration, Cell Biology, medicine.disease, miR-9-5p, Gene Expression Regulation, Neoplastic, MicroRNAs, medicine.anatomical_structure, Cancer research, Adenocarcinoma, RNA, Long Noncoding, Carcinogenesis, Research Paper
Abstract

Increasing evidence confirms that long noncoding RNAs (lncRNAs) exert vital functions in multiple biological process among malignant cancers. In the current study, we uncovered that linc00968 was downregulated in lung adenocarcinoma (LUAD). Furthermore, the low level of linc00968 was correlated with worse prognosis in patients with LUAD. Upregulation of linc00968 restrained the growth and metastatic phenotypes of LUAD cell in vitro and in vivo. Using bioinformation methods and luciferase reporter assay, we identified that linc00968 acted as a competing endogenous RNA (ceRNA) via sponging miR-9-5p to modulate the level of Cytoplasmic Polyadenylation Element Binding Protein 3 (CPEB3) in LUAD. In addition, LUAD cell migration, colony formation and epithelial-mesenchymal transition (EMT) process were suppressed by linc00968 while these aggressive traits were reversed by miR-142-5p or CPEB3 silencing. Altogether, our work disclosed that linc00968 played a critical role in LUAD and linc00968/miR-9-5p/CPEB3 regulatory axis might be a potential treatment target in LUAD.

Published
2020

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