MiR-181a inhibits non-small cell lung cancer cell proliferation by targeting CDK1

“…miR‐181a can function as a prognostic biomarke in acute myeloid leukemia (Guo et al, ). miR‐181a can inhibit NSCLC proliferation by inhibiting CDK1 (Shi et al, ). miR‐181a is able to inhibit macrophage activation in chronic liver injury (Li, Chang et al, ).…”

Section: Discussionmentioning

confidence: 99%

MiR‐181a inhibits vascular inflammation induced by ox‐LDL via targeting TLR4 in human macrophages

Yin

2018

Journal Cellular Physiology

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Atherosclerosis is a kind of chronic inflammation disease with lipid accumulation in in blood vessel linings. Increasing evidence has reported that microRNAs can exert crucial roles in atherosclerosis. In previous study, miR-181a has been implicated to be abnormally expressed in atherosclerosis mice, however its detailed function in atherosclerosis remains uninvestigated. Hence, in our current study, we focused on the biological role of miR-181a in atherosclerosis progression. Ox-LDL has been commonly identified as an important atherosclerosis regulator. We observed that ox-LDL induced THP-1 cell apoptosis dose-dependently and time- dependently. Meanwhile, 25 µg/ml ox-LDL can promote foam cell formation and increased miR-181a expression significantly. CD36 has been involved in atherosclerosis progression and it was found that overexpression of miR-181a inhibited its protein levels. Moreover, miR-181a mimics repressed foam cell formation, TC and TG levels induced by ox-LDL dramatically. In addition, miR-181a mimics were able to reverse THP-1 cell apoptosis, increased IL-6, IL-1β, and TNF-α protein expression triggered by 25 µg/ml ox-LDL. TLR4 has been linked to various inflammation-associated diseases. In our present study, TLR4 was indicated as miR-181a target and the binding correlation between them was validated by dual-luciferase reporter assay. In conclusion, these results improves the understanding of atherosclerosis modulated by miR-181a/TLR4 and can contribute to development of new approaches for atherosclerosis.

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“…However, the researchers observed that CDK1 and PIK3R1 genes shared the most abundant edges than the above genes in the sub-network, and were significantly up-regulated and down-regulated in NSCLC, separately. Currently, a few studies reported that the CDK1 gene were associated with carcinomas, including gastric, colorectal, breast, and lung cancers (36)(37)(38)(39). Moreover, published results showed that some non-coding RNA inhibited cell proliferation of NSCLC by targeting CDK1 (39,40).…”

Section: Discussionmentioning

confidence: 99%

“…Currently, a few studies reported that the CDK1 gene were associated with carcinomas, including gastric, colorectal, breast, and lung cancers (36)(37)(38)(39). Moreover, published results showed that some non-coding RNA inhibited cell proliferation of NSCLC by targeting CDK1 (39,40). Despite these results, the role of CDK1 in NSCLC is still vague.…”

Section: Discussionmentioning

confidence: 99%

Cross-Sectional Study of Gene Expression Analysis Identifies Critical Biological Pathways and Key Genes Implicated in Non-Small Cell Lung Cancer

Wang

et al. 2018

Iran Red Crescent Med J

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Background: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, which accounts for about 85% of all lung cancer types. However, critical biological pathways and key genes implicated in NSCLC remain ambiguous. Objectives: The present study aimed at identifying the critical biological pathways and key genes implicated in NSCLC, and providing insight in the molecular mechanism underlying NSCLC. Methods: In this case-control bioinformatics study, the researchers used four microarray data of NSCLC from public gene expression omnibus (GEO) database at the national center for biotechnology information (NCBI) website. The microarray data came from studies of American, Spanish, and Taiwanese NSCLC patients, and in total contained 190 NSCLC tissue and 180 normal lung tissue. A standardized microarray preprocessing and gene set enrichment analysis (GSEA) were used to analyze each microarray data and obtained significantly regulated pathways. Venn analysis was used to identify the common significantly regulated biological pathways. Protein and protein interaction (PPI) network analysis was used to identify the key genes within common significantly regulated pathways. The PPI information was retrieved from STRING database, and cytoscape software was used to construct and visualize the PPI network. Results: Through integrating GSEA results of four microarray data, finally, the researchers identified 22 common up-regulated and 85 common down-regulated pathways. Many genes within 107 common significantly regulated pathways were significantly enriched within cell cycle pathway (P value of 2.58e-79) and focal adhesion pathway (P value of 2.44e-81). The PPI network showed that up-regulated CDK1 (P value = 1.33e-18 and logFC = 1.41) and down-regulated PIK3R1 (P value = 5.09e-22 and logFC = -1.13) genes shared the most abundant edges, and were associated with NSCLC. Conclusions: This cross-sectional study showed increased concordance between gene expression profiling data. These identified pathways and genes provide some insight in the molecular mechanisms of NSCLC, and the genes may serve as candidate diagnostic and therapeutic targets of NSCLC.

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MiR-181a inhibits non-small cell lung cancer cell proliferation by targeting CDK1

Abstract: These data suggested that miR-181a plays a tumor suppressor and may be a potential therapeutic target for NSCLC patients.

Cited by 65 publications

References 18 publications

Identification of a panel of mitotic spindle‐related genes as a signature predicting survival in lung adenocarcinoma

Identification of a panel of mitotic spindle‐related genes as a signature predicting survival in lung adenocarcinoma

MiR‐181a inhibits vascular inflammation induced by ox‐LDL via targeting TLR4 in human macrophages

Cross-Sectional Study of Gene Expression Analysis Identifies Critical Biological Pathways and Key Genes Implicated in Non-Small Cell Lung Cancer

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