Silencing Aurora-A with siRNA inhibits cell proliferation in human lung adenocarcinoma cells

Zhong, Ning; Shi, Sixiang; Wang, Hongzhen; Wu, Guangzhou; Wang, Yunliang; Ma, Qiang; Wang, Hongwei; Liu, Yuanhua; Wang, Jinzhi

doi:10.3892/ijo.2016.3605

Cited by 19 publications

(16 citation statements)

References 42 publications

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“…Cell-division cycle protein 20 interacts with cadherin-1 to regulate anaphase-promoting complex and cyclin-dependent kinases during cell cycle. Dysregulation of Aurora kinase A has been associated with cancers of the lung, 30 prostate, 31 and breast. 32 We have performed oral gavage using human stool in this experiment.…”

Section: Basic and Translational Atmentioning

confidence: 99%

Gavage of Fecal Samples From Patients With Colorectal Cancer Promotes Intestinal Carcinogenesis in Germ-Free and Conventional Mice

et al. 2017

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We fed stool samples from patients with CRC and heathy individuals to germ-free mice and conventional mice with azoxymethane. We found stool from patients with CRC to increase the numbers of polyps, levels of intestinal dysplasia and proliferation, markers of inflammation, and proportions of Th1 and Th17 cells in colon, compared with stool from individuals without CRC. This study provides evidence that the fecal microbiota from patients with CRC can promote tumorigenesis in germ-free mice and mice given a carcinogen.

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Section: Basic and Translational Atmentioning

confidence: 99%

Gavage of Fecal Samples From Patients With Colorectal Cancer Promotes Intestinal Carcinogenesis in Germ-Free and Conventional Mice

et al. 2017

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“…[ 32 , 36 , 37 ] Knockdown of AURKA and FEN1 inhibit the migration, invasion, and proliferation of LUAD cells and induce apoptosis. [ 38 , 39 ] More importantly, AURKA is a driving force for the evolution of resistance to third-generation EGFR inhibitors in LUAD and associated with epithelial mesenchymal transition. [ 40 ] Recently, it is found that the deregulation of transcriptional levels and posttranscriptional modification of GAPDH, which is traditionally considered as a critical enzyme of glycolytic process, is an important determinant for tumor cell survival.…”

Section: Discussionmentioning

confidence: 99%

Integrated bioinformatics analysis reveals CDK1 and PLK1 as potential therapeutic targets of lung adenocarcinoma

Cao

et al. 2021

Medicine

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This study is to identify potential biomarkers and therapeutic targets for lung adenocarcinoma (LUAD). GSE6044 and GSE118370 raw data from the Gene Expression Omnibus database were normalized with Robust Multichip Average. After merging these two datasets, the combat function of sva packages was used to eliminate batch effects. Then, limma packages were used to filtrate differentially expressed genes. We constructed protein–protein interaction relationships using STRING database and hub genes were identified based on connectivity degrees. The cBioportal database was used to explore the alterations of the hub genes. The promoter methylation of cyclin dependent kinase 1 (CDK1) and polo-like Kinase 1 (PLK1) and their association with tumor immune infiltration in patients with LUAD were investigated using DiseaseMeth version 2.0 and TIMER databases. The Cancer Genome Atlas-LUAD dataset was used to perform gene set enrichment analysis. We identified 10 hub genes, which were upregulated in LUAD, among which 8 were successfully verified in the Cancer Genome Atlas and Oncomine databases. Kaplan–Meier analysis indicated that the expressions of CDK1 and PLK1 in LUAD patients were associated with overall survival and disease-free survival. The methylation levels in the promoter regions of these 2 genes in LUAD patients were lower than those in normal lung tissues. Their expressions in LUAD were associated with tumor stages and relative abundance of tumor infiltrating immune cells, such as B cells, CD4+ T cells, and macrophages. Moreover, cell cycle, DNA replication, homologous recombination, mismatch repair, P53 signaling pathway, and small cell lung cancer signaling were significantly enriched in CDK1 and PLK1 high expression phenotype. CDK1 and PLK1 may be used as potential biomarkers and therapeutic targets for LUAD.

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“…Among these 10 candidates, six have been reported as Lung cancer‐related genes. It has been discovered AURKA was highly expressed in LUAD and played important roles in the cell cycle and apoptosis of human LUAD cells . Chen et al unraveled HMGA1, a NF‐κB signaling related factor, can be regulated by miR‐26 and associated with prognosis of LUAD patients.…”

Section: Discussionmentioning

confidence: 99%

Aberrant CpG‐methylation affects genes expression predicting survival in lung adenocarcinoma

Zhang

et al. 2018

Cancer Medicine

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Lung adenocarcinoma (LUAD) is a common diagnosed disease with high‐mortality rate, and its prognostic implications are under discovered. DNA methylation aberrations are not only an important event for dysregulation of gene expression during tumorigenesis but also a revolution in epigenetics by identifying key prognostic biomarkers for multiple cancers. In this study, we analyzed methylation status of 485 578 CpG sites and RNA‐seq transcriptomes of 20 532 genes for 1095 LUAD samples in TCGA database. The association between DNA methylation and the prognostic value of the corresponding gene expression was identified as well. In total, ten aberrantly methylated and dysregulated genes (AURKA, BLK, CNTN2, HMGA1, PTTG1, TNS4, DAPK2, MFSD2A, THSD1, and WNT7A) were highlighted which were significantly correlated with overall survival of 492 LUAD patients, which were all reported as tumor‐associated genes in other various cancers and worthy of further investigated and might be used as therapeutic targets for LUAD. Together, methylation aberrances regulate gene expression level during tumorigenesis and influence prognosis of LUAD patients. Integrating knowledge of epigenetics and expression of genes can be useful for an in‐depth understanding of cancer mechanism and for the eventual purpose of precisely prognostic and therapeutic target verification.

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Silencing Aurora-A with siRNA inhibits cell proliferation in human lung adenocarcinoma cells

Cited by 19 publications

References 42 publications

Gavage of Fecal Samples From Patients With Colorectal Cancer Promotes Intestinal Carcinogenesis in Germ-Free and Conventional Mice

Gavage of Fecal Samples From Patients With Colorectal Cancer Promotes Intestinal Carcinogenesis in Germ-Free and Conventional Mice

Integrated bioinformatics analysis reveals CDK1 and PLK1 as potential therapeutic targets of lung adenocarcinoma

Aberrant CpG‐methylation affects genes expression predicting survival in lung adenocarcinoma

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