scholarly journals Expression of the Long Intergenic Non-Protein Coding RNA 665 (LINC00665) Gene and the Cell Cycle in Hepatocellular Carcinoma Using The Cancer Genome Atlas, the Gene Expression Omnibus, and Quantitative Real-Time Polymerase Chain Reaction

2018 ◽  
Vol 24 ◽  
pp. 2786-2808 ◽  
Author(s):  
Dong-Yue Wen ◽  
Peng Lin ◽  
Yu-Yan Pang ◽  
Gang Chen ◽  
Yun He ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Chain Reaction ◽  
Protein Coding ◽  
Cancer Genome Atlas ◽  
Polymerase Chain ◽  
Genome Atlas

scholarly journals Clinical value of miR-452-5p expression in lung adenocarcinoma: A retrospective quantitative real-time polymerase chain reaction study and verification based on The Cancer Genome Atlas and Gene Expression Omnibus databases

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770575 ◽  
Author(s):  
Xiao-ning Gan ◽  
Jie Luo ◽  
Rui-xue Tang ◽  
Han-lin Wang ◽  
Hong Zhou ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Gene Expression Omnibus ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Chain Reaction ◽  
Clinical Value ◽  
Node Metastasis ◽  
Cancer Genome Atlas ◽  
Polymerase Chain ◽  
Genome Atlas

The role and mechanism of miR-452-5p in lung adenocarcinoma remain unclear. In this study, we performed a systematic study to investigate the clinical value of miR-452-5p expression in lung adenocarcinoma. The expression of miR-452-5p in 101 lung adenocarcinoma patients was detected by quantitative real-time polymerase chain reaction. The Cancer Genome Atlas and Gene Expression Omnibus databases were joined to verify the expression level of miR-452-5p in lung adenocarcinoma. Via several online prediction databases and bioinformatics software, pathway and network analyses of miR-452-5p target genes were performed to explore its prospective molecular mechanism. The expression of miR-452-5p in lung adenocarcinoma in house was significantly lower than that in adjacent tissues (p < 0.001). Additionally, the expression level of miR-452-5p was negatively correlated with several clinicopathological parameters including the tumor size (p = 0.014), lymph node metastasis (p = 0.032), and tumor–node–metastasis stage (p = 0.036). Data from The Cancer Genome Atlas also confirmed the low expression of miR-452 in lung adenocarcinoma (p < 0.001). Furthermore, reduced expression of miR-452-5p in lung adenocarcinoma (standard mean deviations = −0.393, 95% confidence interval: −0.774 to −0.011, p = 0.044) was validated by a meta-analysis. Five hub genes targeted by miR-452-5p, including SMAD family member 4, SMAD family member 2, cyclin-dependent kinase inhibitor 1B, tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein epsilon, and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein beta, were significantly enriched in the cell-cycle pathway. In conclusion, low expression of miR-452-5p tends to play an essential role in lung adenocarcinoma. Bioinformatics analysis might be beneficial to reveal the potential mechanism of miR-452-5p in lung adenocarcinoma.

scholarly journals The role of miR-92b in cholangiocarcinoma patients

2018 ◽  
Vol 33 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Min-hang Zhou ◽  
Hong-wei Zhou ◽  
Mo Liu ◽  
Jun-zhong Sun
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Gene Expression Omnibus ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Positive Regulation ◽  
Cancer Genome Atlas ◽  
High Level ◽  
Genome Atlas

Purpose: The role of microRNA (miRNA) in cholangiocarcinoma was not clear. The aim of this study was to find the potential diagnostic and prognostic miRNA in cholangiocarcinoma patients. Methods: The miRNA expression profiles in cholangiocarcinoma patients from The Cancer Genome Atlas and Gene Expression Omnibus (GSE53870) were analyzed. The comparison of overall survival was performed using the Kaplan–Meier method. The targeted genes of prognostic miRNA were identified in miRanda, PicTar, or TargetScan, and their cell signaling pathways were analyzed by the Database for Annotation, Visualization and Integrated Discovery. Results: In The Cancer Genome Atlas and the Gene Expression Omnibus miRNA dataset, miR-92b and miR-99a were found with concordant directionality, up-regulated and down-regulated, respectively. In The Cancer Genome Atlas survival data, patients with the high level of miR-99b had obviously shorter overall survival time ( P=0.038). However, the level of miR-99a was not found to be significant. The 17 shared target genes of miR-92b were identified, such as DAB21IP, BCL21L11, SPHK2, PER2, and TSC1. The related pathways included positive regulation of transcription, positive regulation of cellular biosynthetic process, regulation of programmed cell death, etc. Conclusion: miR-92b was up-regulated in cholangiocarcinoma compared with normal controls. The high level of miR-92b was associated with adverse outcomes in cholangiocarcinoma patients, which might be partly explained by the targeted genes of miR-92b and their signaling pathways.

Using machine learning method to identify MYLK as a novel marker to predict biochemical recurrence in prostate cancer

2021 ◽  
Vol 15 (1) ◽  
pp. 29-41
Author(s):  
Peng Qiao ◽  
Di Zhang ◽  
Song Zeng ◽  
Yicun Wang ◽  
Biao Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Biochemical Recurrence ◽  
Surgical Margin ◽  
Gene Expression Omnibus ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Support Vector ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Aim: This study aims to identify novel marker to predict biochemical recurrence (BCR) in prostate cancer patients after radical prostatectomy with negative surgical margin. Materials & methods: The Cancer Genome Atlas database, Gene Expression Omnibus database and Cancer Cell Line Encyclopedia database were employed. The ensemble support vector machine-recursive feature elimination method was performed to select crucial gene for BCR. Results: We identified MYLK as a novel and independent biomarker for BCR in The Cancer Genome Atlas training cohort and confirmed in four independent Gene Expression Omnibus validation cohorts. Multi-omic analysis suggested that MYLK was a DNA methylation-driven gene. Additionally, MYLK had significant positive correlations with immune infiltrations. Conclusion: MYLK was identified and validated as a novel, robust and independent biomarker for BCR in prostate cancer.

Phosphatase and Tensin Homolog Is a Potential Target for Ovarian Cancer Sensitization to Cytotoxic Agents

2016 ◽  
Vol 26 (4) ◽  
pp. 632-639 ◽  
Author(s):  
Aiste McCormick ◽  
Eleanor Earp ◽  
Charlotte Leeson ◽  
Michelle Dixon ◽  
Rachel O’Donnell ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Polymerase Chain Reaction ◽  
The Cancer Genome Atlas ◽  
Chain Reaction ◽  
Phosphatase And Tensin Homolog ◽  
Atlas Data ◽  
Tensin Homolog ◽  
Cancer Genome Atlas ◽  
Polymerase Chain ◽  
Genome Atlas

ObjectivesThe phosphatase and tensin homolog (PTEN) tumor suppressor protein has been found to be inactivated or mutated in various human malignancies and to play a role in cisplatin and poly(ADP-ribose) polymerase inhibitor sensitivity. In this study, we assessed the association of PTEN loss with homologous recombination (HR) deficiency and increased chemosensitivity.Materials and MethodsThe PTEN knockdown models were created using MISSION shRNA lentiviral transduction particles in cell lines derived from normal ovarian surface epithelium and a mixed endometrioid/clear-cell carcinoma. Sensitivity to common therapeutics was assessed using sulforhodamine B assay. Twenty-eight unselected primary epithelial ovarian cancer cultures derived from ascitic fluid collected at the time of surgery and matched genomic DNA were assessed for PTEN mutations using polymerase chain reaction amplification and Sanger sequencing and for mRNA expression using quantitative reverse transcription-polymerase chain reaction; HR was determined using γH2AX/RAD51 assay. The Cancer Genome Atlas data were analyzed using cBioPortal.ResultsIn the carcinoma cell line, the PTEN knockdown enhanced sensitivity to cisplatin, rucaparib, doxorubicin, camptothecin, paclitaxel, and irradiation. In the primary ovarian cancer cultures, 2 point mutations were found (1105T>TG, 25L>L in 6 cultures and 1508G>GA, 159R>R in 4 cultures). The PTEN mRNA expression varied over 40-fold between the cultures, but did not correlate with HR status or in vitro sensitivity to cisplatin or rucaparib. The Cancer Genome Atlas data showed a rate of 8% alteration in PTEN and a trend toward improved survival in PTEN-mutated cases.ConclusionsThese data indicate that although PTEN mutations in ovarian cancer are rare, PTEN inhibition results in therapeutic sensitization. Therefore, PTEN may be an important therapeutic target, in at least some cancers.

scholarly journals Cell Cycle Genes Are Potential Diagnostic and Prognostic Biomarkers in Hepatocellular Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Xu Liping ◽  
Li Jia ◽  
Chen Qi ◽  
Yang Liang ◽  
Li Dongen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cancer Recurrence ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Cell Cycle Gene ◽  
Pathway Gene ◽  
Cell Cycle Pathway ◽  
Cell Cycle Gene Expression

Background. The cell cycle pathway genes are comprised of 113 members which are critical to the maintenance of cell cycle and survival of tumor cells. This study was performed to investigate the diagnostic and prognostic values of cell cycle gene expression in hepatocellular carcinoma (HCC) patients. Methods. Clinical features and cell cycle pathway gene expression data were obtained from the Gene Expression Omnibus and The Cancer Genome Atlas databases. Differentially expressed genes (DEGs) were determined by the student t-test between HCC and noncancerous samples. Kaplan-Meier survival, univariate, and multivariate survival analyses and validation analysis were performed to characterize the associations between cell cycle gene expression and patients’ overall survival and recurrence-free survival. Results. 47 and 5 genes were significantly upregulated and downregulated genes in HCC samples, respectively. The high expression of BUB3, CDK1, and CHEK1 was associated with increased mortality (adjusted P value = 0.04, odds ratio (OR): 1.89 (95% confidence interval (CI): 1.04-3.46); adjusted P value = 0.02, OR: 2.06 (95% CI:1.15-3.75); and adjusted P value = 0.04, OR: 1.84 (%95 CI: 1.03-3.32), respectively). The expression of PTTG2 and RAD21 was significantly associated with cancer recurrence (adjusted P value = 0.01, OR: 2.17 (95% CI: 1.24-3.86); adjusted P value = 0.03, OR: 1.88[95% CI:1.08-3.28], respectively), while the low expression of MAD1L1 was associated with cancer recurrence (adjusted P value = 0.03, OR: 0.53 (%95 CI: 0.3-0.93)). Conclusions. The present study demonstrated that BUB3, CDK1, and CHEK1 may serve as a prognostic biomarker for HCC patients. PTTG2, RAD21, and MAD1L1 expression is a major factor affecting the recurrence of HCC patients.

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