Bioinformatic Analysis of Potential Biomarker for hsa-miR-196b-5p in Mesothelioma

2021 ◽  
Author(s):  
Eun Jung Sohn
Keyword(s):  
Bioinformatic Analysis ◽  
Potential Biomarker

scholarly journals LINC00942 Promotes Tumor Proliferation and Metastasis in Lung Adenocarcinoma via FZD1 Upregulation

2021 ◽  
Vol 20 ◽  
pp. 153303382097752
Author(s):  
Ronghua Wang ◽  
Xiuyun Wang ◽  
Jingtao Zhang ◽  
Yanpei Liu
Keyword(s):  
Lung Adenocarcinoma ◽  
Wnt Signaling ◽  
Molecular Mechanisms ◽  
Bioinformatic Analysis ◽  
Luciferase Reporter ◽  
Regulatory Relationship ◽  
Potential Biomarker ◽  
Proliferation And Metastasis ◽  
Tumor Proliferation And Metastasis ◽  
Dual Luciferase Reporter Assay

Background: Long non-coding RNAs (lncRNAs) have been reported to play important roles in the progression of human cancers. Herein, bioinformatic analysis identified that LINC00942 was a highly overexpressed lncRNA in lung adenocarcinoma (LUAD). The present study aimed to explore the roles and possible molecular mechanisms of LINC00942 in LUAD. Methods: First, on the basis of TCGA database, the expression and prognosis of LINC00942 were analyzed in LUAD tissues. Then, si-LINC00942 was transfected into A549 and H1299 cells to knockdown the expression of LINC00942. Cell viability was detected by MTT assay. Flow cytometry was used to analyze cell apoptosis. The expressions of PCNA, Bax, Bcl-2, and wnt/β-catenin pathway proteins were detected by western blotting. Dual-luciferase reporter assay was used to evaluate the regulatory relationship between LINC00942 and miR-5006-5p, or miR-5006-5p and FZD1. Results: We discovered that LINC00942 was up-regulated in LUAD tissues compared with adjacent tissues. Besides, we found the increased LINC00942 expression was associated with poor survival. In addition, silencing of LINC00942 suppressed the proliferation, migration, invasion and facilitated the apoptosis of A549 and H1299 cells. Moreover, silencing of LINC00942 repressed the expression of PCNA, Bcl-2, and enhanced Bax expression in A549 and H1299 cells. Mechanically, LINC00942 exerted its effects via enhancing Wnt signaling. LINC00942 functioned as competing endogenous RNA (ceRNA) by binding to miR-5006-5p, upregulating the expression of FZD1, which was a direct target of miR-5006-5p. Conclusion: Our findings indicated that LINC00942/miR-5006-5p/FZD1 axis played important roles in LUAD growth through enhancing Wnt signaling. LINC00942/miR-5006-5p/FZD1 axis might serve as a potential biomarker and therapeutic target for LUAD treatment.

scholarly journals Hsa_circ_0051079 functions as an oncogene by regulating miR-26a-5p/TGF-β1 in osteosarcoma

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Zuojun Zhang ◽  
Ming Zhao ◽  
Guojie Wang
Keyword(s):  
Luciferase Activity ◽  
Bioinformatic Analysis ◽  
Luciferase Assay ◽  
Circular Rnas ◽  
Potential Biomarker ◽  
Luciferase Activity Assay ◽  
Proliferation And Metastasis ◽  
Normal Controls ◽  
Tgf Β1

Abstract Background Osteosarcoma is a most common bone malignant tumor which threatens children and adolescents. Circular RNAs (circRNAs) fundamentally play essential roles in the progress and development of human cancers by sponging with microRNAs (miRNAs). However, the role of circRNAs in osteosarcoma is not clear. The aim of the study was to investigate the roles and molecular mechanism of circRNAs in osteosarcoma. Results The data from qRT-PCR showed that circ_0051079 expression was higher in osteosarcoma cells and tissues compared to their normal controls. Meanwhile, bioinformatic analysis indicated that circ_0051079 was a sponge of miR-26a-5p, which was verified by luciferase activity assay. Subsequently, TGF-β1 was verified as a putative target mRNA of miR-26a-5p by luciferase assay. Cellular function assays were conducted and the findings revealed that circ_0051079/miR-26a-5p/TGF-β1 regulated osteosarcoma proliferation and metastasis. Conclusion The study demonstrated that circ_0051079 could act as an oncogene via regulating miR-26a-5p/TGF-β1 and a potential biomarker for osteosarcoma diagnose.

scholarly journals Evaluation of MT Family Isoforms as Potential Biomarker for Predicting Progression and Prognosis in Gastric Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-15
Author(s):  
Mingfu Tong ◽  
Wenquan Lu ◽  
Hao Liu ◽  
Jian Wu ◽  
Mingzuo Jiang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Mrna Expression ◽  
Promoter Region ◽  
Gene Promoter ◽  
Distinct Type ◽  
Bioinformatic Analysis ◽  
Kaplan Meier ◽  
Potential Biomarker ◽  
Wide Range ◽  
The Individual

Background. Metallothioneins (MTs) family comprises many isoforms, most of which are frequently dysregulated in a wide range of cancers. However, the expression pattern and exact role of each distinct MT family isoform which contributes to tumorigenesis, progression, and drug resistance of gastric cancer (GC) are still unclear. Methods. Publicly available databases including Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), Kaplan-Meier plotter, SurvExpress, MethHC, cBioportal, and GeneMANIA were accessed to perform an integrated bioinformatic analysis and try to detect fundamental relationships between each MT family member and GC. Results. Bioinformatic data indicated that the mRNA expression of all MT family members was almost lowly expressed in GC compared with normal gastric tissue (P<0.05), and patients with reduced mRNA expression of each individual MT member had inconsistent prognostic value (OS, FP, PPS), which depended on the individual isoform of MT. A negative correlation between the methylation in promoter region of majority of MT members and their mRNA expression was detected from MethHC database (p<0.001). Data downloaded from TCGA revealed that MTs were rarely mutated in GC patients and MT2A was frequently regulated by other three genes (FOS, JUN, SP1) in GC patients. Conclusion. MTs were nearly downregulated, and distinct type of MT harbored different prognostic role in GC patients. Methylation in gene promoter region of MTs partially contributed to their reduced expression in GC. Our comprehensive analyses from multiple independent databases may further lead researches to explore MT-targeting reagents or potential diagnostic and prognostic markers for GC patients.

scholarly journals PNO1 promotes cell proliferation in prostate cancer

2020 ◽  
Author(s):  
Jianpeng Hu ◽  
Feilun Cui ◽  
Zhipeng Xv ◽  
Jian Tan ◽  
Zhengyu Wang
Keyword(s):  
Prostate Cancer ◽  
Rna Splicing ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Multiple Cancer ◽  
Translational Initiation ◽  
Normal Tissues ◽  
Potential Biomarker

Abstract BackgroundProstate cancer (PCa) is one of the most commonly diagnosed cancers. The functions of PNO1 in yeasts were involved in regulating ribosome and proteasome biogenesis. Human PNO1 is crucial to the site 3 cleavage at the 3ʹ-end of 18S pre-rRNA. Previous studies indicated that PNO1 may be related to the progression of cancers. However, the functions of PNO1 in PCa remained unclear. MethodsThe present study evaluated the expression levels of PNO1 in PCa by using GSE45016, GSE55945 and GSE17951 datasets. Then, in vivo and in vitro assays were conducted to detect the biological functions of PNO1 in PCa. Microarray and bioinformatic analysis were carried out to detect the downstream targets and pathways regulated by PNO1.ResultsThe present study for the first time demonstrated PNO1 was up-regulated in PCa samples compared to normal tissues. ShRNA mediated knockdown of PNO1 significantly suppressed PCa proliferation and clone formation, however, induced PCa apoptosis. Microarray analysis and bioinformatics analysis revealed PNO1 was involved in regulating multiple cancer related biological processes, such as regulation of DNA repair, single organismal cell-cell adhesion, translational initiation, RNA splicing, transcription, and positive regulation of mRNA catabolic process. OF note, in vivo results showed PNO1 knockdown remarkably reduced the PCa growth rate. ConclusionsDespite more in-depth research is still required, this study showed PNO1 could serve as a potential biomarker for PCa.

scholarly journals Proteomic Characterization of Cerebrospinal Fluid from Ataxia-Telangiectasia (A-T) Patients Using a LC/MS-Based Label-Free Protein Quantification Technology

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Monika Dzieciatkowska ◽  
Guihong Qi ◽  
Jinsam You ◽  
Kerry G. Bemis ◽  
Heather Sahm ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Biomarker Discovery ◽  
Functional Characterization ◽  
Therapeutic Targets ◽  
Bioinformatic Analysis ◽  
Protein Quantification ◽  
Label Free ◽  
Free Protein ◽  
Potential Biomarker

Cerebrospinal fluid (CSF) has been used for biomarker discovery of neurodegenerative diseases in humans since biological changes in the brain can be seen in this biofluid. Inactivation of A-T-mutated protein (ATM), a multifunctional protein kinase, is responsible for A-T, yet biochemical studies have not succeeded in conclusively identifying the molecular mechanism(s) underlying the neurodegeneration seen in A-T patients or the proteins that can be used as biomarkers for neurologic assessment of A-T or as potential therapeutic targets. In this study, we applied a high-throughput LC/MS-based label-free protein quantification technology to quantitatively characterize the proteins in CSF samples in order to identify differentially expressed proteins that can serve as potential biomarker candidates for A-T. Among 204 identified CSF proteins with high peptide-identification confidence, thirteen showed significant protein expression changes. Bioinformatic analysis revealed that these 13 proteins are either involved in neurodegenerative disorders or cancer. Future molecular and functional characterization of these proteins would provide more insights into the potential therapeutic targets for the treatment of A-T and the biomarkers that can be used to monitor or predict A-T disease progression. Clinical validation studies are required before any of these proteins can be developed into clinically useful biomarkers.

scholarly journals Identification of the miRNA signature and key genes in colorectal cancer lymph node metastasis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xi Wang ◽  
Guangyu Gao ◽  
Zhengrong Chen ◽  
Zhihao Chen ◽  
Mingxiao Han ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Expression Profiles ◽  
Bioinformatic Analysis ◽  
The Cancer Genome Atlas ◽  
Node Metastasis ◽  
Novel Mirna ◽  
Potential Biomarker

Abstract Background Because its metastasis to the lymph nodes are closely related to poor prognosis, miRNAs and mRNAs can serve as biomarkers for the diagnosis, prognosis, and therapy of colorectal cancer (CRC). This study aimed to identify novel gene signatures in the lymph node metastasis of CRC. Methods GSE56350, GSE70574, and GSE95109 datasets were downloaded from the Gene Expression Omnibus (GEO) database, while data from 569 colorectal cancer cases were also downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed miRNAs (DE-miRNAs) were calculated using R programming language (Version 3.6.3), while gene ontology and enrichment analysis of target mRNAs were performed using FunRich (http://www.funrich.org). Furthermore, the mRNA–miRNA network was constructed using Cytoscape software (Version 3.8.0). Gene expression levels were verified using the GEO datasets. Similarly, quantitative real-time PCR (qPCR) was used to examine expression profiles from 20 paired non-metastatic and metastatic lymph node tissue samples obtained from patients with CRC. Results In total, five DE-miRNAs were selected, and 34 mRNAs were identified after filtering the results. Moreover, two key miRNAs (hsa-miR-99a, hsa-miR-100) and one gene (heparan sulfate-glucosamine 3-sulfotransferase 2 [HS3ST2]) were identified. The GEO datasets analysis and qPCR results showed that the expression of key miRNA and genes were consistent with that obtained from the bioinformatic analysis. A novel miRNA–mRNA network capable of predicting the prognosis and confirmed experimentally, hsa-miR-99a-HS3ST2-hsa-miR-100, was found after expression analysis in metastasized lymph node tissue from CRC samples. Conclusion In summary, miRNAs and genes with potential as biomarkers were found and a novel miRNA–mRNA network was established for CRC lymph node metastasis by systematic bioinformatic analysis and experimental validation. This network may be used as a potential biomarker in the development of lymph node metastatic CRC.

scholarly journals PNO1 promotes cell proliferation in prostate cancer

2019 ◽  
Author(s):  
Jianpeng Hu ◽  
Feilun Cui ◽  
Zhipeng Xv ◽  
Jian Tan ◽  
Zhengyu Wang
Keyword(s):  
Prostate Cancer ◽  
Rna Splicing ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Multiple Cancer ◽  
Translational Initiation ◽  
Normal Tissues ◽  
Potential Biomarker

Abstract Background Prostate cancer (PCa) is one of the most commonly diagnosed cancers. The functions of PNO1 in yeasts were involved in regulating ribosome and proteasome biogenesis. However, its roles in PCa remained largely unclear. Methods The present study evaluated the expression levels of PNO1 in PCa by using GSE45016, GSE55945 and GSE17951 datasets. Then, in vivo and in vitro assays were conducted to detect the biological functions of PNO1 in PCa. BALB/c mice were used for in vivo assay in this study. Microarray and bioinformatic analysis were carried out to detect the downstream targets and pathways regulated by PNO1. Results The present study for the first time demonstrated PNO1 was up-regulated in PCa samples compared to normal tissues. ShRNA mediated knockdown of PNO1 significantly suppressed PCa proliferation and clone formation, however, induced PCa apoptosis. Microarray analysis and bioinformatics analysis revealed PNO1 was involved in regulating multiple cancer related biological processes, such as regulation of DNA repair, single organismal cell-cell adhesion, translational initiation, RNA splicing, transcription, and positive regulation of mRNA catabolic process. OF note, in vivo results showed PNO1 knockdown remarkably reduced the PCa growth rate. Conclusions Despite more in-depth research is still required, this study showed PNO1 could serve as a potential biomarker for PCa.

scholarly journals Identification and characterization of miR-96, a potential biomarker of NSCLC, through bioinformatic analysis

2017 ◽  
Vol 38 (2) ◽  
pp. 1213-1223 ◽  
Author(s):  
Tonghui Cai ◽  
Jie Long ◽  
Hongyan Wang ◽  
Wanxia Liu ◽  
Yajie Zhang
Keyword(s):  
Bioinformatic Analysis ◽  
Potential Biomarker ◽  
Identification And Characterization

LPA3 Is a Precise Therapeutic Target And Potential Biomarker For Ovarian Cancer

2021 ◽  
Author(s):  
Pengfei Zhao ◽  
Qingru Yun ◽  
Aodungerile Li ◽  
Rong Li ◽  
Yali Yan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Bioinformatic Analysis ◽  
Ovarian Cancer Cells ◽  
Cancer Tissue ◽  
Lpa Receptor ◽  
Ovarian Cancer Tissue ◽  
Potential Biomarker

Abstract Current studies have demonstrated that significant increased LPA levels to be observed in ascites in patients with ovarian cancer. Although several studies have shown that Lysophosphatidic acid (LPA) related to the progression of ovarian cancer, which LPA receptors (LPARs) and G coupled protein subtypes mediated in LPA actions have not been clearly elucidated. This study aimed to clarify the roles of LPA and it’s subtype-specific LPARs mediating mechanisms in ovarian cancer by integrated using bioinformatic analysis and biological experimental approaches. The big data analysis shown that LPA3 was the only differentially expressed LPA receptor among the six LPARs in ovarian cancer and further verified in immunohistochemistry of tissue microarrays. Also found that LPA3 was also highly expressed in ovarian cancer tissue and ovarian cancer cells. Importantly, LPA significantly promoted the proliferation and migration of LPA3-overexpressing ovarian cancer cells, while the LPA-induced actions blocked by Ki16425, a LPAR1/3 antagonist treated, and LPA3-shRNA transfected. In vivo study indicated that the LPA3-overexpressing cell derived tumors metastasis, tumors volume and tumors mass were apparently increased in xenografted nude mice. In addition, we also observed that LPA3 was differential high-expression in ovarian cancer tissue of the patients. Our studies further confirmed the LPA3/Gi/MAPKs/NF-κB signals were involved in LPA-induced oncogenic actions in ovarian cancer cells. Our findings indicated that the LPA3 might be a novel precise therapeutic target and potential biomarker for ovarian cancer.

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