scholarly journals Long non-coding RNA MALAT1 regulates BLCAP mRNA expression through binding to miR-339-5p and promotes poor prognosis in breast cancer

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Liuhong Zheng ◽  
Yuhan Zhang ◽  
Yajun Fu ◽  
Hangdi Gong ◽  
Jianjun Guo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Ductal Carcinoma ◽  
The Cancer Genome Atlas ◽  
Clinical Samples ◽  
Non Coding Rna ◽  
Competitive Endogenous Rnas ◽  
Tumorigenesis And Progression ◽  
Non Coding Rnas ◽  
Cancer Tissues

AbstractThe human genome transcribes a large amount of non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs. LncRNAs and microRNAs have been shown to play a critical regulatory role in tumorigenesis and progression. Competitive endogenous RNAs (ceRNAs) affect other RNAs transcription through competitively binding to common microRNAs (miRNAs). MALAT1 is a typical lncRNA that is markedly up-regulated in breast cancer. However, current understanding of the involvement of MALAT1 in breast cancer development and prognosis remains unclear. In the present study, the expression of MALAT1 in clinical samples of breast cancer tissues was found to be significantly up-regulated that was consistent with the result based on the dataset of the Cancer Genome Atlas (TCGA) at cBioportal. A negative correlation between overall survival and the expression of MALAT1 was statistically significant in the group of diagnosis age below 60 or in the group of infiltrating ductal carcinoma analyzed by TCGA database, which declared that MALAT1 might be a potentially useful prognostic factor. Furthermore, the combination of bioinformatics prediction with experimental verifications indicated that lncRNA MALAT1 can regulate BLCAP mRNA expression through binding to miR-339-5p.

scholarly journals The Prognostic Value of the Expression of SMC4 mRNA in Breast Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Rui-min Ma ◽  
Fan Yang ◽  
Du-ping Huang ◽  
Min Zheng ◽  
Yi-luan Wang
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Mrna Level ◽  
The Cancer Genome Atlas ◽  
Paired Samples ◽  
Cancer Genome Atlas ◽  
Advanced Stages ◽  
Independent Risk Factors ◽  
Cancer Tissues ◽  
Structural Maintenance Of Chromosomes

Aim. To investigate the mRNA expression and clinical significance of structural maintenance of chromosomes protein 4 (SMC4) in breast cancer. Methods. A total of 23 paired samples were sequenced, and data from the Cancer Genome Atlas were analyzed. Results. SMC4 mRNA level was significantly upregulated in breast cancer tissues (P<0.001). Patients with high mRNA expression of SMC4 had significantly poor survival (P=0.012). Subgroup analyses show that in nontriple negative breast cancer (non-TNBC) patients, the high SMC4 mRNA expression, older age (>65), negative progesterone receptor, and advanced stages (III-IV) were independent risk factors (HR=3.293, 95% CI 1.257-8.625, P=0.015). In patients with TNBC, high mRNA expression of SMC4 correlated with better survival rate (P<0.046). Conclusion. SMC4 mRNA level is a good prognostic biomarker for patients with breast cancer.

scholarly journals Long non-coding RNA ARAP1-AS1 accelerates cell proliferation and migration in breast cancer through miR-2110/HDAC2/PLIN1 axis

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Chong Lu ◽  
Xiuhua Wang ◽  
Xiangwang Zhao ◽  
Yue Xin ◽  
Chunping Liu
Keyword(s):  
Breast Cancer ◽  
Normal Breast ◽  
Tumor Promoter ◽  
Women Health ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Breast Tissues ◽  
Long Non Coding Rna

Abstract Breast cancer (BC) poses a great threaten to women health. Numerous evidences suggest the important role of long non-coding RNAs (lncRNAs) in BC development. In the present study, we intended to investigate the role of ARAP1-AS1 in BC progression. First of all, the GEPIA data suggested that ARAP1-AS1 was highly expressed in breast invasive carcinoma (BRAC) tissues compared with the normal breast tissues. Meanwhile, the expression of ARAP1-AS1 was greatly up-regulated in BC cell lines. ARAP1-AS1 knockdown led to repressed proliferation, strengthened apoptosis and blocked migration of BC cells. Moreover, ARAP1-AS1 could boost HDAC2 expression in BC through sponging miR-2110 via a ceRNA mechanism. Of note, the UCSC predicted that HDAC2 was a potential transcriptional regulator of PLIN1, an identified tumor suppressor in BC progression. Moreover, we explained that the repression of HDAC2 on PLIN1 was owing to its deacetylation on PLIN1 promoter. More importantly, depletion of PLIN1 attenuated the mitigation function of ARAP1-AS1 silence on the malignant phenotypes of BC cells. To sum up, ARAP1-AS1 serves a tumor-promoter in BC development through modulating miR-2110/HDAC2/PLIN1 axis, which may help to develop novel effective targets for BC treatment.

scholarly journals Competing endogenous RNA (ceRNA) hypothetic model based on comprehensive analysis of long non-coding RNA expression in lung adenocarcinoma

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e8024 ◽  
Author(s):  
Xiwen Wang ◽  
Rui Su ◽  
Qiqiang Guo ◽  
Jia Liu ◽  
Banlai Ruan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Inverse Correlation ◽  
The Cancer Genome Atlas ◽  
Competing Endogenous Rna ◽  
Cerna Network ◽  
Kaplan Meier ◽  
Non Coding Rna ◽  
Pathway Analyses ◽  
Lung Adenocarcinomas ◽  
Cancer Tissues

Background Non-small cell lung cancer (NSCLC) is a major subtype of lung cancer with high malignancy and bad prognosis, consisted of lung adenocarcinomas (LUAD) and lung squamous cell carcinomas (LUSC) chiefly. Multiple studies have indicated that competing endogenous RNA (ceRNA) network centered long noncoding RNAs (lncRNAs) can regulate gene expression and the progression of various cancers. However, the research about lncRNAs-mediated ceRNA network in LUAD is still lacking. Methods In this study, we analyzed the RNA-seq database from The Cancer Genome Atlas (TCGA) and obtained dysregulated lncRNAs in NSCLC, then further identified survival associated lncRNAs through Kaplan–Meier analysis. Quantitative real time PCR (qRT-PCR) was performed to confirm their expression in LUAD tissues and cell lines. The ceRNA networks were constructed based on DIANA-TarBase and TargetScan databases and visualized with OmicShare tools. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to investigate the potential function of ceRNA networks. Results In total, 1,437 and 1,699 lncRNAs were found to be up-regulated in LUAD and LUSC respectively with 895 lncRNAs overlapping (|log2FC| > 3, adjusted P value <0.01). Among which, 222 lncRNAs and 46 lncRNAs were associated with the overall survival (OS) of LUAD and LUSC, and 18 out of 222 up-regulated lncRNAs were found to have inverse correlation with LUAD patients’ OS (|log2FC| > 3, adjusted P value < 0.02). We selected 3 lncRNAs (CASC8, LINC01842 and VPS9D1-AS1) out of these 18 lncRNAs and confirmed their overexpression in lung cancer tissues and cells. CeRNA networks were further constructed centered CASC8, LINC01842 and VPS9D1-AS1 with 3 miRNAs and 100 mRNAs included respectively. Conclusion Through comprehensively analyses of TCGA, our study identified specific lncRNAs as candidate diagnostic and prognostic biomarkers for LUAD. The novel ceRNA network we created provided more insights into the regulatory mechanisms underlying LUAD.

The glycobiological landscape of breast cancer: insights into galectins and O-GlcNAc homeostasis-related genes

2021 ◽  
Author(s):  
Rada Tazhitdinova ◽  
Alexander V Timoshenko
Keyword(s):  
Breast Cancer ◽  
Cancer Biology ◽  
Breast Cancer Subtype ◽  
The Cancer Genome Atlas ◽  
Correlation Relationship ◽  
Cancer Data ◽  
Normal Tissues ◽  
Genes Encoding ◽  
Genetic Landscape ◽  
Cancer Tissues

Abstract Purpose This study aimed to assess the functional associations between genes of the glycobiological landscape encoding galectins and O-GlcNAc cycle enzymes in the context of breast cancer biology and clinical applications. Methods An in silico analysis of the breast cancer data from The Cancer Genome Atlas was conducted comparing expression, pairwise correlations, and prognostic value for 17 genes encoding galectins, O-GlcNAc cycle enzymes, and cell stemness-related transcription factors. Results Multiple general and breast cancer subtype-specific differences in galectin/O-GlcNAc genetic landscape markers were observed and classified. Specifically, LGALS12 was found to be significantly downregulated in breast cancer tissues across all subtypes while LGALS2 and GFPT1 showed potential as prognostic markers. Remarkably, there was an overall loss of both correlation strength and correlation relationship between expression of galectin/O-GlcNAc landscape genes in the breast cancer samples versus normal tissues. Six gene pairs (GFPT1/LGALS1, GFPT1/LGALS3, GFPT1/LGALS12, GFPT1/KLF4, OGT/LGALS12, and OGT/KLF4) were found to be potential diagnostic markers for breast cancer. Conclusions These findings indicate that the glycobiological landscape of breast cancer underwent significant remodeling, which might be associated with switching galectin gene regulation within a framework of O-GlcNAc homeostasis.

Overexpression of long non-coding RNA MCM3AP-AS1 in breast cancer tissues compared to adjacent non-tumour tissues

2020 ◽  
pp. 1-5
Author(s):  
A Riahi ◽  
M Hosseinpour-Feizi ◽  
A Rajabi ◽  
M Akbarzadeh ◽  
V Montazeri ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

scholarly journals Paired Ductal CarcinomaIn Situand Invasive Breast Cancer Lesions in the D-Loop of the Mitochondrial Genome Indicate a Cancerization Field Effect

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Andrea Maggrah ◽  
Kerry Robinson ◽  
Jennifer Creed ◽  
Roy Wittock ◽  
Ken Gehman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mitochondrial Genome ◽  
Invasive Breast Cancer ◽  
Field Effect ◽  
Ductal Carcinoma ◽  
Hypervariable Region ◽  
Clinical Samples ◽  
Paired Samples ◽  
D Loop ◽  
Cancerization Field

Alterations in the mitochondrial genome have been chronicled in most solid tumors, including breast cancer. The intent of this paper is to compare and document somatic mitochondrial D-loop mutations in paired samples of ductal carcinomain situ(DCIS) and invasive breast cancer (IBC) indicating a potential breast ductal epithelial cancerization field effect. Paired samples of these histopathologies were laser-captured microdissected (LCM) from biopsy, lumpectomy, and mastectomy tissues. Blood samples were collected as germplasm control references. For each patient, hypervariable region 1 (HV1) in the D-loop portion of the mitochondrial genome (mtGenome) was sequenced for all 3 clinical samples. Specific parallel somatic heteroplasmic alterations between these histopathologies, particularly at sites 16189, 16223, 16224, 16270, and 16291, suggest the presence of an epithelial, mitochondrial cancerization field effect. These results indicate that further characterization of the mutational pathway of DCIS and IBC may help establish the invasive potential of DCIS. Moreover, this paper indicates that biofluids with low cellularity, such as nipple aspirate fluid and/or ductal lavage, warrant further investigation as early and minimally invasive detection mediums of a cancerization field effect within breast tissue.

scholarly journals Upregulated CDKN2A expression may be an independent protective factor in Luminal-like breast cancer

2020 ◽  
Author(s):  
Yier Qiu ◽  
Guowen Lu ◽  
Yingjie Wu
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Mrna Expression ◽  
Protective Factor ◽  
Killer Cell ◽  
Cytokine Receptor ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Receptor Interactions ◽  
Cancer Tissues

Abstract Background: Previous studies revealed that CDKN2A (cyclin-dependent kinase inhibitor 2A) functioned as a tumour suppressor in various types of malignant tumours. The aim of the study was to clarify the value of CDKN2A expression in the prognosis of breast cancer.Method: Using the Cancer Genome Atlas (TCGA) database, we compared CDKN2A mRNA levels between breast cancer tissues and normal tissues and analyzed the relationship between clinical features and CDKN2A expression with the Wilcox test and the Kruskal-Wallis test. Kaplan-Meier and Cox analyses were performed to determine the correlation between CDKN2A expression and breast cancer prognosis. Gene set enrichment analysis (GSEA) was performed using the TCGA data set.Results: We first found that CDKN2A expression was markedly higher in breast cancer tissues than in normal tissues using the TCGA database (P=0.000). In addition, CDKN2A mRNA expression in breast cancer was positively correlated with age (P=0.018), histological types (P=0.028), ER status (P=0.000), PR status (P=0.000) and molecular subtypes (P=0.000). Kaplan-Meier analysis showed that increased CDKN2A expression was associated with increased survival time in breast cancer patients (P=0.000), especially in Luminal-like subtype. Univariate and multivariate Cox analyses indicated that CDKN2A expression was an independent prognostic biomarker for breast cancer (P=0.037). GSEA suggested that pathways involving cell adhesion molecules (CAMs), cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity were differentially enriched in the CDKN2A-high expression group.Conclusion: Our research demonstrated that high CDKN2A mRNA expression may be an independent protective factor for improved prognosis in Luminal-like breast cancer. Additionally, the signaling pathways related to CAMs, cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity regulated by CDKN2A mRNA expression should be further studied.

scholarly journals Upregulated CDKN2A expression may be an independent protective factor in Luminal-like breast cancer

2020 ◽  
Author(s):  
Yier Qiu ◽  
Guowen Lu ◽  
Yingjie Wu
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Mrna Expression ◽  
Protective Factor ◽  
Killer Cell ◽  
Cytokine Receptor ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Receptor Interactions ◽  
Cancer Tissues

Abstract Background: Previous studies revealed that CDKN2A (cyclin-dependent kinase inhibitor 2A) functioned as a tumour suppressor in various types of malignant tumours. The aim of the study was to clarify the value of CDKN2A expression in the prognosis of breast cancer.Method: Using the Cancer Genome Atlas (TCGA) database, we compared CDKN2A mRNA levels between breast cancer tissues and normal tissues and analyzed the relationship between clinical features and CDKN2A expression with the Wilcox test and the Kruskal-Wallis test. Kaplan-Meier and Cox analyses were performed to determine the correlation between CDKN2A expression and breast cancer prognosis. Gene set enrichment analysis (GSEA) was performed using the TCGA data set.Results: We first found that CDKN2A expression was markedly higher in breast cancer tissues than in normal tissues using the TCGA database (P=0.000). In addition, CDKN2A mRNA expression in breast cancer was positively correlated with age (P=0.018), histological types (P=0.028), ER status (P=0.000), PR status (P=0.000) and molecular subtypes (P=0.000). Kaplan-Meier analysis showed that increased CDKN2A expression was associated with increased survival time in breast cancer patients (P=0.000), especially in Luminal-like subtype. Univariate and multivariate Cox analyses indicated that CDKN2A expression was an independent prognostic biomarker for breast cancer (P=0.037). GSEA suggested that pathways involving cell adhesion molecules (CAMs), cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity were differentially enriched in the CDKN2A-high expression group.Conclusion: Our research demonstrated that high CDKN2A mRNA expression was an independent protective factor for improved prognosis in Luminal-like breast cancer. Additionally, the signaling pathways related to CAMs, cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity regulated by CDKN2A mRNA expression should be further studied.

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