<p>Construction and Analysis of a Long Non-Coding RNA-Associated Competing Endogenous RNA Network Identified Potential Prognostic Biomarkers in Luminal Breast Cancer</p>

Abstract

Purpose: To construct a competing endogenous RNA (ceRNA) topology network of RNAseq data and micro RNA-seq (miRNA-seq) data to identify key prognostic long non-coding RNA (lncRNAs) in luminal breast cancer, and validate the results by human luminal breast cancer samples. Materials and Methods: The RNA-seq data and miRNA-seq data of luminal A breast cancer in the The Cancer Genome Atlas (TCGA) database were downloaded and compared with those in the miRcode database to obtain lncRNA-miRNA relationship pairs. Final target genes were predicted by all three databases (miRDB, miRTarBase, and TargetScan), thereby obtaining the miRNA-messenger RNA (miRNA-mRNA) relationship pairs and a ceRNA topology network was constructed, then mRNA enrichment analysis, ceRNA topological and stability analysis, univariate and multivariate Cox regression analysis were performed. Overall survival (OS) was evaluated and the key prognostic RNAs were identified. The expression difference between normal and tumor, as well as the correlation of high expression in tumor with pathological parameters (Ki-67, Grade, tumor diameter) were validated by human breast cancer specimens. Results: A ceRNA topology network was constructed and six lncRNAs were finally identified (The higher expression of PART1, IGF2.AS, WT1.AS, OIP5.AS1, and SLC25A5. AS1 was associated with poor prognosis while AL035706.1 was adverse) and the poor prognostic ones were higher expressed in tumor tissue and correlated with a higher Ki-67 (>10%), tumor grades (II, III) and tumor diameters (>1.5 cm). Using six lncRNAs, we constructed a prognostic model, which performed well for the classification of prognosis in the module. Conclusion: We identified and verified six biomarkers (OS-predicting) in luminal breast cancer, which significantly enriched the prediction and potential targets of this subtype.

Effect and mechanism of downregulating the long-chain noncoding RNA TM4SF1-AS1 on the proliferation, apoptosis and invasion of gastric cancer cells

“…LncTM4SF1-AS1 in four GC cell lines, MKN28, AGS, MGC803 and SGC7901, was also significantly higher than that in normal gastric mucosa cells. The above results suggest that lncTM4SF1-AS1 was upregulated in GC, which is similar to that reported in the literature in NSCLC [ 9 ] and breast carcinoma [ 10 ]. In view of its upregulation in GC tissues and cells, this study selectively downregulated lncTM4SF1-AS1 in GC cell lines.…”

“…It is also a molecular marker of poor prognosis in patients [ 9 ]. RNA sequencing of breast carcinoma revealed that expression levels of TM4SF1-AS1 in breast carcinoma tissues were higher than those in adjacent tissues [ 10 ]. However, the role and mechanism of TM4SF1-AS1 in GC are still unclear.…”

Identification and Roles of miR-29b-1-3p and miR29a-3p-Regulated and Non-Regulated lncRNAs in Endocrine-Sensitive and Resistant Breast Cancer Cells

“…OIP5-AS1 was higher in breast tumors compared with normal breast tissue and high OIP5-AS1 correlated with tumor size, LN metastasis, and tumor grade [ 81 ]. Another study found that OIP5-AS1 expression correlates with a high risk of worse outcomes for luminal BC patients [ 82 ]. Knockdown of OIP5-AS1 in MDA-MB-231 cells inhibited xenograft tumor growth in BALB/c nude mice, validating its oncogenic activity in vivo [ 81 ].…”

LINC00504 Promotes the Malignant Biological Behavior of Breast Cancer Cells by Upregulating HMGB3 via Decoying MicroRNA-876-3p

“…Previous studies have demonstrated that a variety of lncRNAs are dysregulated in breast cancer and they have an effect on the oncogenesis, progression, and metastasis of breast cancer. 27–29 Continued studies on the role of breast cancer-related lncRNAs will lead to an understanding of the mechanisms that underly breast cancer pathogenesis and identity new targets for therapy. In the present study, we explored the role of LINC00504 in regulating oncogenesis in breast cancer.…”