Microarray data reveal potential genes that regulate triple-negative breast cancer.

Objective: Triple-negative breast cancer (TNBC) is characterized by a lack of targeted therapies and poor patient prognosis, and its underlying pathological mechanisms remain unclear. This study aimed to identify potential key genes and related pathways that are required for TNBC development.

Methods: We screened the Gene Expression Omnibus database for transcriptome data and identified differently expressed genes in TNBC.

LncRNA SNHG11 aggravates cell proliferation and migration in triple-negative breast cancer via sponging miR-2355-5p and targeting CBX5.

Triple-negative breast cancer (TNBC) is one of the most common malignances worldwide. Concurrently, the incidence of TNBC has continued to rise in recent years. It is reported that long non-coding RNAs (lncRNAs) are involved in biological processes in numerous cancers including TNBC.

Silencing lncRNA AFAP1-AS1 Inhibits the Progression of Esophageal Squamous Cell Carcinoma Cells via Regulating the miR-498/VEGFA Axis.

Purpose: In view of the continuous increase of the mortality rate, esophageal squamous cell carcinoma (ESCC) develops into a major health concern. In this study, we aimed to investigate the underlying mechanism of long noncoding RNA (lncRNA) actin filament-associated protein 1 antisense RNA (AFAP1-AS1)/microRNA-498 (miR-498)/vascular endothelial growth factor A (VEGFA) in ESCC cells.

Methods: The expression levels of AFAP1-AS1, miR-498 and VEGFA in ESCC tissues and cells were detected using quantitative real-time polymerase chain reaction (qRT-PCR).

miRNA-181a-5p Enhances the Sensitivity of Cells to Cisplatin in Esophageal Adenocarcinoma by Targeting CBLB.

Background: Cisplatin (CDDP) is extensively used for esophageal adenocarcinoma (EAC) chemotherapy, while cisplatin resistance is getting worse. microRNA-181a-5p (miR-181a-5p) has been reported to play an important role in various human cancers. However, the effect and underlying mechanism of miR-181a-5p in cisplatin resistance of EAC remain unclear.