LINC00092 Suppresses the Malignant Progression of Breast Invasive Ductal Carcinoma Through Modulating SFRP1 Expression by Sponging miR-1827

Abstract

Breast invasive ductal carcinoma (IDC) is a most common kind of breast cancer (BC), yet to date the corresponding effective therapies are limited. Extensive evidence has indicated that lncRNAs are involved in multiple cancers, and the potential mechanism of lncRNAs, such as LINC00092, mentioned in IDC remains elusive. IDC clinical samples from TCGA database were used to analyze the expression levels of LINC00092, miR-1827 and SFRP1. Kaplan-Meier method was applied to plot the overall survival curves. KEGG and GO were employed to screen the pathway that LINC00092 participated in. Pearson’s correlation analysis determined the relationship between LINC00092 and SFRP1. Bioinformatics analysis and dual-luciferase reporter assay examined the association among LINC00092, miR-1827, and SFRP1. Cell counting kit-8, colony formation and transwell assays were performed to detect cell viability, colony formation, and migration and invasion, respectively. Quantitative reverse-transcription polymerase chain reaction and western blot were utilized to investigate the expression at RNA and protein levels. LINC00092 expression was down-regulated in IDC tissues and cells, which was correlated with poor prognosis. Down-regulated LINC00092 facilitated cell proliferation, colony formation, and cell migration and invasion, while up-regulated LINC00092 inhibited cell malignant behaviors. LINC00092/SFRP1 physically bound to miR-1827 in IDC. SFRP1 expression was proportional to LINC00092 expression and inversely proportional to miR-1827 expression. The inhibitory effects of LINC00092 on cell aggressive behaviors were partially regulated by miR-1827/SFRP1. In summary, our results indicated that overexpression of LINC00092 inhibited the development of IDC through modulating miR-1827/SFRP1 axis, suggesting new therapeutic targets to treat IDC.

LINC00092 Modulates Oxidative Stress and Glycolysis of Breast Cancer Cells via Pyruvate Carboxylase-Mediated AKT/mTOR Pathway

“…Wu et al [ 16 ] reported that LINC00092 expression was significantly associated with the survival of BC patients. Zhao et al [ 43 ] discovered that LINC00092 expression was downregulated in breast invasive ductal carcinoma (BIDC) tissues and cells, which promoted malignant progression of BIDC via regulating secreted frizzled related protein 1 (SFRP1) by sponging microRNA-1827. Herein, we revealed that LINC00092 had lower expression level in BC tissues and cells and negatively related to BC tumor size and histological grade, as well as positively related to survival probability of BC patients.…”

“…As a type of ncRNAs with 18-24 nucleotides, microRNAs are main downstream targets of lncRNA [ 66 ]. Zhao et al [ 43 ] reported that LINC00092 sponged microRNA-1827 in BIDC cells to modulate BIDC malignant progression, which implied that LINC00092 regulated BC progression not only by modulating PC expression but also via regulating other molecules. Besides, the in vivo experiment in our research was relatively simple.…”

LINC00092 Enhances LPP Expression to Repress Thyroid Cancer Development via Sponging miR-542-3p

“…LINC00092 is an lncRNA, and has been found to be under-expressed in multiple neoplasms to play the antineoplastic role [15,36]. In TC, only Zhang et al revealed the levels of LINC00092 by analyzing the data from TCGA database [16].…”

In silico evaluation of the role of the long non-coding RNA LINC00092 in thyroid cancer progression ; regulation of the miR-34a-5p/RCAN1 axis

“…This study found that LINC00092 acts as a sponge for miR-1827. Considering that secreted frizzled-related protein 1 (SFRP1) can directly be targeted by miR-1827, LINC00092/miR-1827/SFRP1 is a signal axis to regulate malignant cell behaviors in IDC (46).…”