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Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
Published on: June 7, 2016
LINC00092 Suppresses the Malignant Progression of Breast Invasive Ductal Carcinoma Through Modulating SFRP1
Chun-Ming Zhao1, Lin-Lin Li1, Jia-Wen Xu1
1Department of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
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.
Insights
Overexpression of LINC00092 inhibits invasive ductal carcinoma (IDC) development by regulating the miR-1827/SFRP1 axis. This finding suggests LINC00092 as a potential therapeutic target for breast cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Invasive ductal carcinoma (IDC) is the most common breast cancer subtype with limited effective therapies.
- Long non-coding RNAs (lncRNAs) play roles in various cancers, but their specific mechanisms in IDC are not fully understood.
- LINC00092's role in IDC progression and its molecular interactions require further investigation.
Purpose of the Study:
- To investigate the expression and function of LINC00092 in IDC.
- To elucidate the molecular mechanism of LINC00092 in regulating IDC progression.
- To explore the potential of LINC00092 as a therapeutic target for IDC.
Main Methods:
- Analysis of LINC00092, miR-1827, and SFRP1 expression in IDC clinical samples (TCGA database).
- Kaplan-Meier survival analysis, KEGG, and GO pathway analysis.
- Bioinformatics, dual-luciferase reporter assays, cell proliferation, migration, and invasion assays (CCK-8, colony formation, Transwell).
- Quantitative reverse-transcription polymerase chain reaction and Western blot.
Main Results:
- LINC00092 was downregulated in IDC tissues and correlated with poor prognosis.
- Downregulated LINC00092 promoted IDC cell proliferation, colony formation, migration, and invasion.
- LINC00092 directly interacted with miR-1827 and SFRP1, forming a regulatory axis that inhibited IDC progression.
Conclusions:
- Overexpression of LINC00092 inhibits IDC development by modulating the miR-1827/SFRP1 axis.
- LINC00092 acts as a tumor suppressor in IDC.
- The LINC00092/miR-1827/SFRP1 pathway represents a promising therapeutic target for IDC treatment.
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