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Updated: Feb 13, 2026

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Published on: May 1, 2019
Targeting the LINC01515/miR-325-3p/ERBB4 axis suppresses gastric cancer progression
Qiang Ji1, Bibo Tan1, Fang Li2
1Third Department of Surgery, The Fourth Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Background:
Globally, gastric cancer (GC) remains the leading cause of cancer-related death. Research on circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) is mostly focused on cancer. lncRNAs can influence gene expression by functioning as ceRNAs to sponge miRNAs. This study sought to characterize the expression patterns of miR-325-3p and LINC01515 and investigate their possible mechanisms in GC.
Methods:
Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect miR-325-3p expression. The target mRNAs and competitive lncRNAs of miR-325-3p were screened via bioinformatics analysis. Cell counting, Transwell assay, and wound-healing experiments were conducted to measure cell growth, migration, and invasion. The relationships between LINC01515, miR-325-3p, and erythroblastic oncogene B4 (ERBB4) were confirmed through the dual luciferase reporter gene assay.
Results:
GC cell lines and tissues showed upregulated LINC01515 and ERBB4 expression, accompanied by downregulated miR-325-3p expression. These expression patterns were associated with tumor proliferation, invasion, and migration. ERBB4 was positively correlated with LINC01515 in the context of differentially expressed miR-325-3p. These findings suggest that LINC01515 may regulate ERBB4 by functioning as a ceRNAs to sponge miR-325-3p.
Conclusion:
LINC01515 upregulates ERBB4 expression in GC by sponging miR-325-3p, thereby promoting tumor growth. These findings highlight the LINC01515/miR-325-3p/ERBB4 axis as a potential therapeutic target for GC.
Insights
Long non-coding RNA LINC01515 promotes gastric cancer (GC) growth by upregulating ERBB4 via sponging miR-325-3p. This LINC01515/miR-325-3p/ERBB4 pathway presents a potential therapeutic target for GC.
Area of Science:
- Molecular Oncology
- Cancer Biology
- RNA Biology
Background:
- Gastric cancer (GC) is a leading cause of cancer mortality worldwide.
- Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play crucial roles in cancer development.
- lncRNAs can act as competing endogenous RNAs (ceRNAs) to regulate miRNA activity.
Purpose of the Study:
- To investigate the expression patterns of miR-325-3p and LINC01515 in GC.
- To elucidate the underlying molecular mechanisms of LINC01515 and miR-325-3p in GC progression.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) for expression analysis.
- Bioinformatics analysis to identify target genes and interacting lncRNAs.
- Cell proliferation, migration, and invasion assays (Cell counting, Transwell, wound-healing).
- Dual-luciferase reporter assay to confirm interactions between LINC01515, miR-325-3p, and ERBB4.
Main Results:
- LINC01515 and ERBB4 were upregulated, while miR-325-3p was downregulated in GC tissues and cell lines.
- Altered expression levels correlated with increased tumor proliferation, invasion, and migration.
- LINC01515 positively correlated with ERBB4, suggesting a regulatory relationship mediated by miR-325-3p.
Conclusions:
- LINC01515 promotes GC progression by upregulating ERBB4 through sponging miR-325-3p.
- The LINC01515/miR-325-3p/ERBB4 axis represents a promising therapeutic target for gastric cancer treatment.
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