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Updated: Feb 14, 2026

Establishment of Gastric Cancer Patient-derived Xenograft Models and Primary Cell Lines
Published on: July 19, 2019
miR-613 inhibits gastric cancer progression through repressing brain derived neurotrophic factor
Dayong Ding1, Ruizhi Hou1, Yongjian Gao1
1Department of Gastrointestinal Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130000, P.R. China.
Abstract:
MicroRNA (miR)-613 has been reported to function as a tumor suppressor in several types of cancer. However, the biological function and underlying mechanism in gastric cancer (GC) has remained elusive. Therefore, the aim of the present study was to assess the expression and biological role of miR-613 in GC tissues and cell lines. miR-613 expression was found to be downregulated in 38 GC tissue samples compared to that in their adjacent non-cancerous tissues, and low expression of miR-613 was associated with lymph node metastasis and advanced tumor-nodes-metastasis stage. A gain-of-function assay demonstrated that miR-613 overexpression reduced tumor cell proliferation, migration and invasion of SGC-7901 cells, as determined by MTT and Transwell assays. Furthermore, brain-derived neutrophic factor (BDNF) was identified as a direct target of miR-613 in GC cells by a luciferase reporter assay. BDNF expression was upregulated and inversely correlated with miR-613 levels in GC tissues. In addition, knockdown of BDNF expression mimicked the tumor suppressive effect of miR-613 in GC cells. In conclusion, these findings demonstrated that miR-613 functions as a tumor suppressor in GC by targeting BDNF. Thus, miR-613 is a potential therapeutic target for GC.
Insights
MicroRNA-613 (miR-613) acts as a tumor suppressor in gastric cancer (GC). It targets brain-derived neurotrophic factor (BDNF), inhibiting GC cell proliferation, migration, and invasion, suggesting miR-613 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA-613 (miR-613) is a known tumor suppressor in various cancers.
- Its specific role and mechanism in gastric cancer (GC) remain largely uncharacterized.
Purpose of the Study:
- To investigate the expression, biological function, and molecular mechanism of miR-613 in gastric cancer.
- To determine if miR-613 acts as a tumor suppressor in GC and identify its direct targets.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) for miR-613 expression analysis.
- Gain-of-function assays (MTT and Transwell) to assess effects on GC cell proliferation, migration, and invasion.
- Luciferase reporter assay to validate brain-derived neurotrophic factor (BDNF) as a direct target of miR-613.
Main Results:
- miR-613 expression was significantly downregulated in GC tissues compared to adjacent non-cancerous tissues.
- Low miR-613 expression correlated with lymph node metastasis and advanced tumor-nodes-metastasis (TNM) stage.
- Overexpression of miR-613 suppressed GC cell proliferation, migration, and invasion.
- BDNF was identified as a direct target of miR-613, with its expression upregulated and inversely correlated with miR-613 levels in GC tissues.
- Knockdown of BDNF mimicked the tumor-suppressive effects of miR-613.
Conclusions:
- miR-613 functions as a tumor suppressor in gastric cancer by directly targeting and downregulating BDNF.
- miR-613 holds potential as a therapeutic target for gastric cancer treatment.
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