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Updated: Jul 11, 2025
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Published on: August 23, 2019
Decreased KLF3 Expression via miR-660-5p Targeting Suppresses Gastric Cancer Cell Progression
Wei Yu1,2, Jie Shen2, Xiaoguang Wang2
1Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Objective:
Gastric cancer (GC) is one of the most frequent cancers in the world. Recent studies have suggested that microRNAs (miRNAs/miRs) may act as novel therapeutic regimens for GC. This study revealed that miR-660-5p regulated the proliferation, migration, invasion, and apoptosis of GC cells via controlling the level of Krüppel-like factor 3 (KLF3).
Methods:
The level of miR-660-5p was measured in clinical GC tissues. Then, the miRNA targeting relationship between miR-660-5p and KLF3 was explored in vitro. GC cell lines, including HGC-27, SNU-1, HS-746T, NCI-N87, and human gastric epithelial GES-1 cells, were used. The impact of miR-660-5p on cell proliferation, colony formation, invasion, migration, and apoptosis were determined by knocking down KLF3.
Results:
It was demonstrated that the KLF3 expressions were significantly increased in GC tissues and cell lines compared to normal tissues or cells, and GC cell development was suppressed following KLF3 knockdown. Moreover, it was also revealed that miR-660-5p expression was significantly decreased in GC cells, and miR-660-5p acted as the direct regulator of KLF3.
Conclusions:
This study firstly reported the miR-660-5p/KLF3 interaction in GC, and the results provided a potential promising therapeutic target for GC.
Insights
This study found that reduced miR-660-5p levels in gastric cancer (GC) correlate with increased Krüppel-like factor 3 (KLF3). Targeting this miR-660-5p/KLF3 interaction offers a promising therapeutic strategy for GC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gastric cancer (GC) is a prevalent malignancy worldwide.
- MicroRNAs (miRNAs) are emerging as potential therapeutic targets for GC.
- Dysregulation of miRNA and gene expression is implicated in GC pathogenesis.
Purpose of the Study:
- To investigate the role of miR-660-5p in regulating gastric cancer cell behavior.
- To elucidate the interaction between miR-660-5p and Krüppel-like factor 3 (KLF3) in GC.
- To assess the therapeutic potential of targeting the miR-660-5p/KLF3 axis in GC.
Main Methods:
- Quantification of miR-660-5p and KLF3 expression in clinical GC tissues and cell lines.
- In vitro investigation of the miRNA-target relationship between miR-660-5p and KLF3.
- Assessment of GC cell proliferation, migration, invasion, and apoptosis following KLF3 knockdown.
Main Results:
- KLF3 expression was significantly elevated in GC tissues and cells, while miR-660-5p expression was decreased.
- Knockdown of KLF3 suppressed GC cell proliferation, migration, and invasion.
- miR-660-5p was identified as a direct regulator of KLF3 expression in GC cells.
Conclusions:
- This study establishes a novel interaction between miR-660-5p and KLF3 in gastric cancer.
- The miR-660-5p/KLF3 pathway represents a potential therapeutic target for gastric cancer treatment.
- Further research into this interaction could lead to new strategies for managing GC.
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