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Updated: Dec 25, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
DLX6 Antisense RNA 1 Modulates Glucose Metabolism and Cell Growth in Gastric Cancer by Targeting microRNA-4290
1Department of Gastric, The Affiliated Huaian N0.1 People's Hospital of Nanjing Medical University, No. 1 Huanghe West Road, Huaiyin District, Huai'an City, 223300, Jiangsu Province, China.
Background:
Gastric cancer (GC) is one of the most commonly diagnosed malignancy worldwide. DLX6 antisense RNA 1 (DLX6-AS1) is a long noncoding RNA (lncRNA) that exhibits oncogenic effects on multiple human carcinomas.
Aims:
This study aimed to investigate the regulatory effect of DLX6-AS1 in GC progression.
Methods:
The expression of DLX6-AS1 in GC tissues and cell lines was examined. The cell viability, number of clones, and apoptosis, aerobic glycolysis, and mitochondrial respiration was assessed. The effect of DLX6-AS1 on tumor growth in nude mice was also evaluated.
Results:
DLX6-AS1 was overexpressed in GC tissues and cell lines. DLX6-AS1 knockdown by short hairpin RNA (shRNA) significantly inhibited cell viability and colony formation, and induced apoptosis. DLX6-AS1 silencing impaired aerobic glycolysis but stimulated mitochondrial respiration in GC cells. miR-4290 was confirmed as a downstream target of DLX6-AS1, and their expression levels were inversely correlated. GC cells expressing sh-DLX6-AS1 showed significantly lower level of 3-phosphoinositide-dependent protein kinase 1 (PDK1), a target of miR-4290, compared to cells expressing control shRNA. In addition, the suppressed GC cell malignancy upon DLX6-AS1 knockdown could be prominently reversed by PDK1 overexpression. Meanwhile, PDK1 overexpression enhanced aerobic glycolysis but repressed mitochondrial respiration under sh-DLX6-AS1 treatment. Furthermore, DLX6-AS1 knockdown significantly delayed the tumor growth in a mouse xenograft model inoculated with GC cells.
Conclusions:
LncRNA DLX6-AS1 regulated tumor growth and aerobic glycolysis in GC by targeting miR-4290 and PDK1, suggesting DLX6-AS1 might serve as a novel potential therapeutic target for GC treatment from bench to clinic.
Insights
Long noncoding RNA DLX6-AS1 promotes gastric cancer (GC) progression by affecting cell viability, apoptosis, and metabolism. Targeting DLX6-AS1 offers a potential therapeutic strategy for gastric cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric cancer (GC) is a prevalent malignancy globally.
- Long noncoding RNA DLX6-AS1 (DLX6-AS1) is implicated as an oncogene in various human carcinomas.
- The specific role of DLX6-AS1 in GC progression requires elucidation.
Purpose of the Study:
- To investigate the regulatory role of DLX6-AS1 in gastric cancer progression.
- To explore the molecular mechanisms underlying DLX6-AS1's function in GC.
Main Methods:
- Examined DLX6-AS1 expression in GC tissues and cell lines.
- Assessed cell viability, colony formation, apoptosis, aerobic glycolysis, and mitochondrial respiration.
- Evaluated the effect of DLX6-AS1 on tumor growth in a mouse xenograft model.
Main Results:
- DLX6-AS1 was overexpressed in GC tissues and cell lines.
- DLX6-AS1 knockdown inhibited cell viability and colony formation, induced apoptosis, impaired aerobic glycolysis, and stimulated mitochondrial respiration.
- DLX6-AS1 targeted miR-4290, which in turn regulated PDK1; DLX6-AS1 knockdown suppressed tumor growth in vivo.
Conclusions:
- DLX6-AS1 promotes gastric cancer growth and alters cellular metabolism by targeting miR-4290 and PDK1.
- DLX6-AS1 represents a potential therapeutic target for gastric cancer treatment.
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