Related Experiment Video
Updated: Oct 16, 2025
Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
Published on: January 31, 2025
MiR-144-3p inhibits gastric cancer progression and stemness via directly targeting GLI2 involved in hedgehog pathway
Yixun Lu1,2, Benlong Zhang1,2, Baohua Wang1,2
1Medical School of Chinese PLA, Beijing, 100853, China.
Background:
Gastric cancer (GC) is the fifth most commonly diagnosed cancer worldwide. Due to the dismal prognosis, identifying novel therapeutic targets in GC is urgently needed. Evidences have shown that miRNAs played critical roles in the regulation of tumor initiation and progression. GLI family zinc finger 2 (GLI2) has been reported to be up-regulated and facilitate cancer progression in multiple malignancies. In this study, we focused on identifying GLI2-targeted miRNAs and clarifying the underlying mechanism in GC.
Methods:
Paired fresh gastric cancer tissues were collected from gastrectomy patients. GLI2 and miRNAs expression were detected in gastric cancer tissues and cell lines. Bioinformatics analysis was used to predict GLI2-targeted miRNAs and dual-luciferase reporter assay was applied for target verification. CCK-8, clone formation, transwell and flow cytometry were carried out to determine the proliferation, migration, invasion and cell cycle of gastric cancer cells. Tumorsphere formation assay and flow cytometry were performed to detail the stemness of gastric cancer stem cells (GCSCs). Xenograft models in nude mice were established to investigate the role of the miR-144-3p in vivo.
Results:
GLI2 was frequently upregulated in GC and indicated a poor survival. Meanwhile, miR-144-3p was downregulated and negatively correlated with GLI2 in GC. GLI2 was a direct target gene of miR-144-3p. MiR-144-3p overexpression inhibited proliferation, migration and invasion of gastric cancer cells. Enhanced miR-144-3p expression inhibited tumorsphere formation and CD44 expression of GCSCs. Restoration of GLI2 expression partly reversed the suppressive effect of miR-144-3p. Xenograft assay showed that miR-144-3p could inhibit the tumorigenesis of GC in vivo.
Conclusions:
MiR-144-3p was downregulated and served as an essential tumor suppressor in GC. Mechanistically, miR-144-3p inhibited gastric cancer progression and stemness by, at least in part, regulating GLI2 expression.
Insights
MicroRNA-144-3p suppresses gastric cancer (GC) progression by targeting GLI2. This study identifies miR-144-3p as a crucial tumor suppressor in GC, offering potential therapeutic avenues.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gastric cancer (GC) is a leading cause of cancer mortality worldwide, necessitating novel therapeutic targets.
- MicroRNAs (miRNAs) are critical regulators of tumor initiation and progression.
- GLI family zinc finger 2 (GLI2) is implicated in various cancers, including GC.
Purpose of the Study:
- To identify miRNAs targeting GLI2 in gastric cancer.
- To elucidate the underlying molecular mechanisms of GLI2 regulation by miRNAs in GC.
Main Methods:
- Analysis of GLI2 and miRNA expression in GC tissues and cell lines.
- Bioinformatic prediction and dual-luciferase reporter assay for miRNA-target validation.
- In vitro assays (proliferation, migration, invasion, cell cycle, stemness) and in vivo xenograft models.
Main Results:
- GLI2 was upregulated in GC, correlating with poor survival.
- miR-144-3p was downregulated and inversely correlated with GLI2.
- GLI2 is a direct target of miR-144-3p.
- miR-144-3p suppressed GC cell proliferation, migration, invasion, and stemness.
- miR-144-3p inhibited tumor growth in vivo.
Conclusions:
- miR-144-3p functions as a tumor suppressor in gastric cancer.
- miR-144-3p inhibits GC progression and stemness by regulating GLI2 expression.
More Related Videos
Related Concept Videos
02:33Hedgehog Signaling Pathway
01:22MicroRNAs