Related Experiment Video
Updated: Nov 10, 2025
Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors
Published on: May 17, 2024
miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
Haibin Yuan1, Fengli Liu1, Tongsheng Ma1
1Department of Neonatal Surgery, Xuzhou Children's Hospital, No.18 Sudi North Road, Quanshan District, 221001, Xuzhou, China.
Abstract:
This study aimed to explore the regulatory mechanisms of miR-338-3p and matrix metalloproteinase-2 (MMP-2) in neuroblastoma. Putative target interaction regions of miR-338-3p on MMP-2 were predicted by miRcode and miRbase bioinformatics tools. Relative expression of miRNA-338-3p and MMP-2 in neuroblastoma tissues and GI-LI-N and SK-N-SH cells was determined by reverse transcription polymerase chain reaction experiment. Furthermore, the cell proliferation was determined by Cell Counting Kit-8 assay, the cell apoptosis rate was analyzed by flow cytometry assay, and the cell invasion was evaluated by transwell assay. miR-338-3p expression was downregulated, whereas MMP-2 expression was upregulated in metastasis tissue site compared to that in primary tissue site in total. Furthermore, miR-338-3p overexpression suppressed proliferation, invasion, and epithelial-mesenchymal transition (EMT) of neuroblastoma cells but promoted apoptosis, and the knockdown of MMP-2 triggered similar effects. Furthermore, MMP-2 was directly targeted by miR-338-3p, and overexpression of MMP-2 rescued the inhibitory effects of miR-338-3p on human neuroblastoma cell progression. Collectively, these data demonstrated that miR-338-3p could suppress cell growth, invasion, and EMT pathway and induce apoptosis in neuroblastoma cells by targeting MMP-2. MiR-338-3p sponged MMP-2 to regulate the PI3K/AKT pathway in human neuroblastoma cells.
Insights
MicroRNA-338-3p (miR-338-3p) suppresses neuroblastoma progression by targeting matrix metalloproteinase-2 (MMP-2). Upregulated MMP-2 and downregulated miR-338-3p correlate with metastasis, with miR-338-3p inhibiting cell growth and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Neuroblastoma is a pediatric cancer with complex regulatory mechanisms.
- MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
- Matrix metalloproteinase-2 (MMP-2) is implicated in tumor invasion and metastasis.
Purpose of the Study:
- To investigate the regulatory relationship between miR-338-3p and MMP-2 in neuroblastoma.
- To elucidate the functional impact of miR-338-3p and MMP-2 on neuroblastoma cell behavior.
Main Methods:
- Bioinformatic prediction of miR-338-3p and MMP-2 interactions.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) for gene expression analysis.
- Cell Counting Kit-8, flow cytometry, and Transwell assays for proliferation, apoptosis, and invasion assessments.
Main Results:
- miR-338-3p was downregulated, while MMP-2 was upregulated in metastatic neuroblastoma tissues and cells.
- Overexpression of miR-338-3p inhibited neuroblastoma cell proliferation, invasion, and epithelial-mesenchymal transition (EMT), while promoting apoptosis.
- Knockdown of MMP-2 mimicked the effects of miR-338-3p.
- MMP-2 was identified as a direct target of miR-338-3p, and its overexpression reversed the inhibitory effects of miR-338-3p.
Conclusions:
- miR-338-3p acts as a tumor suppressor in neuroblastoma by directly targeting MMP-2.
- The miR-338-3p/MMP-2 axis regulates neuroblastoma cell growth, invasion, EMT, and apoptosis, potentially through the PI3K/AKT pathway.
More Related Videos
09:37Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
06:54Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
