Related Experiment Video
Updated: Mar 17, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
miR-338 inhibits the metastasis of lung cancer by targeting integrin β3
Xiao Chen1, Li Wei2, Song Zhao1
1Department of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450003, P.R. China.
Abstract:
miR-338 as an intronic miRNA from apoptosis-associated tyrosine kinase (AATK) is involved in tumor proliferation and apoptosis, but its function and regulatory mechanism in lung cancer is still obscure. In the present study, we found that miR-338 was strikingly downregulated in 115 lung cancer tissues and 5 lung cancer cell lines. Besides, low level of miR-338 was associated with tumor emboli, TNM stage, tumor recurrence and poor survival. Regaining the expression of miR-338 in lung cancer cell lines significantly impaired cellular adhesion, migration, invasion and lung tumor formation in nude mice. Furthermore, we also identified a metastasis related protein, integrin β3 (ITGB3), as a novel target gene of miR-338. Our results reveal a new regulatory mechanism of miR-338 which may help us better understand the metastasis of lung cancer.
Insights
MicroRNA-338 (miR-338) is downregulated in lung cancer, suppressing tumor metastasis and formation. Its restoration inhibits cell adhesion, migration, and invasion, identifying integrin β3 (ITGB3) as a key target.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- MicroRNA-338 (miR-338), an intronic miRNA from apoptosis-associated tyrosine kinase (AATK), is implicated in tumor proliferation and apoptosis.
- Its specific role and regulatory mechanisms in lung cancer remain largely unknown.
Purpose of the Study:
- To investigate the function and regulatory mechanism of miR-338 in lung cancer.
- To determine the association of miR-338 expression with clinical features and patient outcomes.
Main Methods:
- Analysis of miR-338 expression in lung cancer tissues and cell lines.
- In vitro functional assays (adhesion, migration, invasion) and in vivo tumor formation studies in nude mice.
- Identification of miR-338 target genes using molecular biology techniques.
Main Results:
- miR-338 was significantly downregulated in 115 lung cancer tissues and 5 cell lines.
- Low miR-338 levels correlated with tumor emboli, advanced TNM stage, recurrence, and poor survival.
- Restoring miR-338 impaired lung cancer cell adhesion, migration, invasion, and in vivo tumor formation.
- Integrin β3 (ITGB3) was identified as a novel direct target of miR-338.
Conclusions:
- miR-338 acts as a tumor suppressor in lung cancer, inhibiting metastasis.
- The miR-338/ITGB3 axis represents a new regulatory mechanism in lung cancer progression.
- miR-338 may serve as a potential therapeutic target for lung cancer treatment.
Related Concept Videos
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Integrins
Some ECM proteins assemble into a basement membrane to which the remaining components adhere. Proteoglycans typically form the bulk of the ECM while fibrous proteins, like collagen,...
MicroRNAs
MicroRNAs
Activation of Integrins
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...

