ArticleComputational and mathematical methods in medicine2022
TRIM66 Promotes Malignant Progression of Non-Small-Cell Lung Cancer Cells via Targeting MMP9.
Article in Computational and mathematical methods in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 7 citations in OpenAlex.
- Bioinformatics-Based Discovery of Therapeutic Targets in Cadmium-Induced Lung Adenocarcinoma: The Role of Oxyresveratrol.Biological trace element research · 2026Article
- Genome-wide association study of lung function decline using elastic-net regression: a prospective analysis in Korean cohort.Human genomics · 2025Article
- Unraveling the molecular-pathological characteristics and cellular complexity of the tumor immune microenvironment in metastatic non-small cell lung cancer.Cell communication and signaling : CCS · 2025Review
- Integrating network pharmacology and molecular modeling to decipher the anti-esophageal squamous cell carcinoma mechanisms of Bidens pilosa L.Discover oncology · 2025Article
- [Research Progress on the Mechanism and Diagnostic Markers of Bone Metastasis in Small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Enhancing the revelation of key genes and interaction networks in non-small cell lung cancer with major depressive disorder: A bioinformatics analysis.Health science reports · 2024Article
- Diagnostic value of matrix metalloproteinases 2, 7 and 9 in urine for early detection of colorectal cancer.World journal of gastrointestinal surgery · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer has a higher incidence and mortality rate than other cancers, and over 80% of lung cancer cases were classified as non-small-cell lung cancer (NSCLC). TRIM66 is one of the crucial members of TRIM, which has a deep connection with the behavior of various malignant tumors. But it remains uncertain regarding its exact function and underlying mechanism in NSCLC. In our study, qRT-PCR and Western blot were employed to validate that TRIM66 was overexpressed in NSCLC. The migration, invasion, and epithelial-mesenchymal transformation (EMT) progression of NSCLC cells were determined by Western blotting and Transwell experiments after knocking down TRIM66, and it was found that knockdown TRIM66 inhibited the migration, invasion, and EMT processes of NSCLC cells. Next, the binding relationship between TRIM66 and MMP9 was verified by Co-IP assay. After determining the interaction between them, rescue assays showed that overexpression of MMP9 was capable to promote the migration, invasion, and EMT of NSCLC cells. However, the transfection of si-TRIM66 could reverse this facilitating effectiveness. To sum up, we concluded that by targeting MMP9, TRIM66 could exert a cancer-promoting role in the progression of NSCLC cells.
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