ArticleMolecular medicine reports2019
MT1‑MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E‑cadherin.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer.Molecular therapy. Nucleic acids · 2026Article
- Potential target within the tumor microenvironment - MT1-MMP.Frontiers in immunology · 2025Review
- Aaptamine Alters Vimentin Expression and Migration Capability of Triple-Negative Breast Cancer Cells.Journal of experimental pharmacology · 2025Article
- Intermediate Filaments in Breast Cancer Progression, and Potential Biomarker for Cancer Therapy: A Narrative Review.Breast cancer (Dove Medical Press) · 2024Review
- Review
- MT1-MMP as a Key Regulator of Metastasis.Cells · 2023Review
- Proteolytic Landscapes in Gastric Pathology and Cancerogenesis.International journal of molecular sciences · 2022Review
- TIMP-2 regulates proliferation, invasion and STAT3-mediated cancer stem cell-dependent chemoresistance in ovarian cancer cells.BMC cancer · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to explore the possible effects of membrane‑type 1 matrix metalloproteinase (MT1‑MMP) on gastric carcinoma cells proliferation and invasion. Immunohistochemistry analysis was conducted to measure MT1‑MMP expression level in 15 patients with gastric carcinoma. Subsequently, recombinant short hairpin RNA (shRNA) vectors targeting MT1‑MMP were constructed to silence the expression of MT1‑MMP in gastric carcinoma cells. Then, the inhibitive efficiency was verified via reverse transcription quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. The effects of MT1‑MMP silencing on cell proliferation and invasion were detected through Cell Counting Kit‑8 test and Transwell assays. The expression levels of vimentin and epithelial cadherin (E‑cadherin) were detected by RT‑qPCR. The immunohistochemistry analysis results revealed that MT1‑MMP expression in gastric carcinoma tissues was markedly overexpressed compared with non‑cancerous adjacent tissues. The MT1‑MMP expression level in cancer‑derived cell line AGS cells was also significantly increased compared with that in non‑cancer‑derived GES‑1 cells. In addition, the MT1‑MMP expression level in AGS cells was significantly decreased via shRNA transfection. Cell proliferation and invasion were markedly inhibited following knockdown of MT1‑MMP level in AGS cells. These inhibitory effects were associated with the decreased expression of vimentin and increased expression of E‑cadherin. MT1‑MMP was overexpressed in gastric carcinoma cells, and silencing of MT1‑MMP inhibited the proliferation and invasion of cells via regulating the expression of vimentin and E‑cadherin.
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