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ADAMTS1 induces epithelial-mesenchymal transition pathway in non-small cell lung cancer by regulating TGF-β
Xueqian Hu1, Chunqi Jiang1, Ning Hu2
1Department of Oncology, Ningbo Municipal Hospital of TCM, Affiliated Hospital of Zhejiang Chinese Medical University, Ningbo, China.
Abstract:
Non-small cell lung cancer (NSCLC) accounts for approximately 80% of all lung cancers. Identifying key molecular targets related to the initiation, development, and metastasis of lung cancer is important for its diagnosis and target therapy. The ADAMTS families of multidomain extracellular protease enzymes have been reported to be involved in many physiological processes. In this study, we found that ADAMTS1 was highly expressed in NSCLC tissues, which promoted cell proliferation, migration, invasion, and epithelial to mesenchymal transition (EMT) of NSCLC cells. In the NSCLC tumor metastasis model involving nude mice, overexpression of ADAMTS1 promoted EMT and lung metastasis of tumor cells. Moreover, ADAMTS1 positively regulated TGF-β expression, and TGF-β was highly expressed in NSCLC tumor tissues. si-TGF-β or inhibition of TGF-β expression through the short peptide KTFR on ADAMTS1 protein could reverse the oncogenic effects of ADAMTS1 on lung cancer cells. Taken together, ADAMTS1 functioned as an oncogene in NSCLC cells by promoting TGF-β expression, indicating that ADAMTS1 has important regulatory roles in the progression of NSCLC.
Insights
ADAMTS1 acts as an oncogene in non-small cell lung cancer (NSCLC). It promotes tumor growth, metastasis, and epithelial to mesenchymal transition by increasing TGF-β expression, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Non-small cell lung cancer (NSCLC) is the most common form of lung cancer.
- Identifying molecular targets is crucial for NSCLC diagnosis and therapy.
- ADAMTS family proteases are implicated in various physiological processes.
Purpose of the Study:
- To investigate the role of ADAMTS1 in NSCLC progression.
- To explore the relationship between ADAMTS1, epithelial to mesenchymal transition (EMT), and TGF-β signaling in NSCLC.
Main Methods:
- Analysis of ADAMTS1 expression in NSCLC tissues.
- In vitro studies on NSCLC cell proliferation, migration, and invasion.
- In vivo metastasis models using nude mice.
- Investigation of TGF-β regulation by ADAMTS1.
- Experimental inhibition of TGF-β signaling.
Main Results:
- ADAMTS1 was highly expressed in NSCLC tissues.
- ADAMTS1 overexpression promoted NSCLC cell proliferation, migration, invasion, and EMT.
- ADAMTS1 enhanced tumor cell metastasis in vivo.
- ADAMTS1 positively regulated TGF-β expression, which was also elevated in NSCLC.
- Inhibition of TGF-β reversed the oncogenic effects of ADAMTS1.
Conclusions:
- ADAMTS1 functions as an oncogene in NSCLC.
- ADAMTS1 promotes NSCLC progression and metastasis by upregulating TGF-β.
- ADAMTS1 represents a potential therapeutic target for NSCLC treatment.
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