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Updated: Feb 10, 2026

A Permanent Window for Investigating Cancer Metastasis to the Lung
Published on: July 1, 2021
Met is involved in TIGAR-regulated metastasis of non-small-cell lung cancer
Mengqin Shen1,2, Xiaoping Zhao1,2, Li Zhao1,2
1Department of Nuclear Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Abstract:
TIGAR is a p53 target gene that is known to protect cells from ROS-induced apoptosis by promoting the pentose phosphate pathway. The role of TIGAR in tumor cell invasion and metastasis remains elusive. Here we found that downregulation of TIGAR reduced the invasion and metastasis of NSCLC cells in vitro and in vivo. Immunohistochemical analysis of 72 NSCLC patients showed that TIGAR and Met protein expression was positively correlated with late stages of lung cancer. Besides, patients with high co-expression of TIGAR and Met presented a significantly worse survival. In addition, we found that Met signaling pathway is involved in TIGAR-induced invasion and metastasis. Our study indicates that TIGAR/Met pathway may be a novel target for NSCLC therapy. It is necessary to evaluate the expression of TIGAR before Met inhibitors are used for NSCLC treatment.
Insights
Downregulation of TIGAR (TP53-inducible glycolysis regulator) inhibits non-small cell lung cancer (NSCLC) invasion and metastasis. The TIGAR/Met pathway presents a potential therapeutic target for NSCLC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- TIGAR (TP53-inducible glycolysis regulator) is a p53 target gene.
- It protects cells from reactive oxygen species (ROS)-induced apoptosis by promoting the pentose phosphate pathway.
- The function of TIGAR in tumor cell invasion and metastasis is not well understood.
Purpose of the Study:
- To investigate the role of TIGAR in non-small cell lung cancer (NSCLC) cell invasion and metastasis.
- To explore the correlation between TIGAR expression and clinical outcomes in NSCLC patients.
- To elucidate the underlying molecular mechanisms involving the Met signaling pathway.
Main Methods:
- In vitro and in vivo assays were used to assess the effects of TIGAR downregulation on NSCLC cell invasion and metastasis.
- Immunohistochemical analysis was performed on 72 NSCLC patient samples.
- Correlation analysis and survival analysis were conducted to evaluate the clinical significance of TIGAR and Met expression.
Main Results:
- Downregulation of TIGAR significantly reduced NSCLC cell invasion and metastasis both in vitro and in vivo.
- TIGAR and Met protein expression levels were positively correlated with advanced stages of lung cancer.
- High co-expression of TIGAR and Met was associated with significantly worse patient survival.
- The Met signaling pathway was found to be involved in TIGAR-mediated invasion and metastasis.
Conclusions:
- The TIGAR/Met pathway represents a novel therapeutic target for NSCLC.
- Evaluating TIGAR expression is crucial before administering Met inhibitors for NSCLC treatment.
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