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Published on: March 30, 2019
Insulin-like growth factor binding protein-4 inhibits cell growth, migration and invasion, and downregulates COX-2
Weiwen Li1, Debin Sun1, Zhuqing Lv1
1Department of Pulmonary Medicine, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui Hospital of Zhejiang University, Lishui, 323000, China.
Abstract:
Insulin-like growth factor binding protein 4 (IGFBP-4) and cyclooxygenase2 (COX-2) are associated with tumor inflammatory microenvironment which is involved in the progression of tumor. However, it is unclear that the roles of IGFBP-4 in lung cancer and the effects of IGFBP-4 on COX-2 expression. In this study, we showed that IGFBP-4 could decrease COX-2 production in lung cancer A549 cells. IGFBP-4 expression was significantly lower but COX-2 expression was higher in lung cancer tissues compared to matched adjacent normal tissues. In addition, IGFBP-4 could inhibit lung cancer cell proliferation, migration and invasion, and suppress the phosphorylation of PI3 K/AKT, ERK, and CREB. These results indicate that IGFBP-4 has potent antitumor effects in non-small cell lung cancer cells.
Insights
Insulin-like growth factor binding protein 4 (IGFBP-4) exhibits antitumor effects in lung cancer. Lower IGFBP-4 levels correlate with higher cyclooxygenase-2 (COX-2) expression and increased tumor progression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Tumor inflammatory microenvironment, involving Insulin-like Growth Factor Binding Protein 4 (IGFBP-4) and Cyclooxygenase-2 (COX-2), influences tumor progression.
- The specific roles of IGFBP-4 in lung cancer and its impact on COX-2 expression remain largely uncharacterized.
Purpose of the Study:
- To investigate the role of IGFBP-4 in lung cancer progression.
- To determine the effect of IGFBP-4 on COX-2 expression in lung cancer cells.
Main Methods:
- Analysis of IGFBP-4 and COX-2 expression in lung cancer tissues and adjacent normal tissues.
- Assessment of IGFBP-4's effects on lung cancer cell proliferation, migration, and invasion in vitro.
- Evaluation of IGFBP-4's impact on signaling pathways including PI3K/AKT, ERK, and CREB phosphorylation.
Main Results:
- IGFBP-4 expression was significantly lower, while COX-2 expression was higher in lung cancer tissues compared to normal tissues.
- IGFBP-4 suppressed lung cancer cell proliferation, migration, and invasion.
- IGFBP-4 inhibited the phosphorylation of PI3K/AKT, ERK, and CREB signaling pathways.
Conclusions:
- IGFBP-4 demonstrates significant antitumor effects in non-small cell lung cancer (NSCLC).
- IGFBP-4 downregulates COX-2 production and inhibits key pro-tumorigenic signaling pathways in lung cancer cells.
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