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<p>Dual-specificity protein phosphatase 7 (DUSP7) is a protein coding gene that has shown dysregulated expression in multiple types of human cancers, including lung adenocarcinoma. However, its specific role in lung adenocarcinoma pathogenesis remains poorly understood. The current study aimed to characterize the expression pattern and functional role of DUSP7 in lung adenocarcinoma. We analyzed data from the Gene Expression Profiling Interactive Analysis database. Additionally, we examined the expression levels of DUSP7 in lung adenocarcinoma tissues and cell lines, and evaluated the impact of DUSP7 overexpression on cellular functions in vitro and tumor growth in a mouse model of lung adenocarcinoma. DUSP7 showed significant downregulation in lung adenocarcinoma tissues and cell lines compared to normal controls. Low expression of DUSP7 was associated with poor survival outcomes in patients with lung adenocarcinoma. Forced DUSP7 overexpression significantly inhibited the proliferation and invasion of lung adenocarcinoma cells as well as the M2 macrophage polarization induced by lung adenocarcinoma cells in co-culture. Furthermore, the effects of DUSP7 overexpression were reversed by a JAK2/STAT3 inhibitor. DUSP7 overexpression significantly reduced tumor growth in a mouse xenograft model, with decreased Ki-67, CD206, and CD163 expression in tumor tissues. DUSP7 functions as a tumor suppressor to inhibit the malignant features of lung adenocarcinoma cells and tumorigenesis in vivo, and its overexpression in cancer cells inhibits M2 macrophage polarization. These findings suggest that DUSP7 represents a promising therapeutic target and prognostic biomarker for lung adenocarcinoma.</p>

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DUSP7 Overexpression Suppresses Lung Adenocarcinoma Cell Proliferation, Invasion, and M2 Macrophage Polarization Through JAK2/STAT3 Pathway Inhibition

  • 期刊论文

  • 发表日期：

    2026年1月3日

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  • Hui Tian,
  • Shanshan Li,
  • Xiuping Gu,
  • Gaofeng Liang,
  • Jinxian He

摘要

Dual-specificity protein phosphatase 7 (DUSP7) is a protein coding gene that has shown dysregulated expression in multiple types of human cancers, including lung adenocarcinoma. However, its specific role in lung adenocarcinoma pathogenesis remains poorly understood. The current study aimed to characterize the expression pattern and functional role of DUSP7 in lung adenocarcinoma. We analyzed data from the Gene Expression Profiling Interactive Analysis database. Additionally, we examined the expression levels of DUSP7 in lung adenocarcinoma tissues and cell lines, and evaluated the impact of DUSP7 overexpression on cellular functions in vitro and tumor growth in a mouse model of lung adenocarcinoma. DUSP7 showed significant downregulation in lung adenocarcinoma tissues and cell lines compared to normal controls. Low expression of DUSP7 was associated with poor survival outcomes in patients with lung adenocarcinoma. Forced DUSP7 overexpression significantly inhibited the proliferation and invasion of lung adenocarcinoma cells as well as the M2 macrophage polarization induced by lung adenocarcinoma cells in co-culture. Furthermore, the effects of DUSP7 overexpression were reversed by a JAK2/STAT3 inhibitor. DUSP7 overexpression significantly reduced tumor growth in a mouse xenograft model, with decreased Ki-67, CD206, and CD163 expression in tumor tissues. DUSP7 functions as a tumor suppressor to inhibit the malignant features of lung adenocarcinoma cells and tumorigenesis in vivo, and its overexpression in cancer cells inhibits M2 macrophage polarization. These findings suggest that DUSP7 represents a promising therapeutic target and prognostic biomarker for lung adenocarcinoma.