ArticleApplied biochemistry and biotechnology2026
DUSP7 Overexpression Suppresses Lung Adenocarcinoma Cell Proliferation, Invasion, and M2 Macrophage Polarization Through JAK2/STAT3 Pathway Inhibition.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
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.
Indexed as
Identifiers
41484728What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.