ArticleClinical and experimental medicine2025
GBP2 regulates lung cancer progression through STAT1 and impacts glycolysis.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Lung cancer remains one of the leading causes of cancer-related mortality worldwide, highlighting the need for novel biomarkers and therapeutic targets. In this study, we sought to assess the role of guanylate-binding protein 2 (GBP2) in lung cancer and its potential as a prognostic marker. Immunohistochemical analysis on tissue microarrays revealed significantly elevated GBP2 expression in lung cancer tissues compared to non-neoplastic adjacent tissues, correlating with advanced tumor stages, lymph node metastasis, and poor patient survival. In vitro experiments using GBP2 knockdown in NCI-H1299 and A549 lung cancer cell lines showed reduced cell proliferation, increased apoptosis, and inhibited cell migration, alongside cell cycle arrest at the G2 phase. In vivo studies confirmed that GBP2 knockdown reduces tumor growth in mouse xenograft models. Mechanistically, GBP2 influences lung cancer progression by regulating STAT1, as its knockdown resulted in decreased STAT1 expression. Furthermore, GBP2 was found to modulate glycolytic metabolism in cancer cells, reducing the expression of key glycolytic enzymes and suppressing metabolic activities essential for cancer cell survival and proliferation. In conclusion, GBP2 emerges as a critical factor in lung cancer progression, influencing both cellular proliferation and metabolic processes, and represents a promising therapeutic target.
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