ArticleOncogene2026
N6-methyladenosine-mediated upregulation of PAICS promotes lung-adenocarcinoma metastasis via the integrin-FAK signaling.
Article in Oncogene, 2026. 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 adenocarcinoma (LUAD) is the most common type of lung cancer, often diagnosed in the advanced stage of diffuse metastasis, highly aggressive and rapidly fatal, lacking early diagnostic markers and effective therapeutic targets. Enzyme phosphoribosylaminoimidazole carboxylase/phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS) is an important bifunctional enzyme in purine de novo synthesis, and rapidly dividing cancer cells are heavily dependent on de novo synthesis of the adenine and guanine pathways. PAICS has been found to be highly expressed in a variety of cancers and has been shown to promote cancer proliferation or metastasis. However, the specific mechanism of action of PAICS in LUAD is unknown. Our study revealed that PAICS mRNA and protein levels were significantly increased in LUAD tumor tissues compared to adjacent normal tissues. Bioinformatics analysis showed that high PAICS expression was associated with LUAD metastasis and could be used as a factor for diagnosis and assessment of prognosis in LUAD patients. PAICS knockdown suppressed tumor cell migration and invasion, whereas overexpression enhanced these phenotypes. Mechanistically, PAICS promotes tumor metastasis by activating the Focal Adhesion Kinase (FAK) signaling through regulating the expression of Integrin α10 (ITGA10). FAK inhibitor Defactinib (VS6063) successfully inhibited PAICS overexpression-induced lung metastasis in vivo. In addition, we found that the high expression of PAICS in LUAD was regulated by m
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