ArticleFrontiers in genetics2026
FANCD2 knockdown suppresses malignant phenotypes and is associated with caspase/PARP-mediated apoptosis in NCI-H2052 pleural mesothelioma cells.
Article in Frontiers in genetics, 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
Background: Malignant pleural mesothelioma (PM) is a highly aggressive thoracic malignancy with an extremely poor prognosis and limited effective therapeutic strategies, representing a critical unmet clinical need. Fanconi anemia complementation group D2 (FANCD2) is a critical effector of the cellular DNA damage response system and plays a central role in maintaining genomic integrity. While the genoprotective functions of Methods: Comprehensive bioinformatics analyses were performed based on public transcriptomic data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to profile Results: Bioinformatics results demonstrated that Conclusion: In summary, FANCD2 may contribute to PM progression by supporting malignant phenotypes and limiting apoptosis. FANCD2 restoration and caspase inhibition partially reversed the growth suppression and apoptosis induced by FANCD2 knockdown, supporting the involvement of caspase-dependent apoptotic signaling. In addition, FANCD2 expression was positively associated with the computationally estimated proportion of M2 macrophages, suggesting that FANCD2 may represent an exploratory prognostic marker and a candidate therapeutic target for further investigation in PM.
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