ANP32B knockdown suppresses glioma malignant progression via the E2F1 pathway

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Background: Glioma is an aggressive primary brain malignancy with a poor prognosis. This study aimed to investigate the mechanism by which ANP32B drives glioma progression, focusing on its regulation of E2F1-mediated cell cycle and malignant phenotypes. Methods: Bioinformatics analysis was first performed to verify the differential expression of ANP32B mRNA in glioma tissues and normal brain tissues. A series of in vitro functional experiments including CCK-8 assay, colony formation assay and wound healing assay were carried out to evaluate the changes in proliferation, colony formation and migration capabilities of LN229 and U87MG glioma cell lines after ANP32B knockdown. Meanwhile, in vivo tumorigenesis experiments were conducted to confirm the regulatory effect of ANP32B downregulation on glioma growth. In addition, RNA sequencing technology combined with functional rescue experiments was applied to screen, analyze, and validate the downstream signaling pathways mediated by ANP32B in glioma cells. Results: Bioinformatics results demonstrated that ANP32B expression was significantly upregulated in glioma tumor tissues compared with normal brain tissues. Cellular functional experiments showed that knockdown of ANP32B markedly weakened the proliferative, migratory and colony-forming abilities of LN229 and U87MG cells, and induced G1-phase cell cycle arrest. Moreover, in vivo experimental data confirmed that ANP32B silencing could effectively suppress the tumorigenic growth of glioma cells. RNA-seq and rescue validation further revealed that ANP32B knockdown suppresses malignant progression strictly by targeting and down-regulating E2F1. Conclusion: These findings demonstrate that downregulating ANP32B restrains glioma progression via the E2F1 axis, providing an experimental basis for evaluating ANP32B as a candidate prognostic biomarker and potential therapeutic target.

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