PHF12 regulates HDAC1 to promote tumorigenesis via EGFR/AKT signaling pathway in non-small cell lung cancer

• DOI: 10.1186/s12967-024-05488-x
• Publication Date: 2024-07-29T14:03:52Z
• Authors: Yiru Kong; Rongrong Jiang; Hui Zhou; Mengxi Ge; Hao Lin; Yu Wang; Rongrong Yao; Qing Wang; Xiaohua Liang; Jing Li; Xinli Zhou
• Keywords: HDAC1

Abstract Background Lung cancer stands as the second most prevalent malignant neoplasm worldwide. Addressing underlying mechanisms propelling progression of non-small cell lung is paramount importance. In this study, we have elucidated pivotal role PHF12 in context. Materials and methods We harnessed clinical tissue samples lines to discern expression pattern PHF12. vitro assays probing proliferation were conducted substantiate functional impact Furthermore, an vivo Xenograft model was employed dissect Employing ChIP qRT-PCR, delved into intricate binding dynamics between HDAC1. Mechanistic insights PHF12-HDAC1 axis pursued via RNA-seq GSEA analyses. Results Notably, exhibited a substantial upregulation within tumor tissue, concomitant with its correlation The trilogy assays, transwell collectively underscored promoting influence on proliferation, both vivo. assay unveiled transcriptional regulatory governing HDAC1 expression. This extended mRNA protein levels. promotes NSCLC through regulating HDCA1 Intriguingly, rescue function post knockdown achievable overexpression. Additionally, our findings capacity activate EGFR/AKT signaling pathway, thereby further corroborating significance progression. Conclusion Our study identified oncogenic migration for first time. transcriptionally regulate pathway may serve important target therapy.