EP300 regulates the SLC16A1-AS1-AS1/TCF3 axis to promote lung cancer malignancies through the Wnt signaling pathway

• DOI: 10.1016/j.heliyon.2024.e27727
• Publication Date: 2024-03-07T08:47:12Z
• Authors: Yunhao Sun; Jian Sun; Kaijun Ying; Jinjin Chen; Tingting Chen; Leilei Tao; Weigang Bian; Limin Qiu
• Keywords: EP300; Social sciences (General); H1-99; 0301 basic medicine; Q1-390; 03 medical and health sciences; Science (General); SLC16A1-AS1; Wnt/β-catenin pathway; Lung cancer; TCF3; Research Article

ObjectiveTo investigate the regulatory mechanism of EP300 in interaction between SLC16A1-AS1 and TCF3 to activate Wnt pathway, thereby promoting malignant progression lung cancer.MethodsIn cancer cell lines, was knocked down, impact this knockdown on cells assessed through clonogenic assays, Transwell apoptosis experiments. The relationship investigated bioinformatic analysis ChIP expression 56 paired tissues examined using RT-qPCR, their correlation analyzed. explored CoIP Activation Wnt/β-catenin pathway by detecting accumulation β-catenin nucleus Western blotting. role regulating effect SLC16A1-AS1/TCF3-mediated signaling validated vitro vivo experiments.ResultsSLC16A1-AS1 is highly expressed regulates its progression. mediates histone modifications promoter, thus controlling expression. exhibits specific interactions with TCF3, SLC16A1-AS1/TCF3 complex activates pathway. plays a critical progression.ConclusionEP300 influencing cancer.