<i>LINC01783</i> Promotes Glioma Tumorigenesis by Enhancing <i>GATA3</i> Expression Through <scp>CBP</scp>‐Mediated <scp>H3K27</scp> Acetylation to Suppress <i>PTEN</i> Expression

This study aims to investigate for the first time the functional role and underlying mechanisms of long intergenic non-coding RNA LINC01783 in glioma progression and development. Glioma tumor tissues of different grades, normal brain tissues, and glioma cell lines were used. Differential expression of LINC01783 and other transcripts was validated in glioma tissues and cell lines using RT-qPCR and western blot assays. Furthermore, the biological functions of LINC01783 were assessed both in vitro and in vivo using various functional assays. We found that LINC01783 was highly expressed in glioma tumor tissues, especially the high-grade glioma samples and glioma cell lines, with its elevated expression associated with glioma cell stemness and progression, while its knockdown had the opposite effects. Functionally, LINC01783 targeted PTEN, and PTEN overexpression significantly suppressed glioma cell proliferation and stemness characteristics, while promoting apoptosis. Mechanistic studies confirmed that GATA3 binds to the PTEN promoter and transcriptionally represses PTEN expression, contributing to glioma progression. Additionally, our findings showed that LINC01783 enhances GATA3 expression by facilitating H3K27 acetylation through its interaction with CBP, which mediates the acetylation process at the GATA3 locus, thereby promoting tumorigenesis in glioma. Collectively, our study provides novel evidence that LINC01783 functions as a tumor promoter and contributes to glioma tumorigenesis by enhancing GATA3 expression via CBP-mediated H3K27 acetylation, thereby suppressing PTEN expression.