Long noncoding RNA LINC01842 enhances disulfidptosis resistance and promotes glioma progression via IQGAP1

Abstract

Abstract Background: Long non-coding RNA (lncRNA) is widely present in cells and is demonstrated to play vital roles in the development and progression of glioma. However, the biological roles and function mechanisms of LINC01842 in glioma are not yet clear. This study aims to elucidate the potential role of LINC01842 in glioma, specifically its association with disulfidptosis. Methods: We obtained sequencing data from The Cancer Gene Atlas (TCGA). Correction analysis was applied to select disulfidptosis-related lncRNAs (DRLs). Prognosis-associated DRLs were identified by least absolute shrinkage and selection operator (LASSO) and support vector machine (SVM). Receiver operating characteristic (ROC) curve and multivariate Cox regression analyses were used to screen our target gene LINC01842. Subsequently, expression of LINC01842, IQGAP1and SLC7A11 in glioma cell lines was detected by real-time quantitative polymerase chain reaction (qPCR). Additionally, CCK8 experiments and wound healing assays were performed to assess cell viability, migration, and invasion. Finally, online database predictions were used to validate the drug sensitivity of glioma. Results: LINC01842 was more highly expressed in high-grade gliomas, and glioma patients with high expression level of LINC01842 had poorer survival. Additionally, tumor cells with high expression of LINC01842 exhibited stronger tumor characteristics, such as migratory and invasive abilities, as well as tolerance to disulfidptosis. Furthermore, strong binding between LINC01842 and the disulfidptosis-related gene IQGAP1 could be predicted, and their expression levels were positively correlated. Ultimately, drug sensitivity analysis suggested glioma patients with high expression level of LINC01842 were sensitive to eight drugs. Conclusion: High expression of LINC01842 is associated with poor prognosis in glioma patients. By interacting with IQGAP1, the resistance to disulfidptosis of LINC0182 was stronger in glioma, which promotes the progression of glioma. Eight discovered sensitive drugs provided important clues for personalized treatment of glioma.