DNA methylation-regulated LINC02587 inhibits ferroptosis and promotes the progression of glioma cells through the CoQ-FSP1 pathway

Author:

Wang Zhengang,Cui Yang,Wang Fanchen,Xu Lixia,Yan Yan,Tong Xiaoguang,Yan Hua

Abstract

Abstract Background Long noncoding RNAs (lncRNAs) are considered key players in the formation and development of tumors. Herein, Gene Expression Profiling Interactive Analysis (GEPIA) was employed as a bioinformatics technology. LINC02587 is differentially expressed in bladder urothelial cancer, glioblastoma, lung adenocarcinoma, lung SCC, melanoma, and other tumor tissue and cells. However, its impact on the emergence of glioma and its mechanism is remaining elusive. Methods Some of the in vitro assays employed in this study were the CCK-8 / Annexin-V / Transwell assays, colony formation, and wound healing, together with Western blot (WB) evaluation. MSP / BSP assays were employed for assessing the CpG island’s methylation status in the LINC02587 promoter. Through transcriptome, ferroptosis-related experiments, and WB evaluation, it was confirmed that LINC02587 is correlated with the regulation of ferroptosis in tumor cells, and CoQ-Fsp1 is one of its regulatory pathways. Moreover, the underlined in-vitro results were further validated by in-vivo studies. Results The current study shows that the promoter sequence of LINC02587 is regulated by methylation. The silencing of LINC02587 can inhibit cellular proliferative, migrative, and invasive properties, and induce ferroptosis within gliomas through the CoQ-FSP1 pathway. Conclusions LINC02587 is likely to be a novel drug target in treating glioma.

Funder

Project of Weifang Municipal Health Commission

Langfang Science and Technology Plan Support Project

The Tianjin Key Medical Discipline (Specialty) Construction Project

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Oncology

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