YTHDF1 promotes the viability and self‑renewal of glioma stem cells by enhancing LINC00900 stability.

Abstract

YTHDF1, an N6‑methyladenosine (m6A)‑binding protein, is significantly upregulated in glioma tissues. The present study investigated the molecular mechanism underlying the regulatory effects of YTHDF1 on the viability, invasion and self‑renewal of glioma stem cells (GSCs). Glioma and normal brain tissues were collected, and reverse transcription‑quantitative PCR and western blotting were used to measure the gene and protein expression levels, respectively. Methylated RNA immunoprecipitation‑PCR was used to assess the m6A modification level of the target gene. Subsequently GSCs were induced, and YTHDF1 and LINC00900 gene regulation was carried out using lentiviral infection. The viability, invasion and self‑renewal of GSCs were assessed by Cell Counting Kit‑8, Transwell and sphere formation assays, respectively. Binding between YTHDF1 and LINC00900 was verified by RNA immunoprecipitation and RNA pull‑down assays. The targeted binding of microRNA (miR)‑1205 to the LINC00900/STAT3 3'‑UTR was verified using a luciferase reporter assay. The results revealed that YTHDF1 and LINC00900 expression levels were significantly upregulated in glioma tissues, and a high m6A modification level in LINC00900 transcripts was detected in glioma tissues. Overexpression of YTHDF1 promoted GSC viability, invasion and self‑renewal, whereas knockdown of YTHDF1 had the opposite effects. In addition, YTHDF1 maintained the stability of LINC00900 and upregulated its expression through binding to it, thereby promoting GSC viability, invasion and self‑renewal. Furthermore, LINC00900 promoted GSC viability, invasion, self‑renewal and tumor growth by regulating the miR‑1205/STAT3 axis. In conclusion, YTHDF1 promotes GSC viability and self‑renewal by regulating the LINC00900/miR‑1205/STAT3 axis.