Downregulation of METTL6 mitigates cell progression, migration, invasion and adhesion in hepatocellular carcinoma by inhibiting cell adhesion molecules

• DOI: 10.3892/ijo.2021.5294
• Publication Date: 2021-12-14T08:08:29Z
• Authors: Amina Bolatkan; Ken Asada; Syuzo Kaneko; Kruthi Suvarna; Noriko Ikawa; Hidenori Machino; Masaaki Komatsu; Shuichiro Shiina; Ryuji Hamamoto
• Keywords: Chromatin immunoprecipitation

RNA modifications have attracted increasing interest in recent years because they been frequently implicated various human diseases, including cancer, highlighting the importance of dynamic post‑transcriptional modifications. Methyltransferase‑like 6 (METTL6) is a member methyltransferase family that has identified many cancers; however, little known about its specific role or mechanism action. In present study, we aimed to study expression levels and functional METTL6 hepatocellular carcinoma (HCC), further investigate relevant pathways. To this end, systematically conducted bioinformatics analysis HCC using gene data clinical information from publicly available dataset. The mRNA <em>METTL6</em> were significantly upregulated tumor tissues compared adjacent non‑tumor strongly associated with poorer survival outcomes patients HCC. CRISPR/Cas9‑mediated knockout cell lines remarkably inhibited colony formation, proliferation, migration, invasion attachment ability. sequencing demonstrated suppressed adhesion‑related genes. However, chromatin immunoprecipitation results revealed no significant differences enhancer activities between cells, which suggests may regulate genes post‑transcriptionally. addition, it was for first time localized cytosol as detected by immunofluorescence analysis, indicates plausible location modification mediated METTL6. Our findings provide insight into function cancer suggest possible therapeutic target