The effect of Epitranscriptomic writer (METTL3) silencing on Hepatocellular carcinoma cell line

Abstract

Worldwide, HCC is the sixth most common malignancy and the third most common cause of cancer-related death. RNA epigenetics becomes a hot topic in recent years. Among more than a hundred different RNA modifications, m6A is the most abundant modification. m6A is involved in regulating mRNA stability, splicing, and translation. However, the implications of m6A modification in human carcinogenesis remain poorly understood. METTL3 is a major RNA methyltransferase implicated in mRNA biogenesis, decay, and translation control through m6A modification. We aimed to target METTL3 in HepG2 cell lines by siRNA (small interfering RNA), and then evaluated the effect of this interference on viability and proliferative activity of HepG2 cells. Material and methods Using HepG2 cell lines, METTL3 was targeted using siRNA. The viability of HepG2 was conducted by Trypan blue exclusion test. The cell proliferation was tested by CellTiter 96® AQueous One Solution Cell Proliferation Assay. Results viable cell number and viability percent were significantly reduced in HepG2 cells transfected with siMETTL3 compared to mock cell lines (treated with transfection reagent only) (p<0.05). The active proliferative cell count was lower in cells transfected with siMETTL3 than mock cells (p<0.05). Conclusions Knockdown of METTL3 in HepG2 cell lines successively reduced cell viability and active proliferative cell count. METTL3 may be involved in liver tumorigenesis and its targeting may be of therapeutic benefit.