E3 Ubiquitin ligase RNF126 regulates the progression of tongue cancer

Abstract

This study aims to analyze the role of RNF126 in the oncogenesis of tongue cancer. The cell proliferation and viability of human tongue cancer cells, SCC25 and SCC9 cells, were determined by cell counting and MTT assay, respectively. The effect of RNF126 on regulating AKT signaling pathway was analyzed through western blotting. The transplantation tumor model of nude mice was used to evaluate the tumorigenecity of RNF126. Knockdown of RNF126 inhibited the proliferation and viability of SCC9 and SCC25 cells. Inhibition of RNF126 also decreased the activity of AKT1 as well as its downstream molecules. Furthermore, RNF126 regulated the tumor volume on mice model. These data suggested that RNF126 might be related to the progression of tongue cancer through regulating AKT signaling pathway.

Keywords: Cell proliferation; E3 ubiquitin ligase; RNF126; tongue cancer; tumor burden.

Figure 1

RNF126 regulates the proliferation and viability of SCC9 and SCC25 cells. Left: Knockdown of RNF126 inhibited the cell growth of SCC9 and SCC25 cells at day 2. Right: Knockdown of RNF126 inhibited the cell viability of SCC9 and SCC25 cells since day 2. *P < 0.05, **P < 0.01.

Figure 2

RNF126 participated in the AKT signaling pathway. (A) The transition of AKT1 into the nucleus decreased when RNF126 was knockeddown. (B) RNF126 regulated the phosphorylation of AKT1.

Figure 3

Knockdown of RNF126 alleviated the tumor burden of transplantation tumor model of nude mice which was originated from the SCC9 cells (left) and SCC25 cells (right).