Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 May 21;11:668424. doi: 10.3389/fonc.2021.668424

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2021 Cheng, Yu, He, Li, Xu, Xue, Shi, Chen, Li, Hong and Xiao

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

SS inhibits the AKT/mTOR/4E-BP3 axis in a ROS-dependent manner. (A) Thyroid cancer cells were treated with vehicle control or different concentrations of SS for 6 h, and the protein levels of p-AKT, total AKT, p-mTOR, total mTOR, p-ERK, and total ERK were detected by western blotting. The expression of β-actin was used as a reference. (B) NAC treatment reversed the inhibitory effect of SS on the AKT/mTOR pathway. (C) 4E-BP3 mRNA expression in SS treatment and control groups. (D) The proliferation of WT and 4E-BP3-knockdown cells under normal conditions. (E) Morphological changes, cell viability, and (G) percentage of G0/G1 phase cells in WT and 4E-BP3-knockdown groups after incubation with SS for 24 h. (F) Colony formation capacity of WT and 4E-BP3-knockdown cells after SS treatment. SS, sodium selenite; NAC, N-acetylcysteine. **P < 0.01; ***P < 0.001.