Endogenous SARI exerts oncogenic functions in human K562 leukemia cells by targeting the PI3K/Akt/mTOR and NF-κB signaling pathways.

Abstract

Suppressor of activator protein-1, regulated by interferon (SARI), is a novel basic leucine zipper containing type I IFN-inducible early response protein that plays an important regulatory role in a wide variety of tumors, including leukemia. However, the functional role of SARI in myeloid leukemia is not thoroughly understood. In this study, we discovered that knock-down of SARI expression suppressed cell growth and colony formation, inhibited invasion, enhanced imatinib (STI571)-mediated apoptosis, and induced G0/G1 and G2/M arrest in human K562 myeloid leukemia cells. Moreover, using immunoblotting, we provide evidence that silencing of SARI resulted in declined expression of cyclinD1 and cyclinA2, as well as down-regulation of mTOR, c-myc p-mTOR, p-PI3K (p85), p-Akt, p70-S6K, p-p70-S6K and NF-κB (p65) that involved in the PI3K/Akt/mTOR and NF-κB signaling pathways. Taken together, our results demonstrate that SARI functions as an oncogenic role in K562 myeloid leukemia cells through regulating the PI3K/Akt/mTOR and NF-κB signaling pathways.

• Authors: Xiaodan Fu, Zhaolei Cui, Yan Chen, Yongjin Tang, Chuncai Wu, Jianping Xu, Donghong Lin
• Journal: International journal of clinical and experimental pathology (Int J Clin Exp Pathol) Vol. 11 Issue 1 Pg. 179-188 ( 2018) ISSN: 1936-2625 [Electronic] United States
• PMID: 31938099 (Publication Type: Journal Article)
• Copyright: IJCEP Copyright © 2018.