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Analytical Cellular Pathology
Volume 2019, Article ID 1575031, 9 pages
https://doi.org/10.1155/2019/1575031
Research Article

ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells

1Department of Experiment Center, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, China
2Department of Pharmacy, Changhai Hospital of Shanghai, 200433, China
3Department of Clinical Laboratory Medicine, Shanghai Tenth People’s Hospital of Tongji University, Shanghai 200072, China
4People’s Hospital of Pudong New District of Shanghai City, No. 490, South Chuanhuan Road, Shanghai 201200, China
5Department of Pharmacy, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, China

Correspondence should be addressed to Kai Li; moc.621@81447iakil and Yanfeng Xu; moc.621@ux_fy

Hui Du and Yun Le contributed equally to this work.

Received 21 July 2018; Revised 12 October 2018; Accepted 20 October 2018; Published 10 February 2019

Academic Editor: Consuelo Amantini

Copyright © 2019 Hui Du et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) is overexpressed and has an oncogenic role in hepatocellular carcinoma (HCC). Interleukin enhancer binding factor 2 (ILF2) has become research hotspot in liver cancer recently. However, it is still unclear whether and how CREB and ILF2 interact with each other. And how this interaction exerts its role in occurrence and development of liver cancer is still unclear. Here, we found that ILF2 directly bound with CREB, and this binding was essential for the malignant phenotypes of liver cancer cells. Moreover, we found that ILF2 acted as one of the upstream proteins of CREB and promoted CREB only in the protein level, whereas ILF2 expression was not regulated by CREB. Mechanistically, ILF2 bound to the pKID domain of CREB and stimulated its phosphorylation at Ser133. Taken together, our study finds a novel interaction between CREB and ILF2 in liver cancer, and this interaction might play a role in the diagnosis and remedy of liver cancer.