Acta Biochim Biophys Sin (Shanghai). 2018 Sep 1;50(9):880-887. doi: 10.1093/abbs/gmy085.
Zhang P1, Ji D1, Hu X2, Ni H3, Ma W1, Zhang X1, Liao S4, Zeng Z4, Zhao Y1,5, Zhou H2.
Author Information
1Cyrus Tang Hematology Center, Soochow University, Suzhou, China.
2Department of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
3Department of Pathology, Medical College of Soochow University, Suzhou, China.
4Department of Oncology, The Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing, China.
5The Collaborative Innovation Center of Hematology, Soochow University, Suzhou, China.
Abstract
Heterogeneous nuclear ribonucleoproteins (hnRNPs) represent a large family of RNA-binding proteins. Heterogeneous nuclear ribonucleoprotein D-like (HNRPDL) is a member of this family. Though aberrant expression of HNRPDL has been reported in a few cancers, whether HNRPDL is deregulated in colon cancer patients and what role this protein plays in these cells are not known yet. In this study, we found that HNRPDL was significantly up-regulated in colon cancer specimens than control. We also demonstrated that HNRPDL silencing inhibited the growth of SW620 cells both in vitro and in vivo. Conversely, we constructed a retroviral vector to deliver HNRPDL into non-malignant NIH-3T3 cells and injected these cells into nude mice. HNRPDL-overexpressing NIH-3T3 cells generated tumors in nude mice but not the control cells. Mechanistically, HNRPDL promoted cell-cycle progression associated with enhanced expressions of cyclin D3 and Ki-67 but decreased expressions of p53 and p21. Taken together, our data demonstrate that HNRPDL is aberrantly expressed in colon cancer cells, which promotes the growth of these cells by activating cell-cycle progression.