nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer
Metrics: PDF 1071 views | HTML 1381 views | ?
Eun Kyung Lee1,*, Seung-Hyun Hong2,*, Sooyong Shin3,4,*, Hyun-Sung Lee5, Ju-Seog Lee6, Eun Jung Park7,8, Sun Shim Choi9, Jae Woong Min9, Daeyoon Park1, Jung-Ah Hwang2, Betty H. Johnson3, Sung Ho Jeon4, In-Hoo Kim8, Yeon-Su Lee2, Yong Sun Lee3,8
1Center for Thyroid Cancer, National Cancer Center, Goyang, 410-769, Korea
2Cancer Genomics Branch, Research Institute, National Cancer Center, Goyang, 410-769, Korea
3Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA
4Department of Life Science and Center for Aging and Health Care, Hallym University, Chuncheon, 200-702, Korea
5Division of Thoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA
6Department of Systems Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
7Cancer Immunology Branch, National Cancer Center, Goyang, 410-769, Korea
8Department of Cancer System Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, 410-769, Korea
9Division of Biomedical Convergence, College of Biomedical Science, and Institute of Bioscience & Biotechnology, Kangwon National University, Chuncheon, 200–701, Korea
*These authors have contributed equally to this work
Yeon-Su Lee, email: firstname.lastname@example.org
Yong Sun Lee, email: email@example.com
Keywords: nc886, thyroid cancer, protein kinase R, oncogene
Received: June 16, 2016 Accepted: August 19, 2016 Published: September 06, 2016
nc886 is a recently identified cellular non-coding RNA and its depletion leads to acute cell death via PKR (Protein Kinase RNA-activated) activation. nc886 expression is increased in some malignancies, but silenced in others. However, the precise role of nc886/PKR is controversial: is it a tumor suppressor or an oncogene? In this study, we have clarified the role of nc886 in thyroid cancer by sequentially generating PKR knockout (KO) and PKR/nc886 double KO cell lines from Nthy-ori 3-1, a partially transformed thyroid cell line. Compared to the wildtype, PKR KO alone does not exhibit any significant phenotypic changes. However, nc886 KO cells are less proliferative, migratory, and invasive than their parental PKR KO cells. Importantly, the requirement of nc886 in tumor phenotypes is totally independent of PKR. In our microarray data, nc886 KO suppresses some genes whose elevated expression is associated with poor survival confirmed by data from total of 505 thyroid cancer patients in the Caner Genome Atlas project. Also, the nc886 expression level tends to be elevated and in more aggressively metastatic tumor specimens from thyroid cancer patients. In summary, we have discovered nc886’s tumor-promoting role in thyroid cancer which has been concealed by the PKR-mediated acute cell death.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.