Elucidation of the regulation of INK4 locus by long noncoding RNA and the oncogenic mechanism by the bankruptcy.

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K07184
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Kindai University
• Principal Investigator: KOTAKE YOJIRO 近畿大学, 産業理工学部, 教授 (90531963)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: long noncoding RNA / INK4 locus / CDK inhibitor p15 / CDK inhibitor p16 / cell cycle / cancer cells

Outline of Final Research Achievements

The aim of this study is to reveal the regulation of INK4 locus by long noncoding RNA (lncRNA) and the oncogenic mechanism by the bankruptcy. In this study, we showed that a novel lncRNA, LOIL (lncRNA on the INK4 locus) functions to promote the proliferation of human lung cancer and colorectal cancer cells. Furthermore, we revealed that LOIL represses the transcription of CDK inhibitors p15 and p16 on INK4 locus. We also showed that another lncRNA, SLOP functions to promote G1 phase progression of cell cycle via repressing p15 transcription.

Free Research Field

腫瘍生物学

Academic Significance and Societal Importance of the Research Achievements

本研究の結果、我々が同定したlncRNA LOILとSLOPが、INK4遺伝子座の転写抑制を介して各種癌細胞の増殖を促進することが明らかとなった。INK4遺伝子座は、多くのヒト癌で変異や転写抑制されていることが報告されていることから、この遺伝子座の転写抑制因子は癌化に関与している可能性が高いと考えられる。従って、LOILとSLOPは将来的に癌治療薬の分子標的や癌診断マーカーになる可能性が示唆された。