Kohno S, Kitajima S, Sasaki N, Takahashi C. Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies. World J Stem Cells 2016; 8(4): 170-184 [PMID: 27114748 DOI: 10.4252/wjsc.v8.i4.170]
Corresponding Author of This Article
Chiaki Takahashi, MD, PhD, Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-1192, Japan. chtakaha@staff.kanazawa-u.ac.jp
Research Domain of This Article
Oncology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Susumu Kohno, Chiaki Takahashi, Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-1192, Japan
Shunsuke Kitajima, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, United States
Nobunari Sasaki, Department of Pharmacy, Graduate School of Medicine, Keio University, Tokyo 106-0016, Japan
Author contributions: All authors wrote the manuscript.
Supported by The Funding Program for Next Generation World-Leading Researchers (NEXT), Grant-in-Aid for Scientific Research (MEXT), Naito Foundation, Daiichi-Sankyo Foundation for Life Science, Hokkoku Foundation for Cancer Research, and IMSUT Joint Research Project.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Chiaki Takahashi, MD, PhD, Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-1192, Japan. chtakaha@staff.kanazawa-u.ac.jp
Telephone: +81-76-2646750 Fax: +81-76-2344521
Received: October 28, 2015 Peer-review started: November 3, 2015 First decision: December 4, 2015 Revised: December 30, 2015 Accepted: February 14, 2016 Article in press: February 16, 2016 Published online: April 26, 2016 Processing time: 168 Days and 6.7 Hours
Abstract
Carcinogenic transformation of somatic cells resembles nuclear reprogramming toward the generation of pluripotent stem cells. These events share eternal escape from cellular senescence, continuous self-renewal in limited but certain population of cells, and refractoriness to terminal differentiation while maintaining the potential to differentiate into cells of one or multiple lineages. As represented by several oncogenes those appeared to be first keys to pluripotency, carcinogenesis and nuclear reprogramming seem to share a number of core mechanisms. The retinoblastoma tumor suppressor product retinoblastoma (RB) seems to be critically involved in both events in highly complicated manners. However, disentangling such complicated interactions has enabled us to better understand how stem cell strategies are shared by cancer cells. This review covers recent findings on RB functions related to stem cells and stem cell-like behaviors of cancer cells.
Core tip: Carcinogenic transformation of somatic cells resembles nuclear reprogramming toward the generation of pluripotent stem cells. The retinoblastoma tumor suppressor product retinoblastoma (RB) seems to be critically involved in both events in highly complicated manners. This review covers recent findings on RB functions related to stem cells and stem cell-like behaviors of cancer cells.
