Targeting Non-Oncogene Addiction for Cancer Therapy

While Next-Generation Sequencing (NGS) and technological advances have been useful in identifying genetic profiles of tumorigenesis, novel target proteins and various clinical biomarkers, cancer continues to be a major global health threat. DNA replication, DNA damage response (DDR) and repair, and...

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Main Authors: Hae Ryung Chang, Eunyoung Jung, Soobin Cho, Young-Jun Jeon, Yonghwan Kim
Format: Article
Language:English
Published: MDPI AG 2021-01-01
Series:Biomolecules
Subjects:
Online Access:https://www.mdpi.com/2218-273X/11/2/129
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author Hae Ryung Chang
Eunyoung Jung
Soobin Cho
Young-Jun Jeon
Yonghwan Kim
author_facet Hae Ryung Chang
Eunyoung Jung
Soobin Cho
Young-Jun Jeon
Yonghwan Kim
author_sort Hae Ryung Chang
collection DOAJ
description While Next-Generation Sequencing (NGS) and technological advances have been useful in identifying genetic profiles of tumorigenesis, novel target proteins and various clinical biomarkers, cancer continues to be a major global health threat. DNA replication, DNA damage response (DDR) and repair, and cell cycle regulation continue to be essential systems in targeted cancer therapies. Although many genes involved in DDR are known to be tumor suppressor genes, cancer cells are often dependent and addicted to these genes, making them excellent therapeutic targets. In this review, genes implicated in DNA replication, DDR, DNA repair, cell cycle regulation are discussed with reference to peptide or small molecule inhibitors which may prove therapeutic in cancer patients. Additionally, the potential of utilizing novel synthetic lethal genes in these pathways is examined, providing possible new targets for future therapeutics. Specifically, we evaluate the potential of TONSL as a novel gene for targeted therapy. Although it is a scaffold protein with no known enzymatic activity, the strategy used for developing PCNA inhibitors can also be utilized to target TONSL. This review summarizes current knowledge on non-oncogene addiction, and the utilization of synthetic lethality for developing novel inhibitors targeting non-oncogenic addiction for cancer therapy.
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spelling doaj.art-36b3158a852f4f1f99530cc072b12b022023-12-03T13:54:33ZengMDPI AGBiomolecules2218-273X2021-01-0111212910.3390/biom11020129Targeting Non-Oncogene Addiction for Cancer TherapyHae Ryung Chang0Eunyoung Jung1Soobin Cho2Young-Jun Jeon3Yonghwan Kim4Department of Biological Sciences and Research Institute of Women’s Health, Sookmyung Women’s University, Seoul 04310, KoreaDepartment of Biological Sciences and Research Institute of Women’s Health, Sookmyung Women’s University, Seoul 04310, KoreaDepartment of Biological Sciences and Research Institute of Women’s Health, Sookmyung Women’s University, Seoul 04310, KoreaDepartment of Integrative Biotechnology, Sungkyunkwan University, Suwon 16419, KoreaDepartment of Biological Sciences and Research Institute of Women’s Health, Sookmyung Women’s University, Seoul 04310, KoreaWhile Next-Generation Sequencing (NGS) and technological advances have been useful in identifying genetic profiles of tumorigenesis, novel target proteins and various clinical biomarkers, cancer continues to be a major global health threat. DNA replication, DNA damage response (DDR) and repair, and cell cycle regulation continue to be essential systems in targeted cancer therapies. Although many genes involved in DDR are known to be tumor suppressor genes, cancer cells are often dependent and addicted to these genes, making them excellent therapeutic targets. In this review, genes implicated in DNA replication, DDR, DNA repair, cell cycle regulation are discussed with reference to peptide or small molecule inhibitors which may prove therapeutic in cancer patients. Additionally, the potential of utilizing novel synthetic lethal genes in these pathways is examined, providing possible new targets for future therapeutics. Specifically, we evaluate the potential of TONSL as a novel gene for targeted therapy. Although it is a scaffold protein with no known enzymatic activity, the strategy used for developing PCNA inhibitors can also be utilized to target TONSL. This review summarizes current knowledge on non-oncogene addiction, and the utilization of synthetic lethality for developing novel inhibitors targeting non-oncogenic addiction for cancer therapy.https://www.mdpi.com/2218-273X/11/2/129non-oncogene addictionDNA damage responseDNA repaircancer therapy
spellingShingle Hae Ryung Chang
Eunyoung Jung
Soobin Cho
Young-Jun Jeon
Yonghwan Kim
Targeting Non-Oncogene Addiction for Cancer Therapy
Biomolecules
non-oncogene addiction
DNA damage response
DNA repair
cancer therapy
title Targeting Non-Oncogene Addiction for Cancer Therapy
title_full Targeting Non-Oncogene Addiction for Cancer Therapy
title_fullStr Targeting Non-Oncogene Addiction for Cancer Therapy
title_full_unstemmed Targeting Non-Oncogene Addiction for Cancer Therapy
title_short Targeting Non-Oncogene Addiction for Cancer Therapy
title_sort targeting non oncogene addiction for cancer therapy
topic non-oncogene addiction
DNA damage response
DNA repair
cancer therapy
url https://www.mdpi.com/2218-273X/11/2/129
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