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Circadian Clock Genes, PER1 and PER2, as Tumor Suppressors
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논문 기본 정보

Type
Academic journal
Author
Beomseok Son (부산대학교) Hyunhee Do (한국교원대학교) EunGi Kim (부산대학교) BuHyun Youn (부산대학교) Wanyeon Kim (한국교원대학교)
Journal
Korean Society Of Life Science Journal of Life Science Vol.27 No.10 KCI Accredited Journals
Published
2017.10
Pages
1,225 - 1,231 (7page)

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Circadian Clock Genes, PER1 and PER2, as Tumor Suppressors
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Disruptive expression patterns of the circadian clock genes are highly associated with many human diseases, including cancer. Cell cycle and proliferation is linked to a circadian rhythm; therefore, abnormal clock gene expression could result in tumorigenesis and malignant development. The molecular network of the circadian clock is based on transcriptional and translational feedback loops orchestrated by a variety of clock activators and clock repressors. The expression of 10~15% of the genome is controlled by the overall balance of circadian oscillation. Among the many clock genes, Period 1 (Per1) and Period 2 (Per2) are clock repressor genes that play an important role in the regulation of normal physiological rhythms. It has been reported that PER1 and PER2 are involved in the expression of cell cycle regulators including cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors. In addition, correlation of the down-regulation of PER1 and PER2 with development of many cancer types has been revealed. In this review, we focused on the molecular function of PER1 and PER2 in the circadian clock network and the transcriptional and translational targets of PER1 and PER2 involved in cell cycle and tumorigenesis. Moreover, we provide information suggesting that PER1 and PER2 could be promising therapeutic targets for cancer therapies and serve as potential prognostic markers for certain types of human cancers.
#Circadian rhythm #clock gene #cell cycle #PER1 #PER2 #tumor suppressor

Contents

Introduction
PER proteins: negative-feedback repressors of circadian rhythm
PER1 and PER2 as tumor suppressors, and their application to cancer therapy
Conclusions
References
초록

References (45)

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Bae, K., Jin, X., Maywood, E. S., Hastings, M. H., Reppert, S. M. and Weaver, D. R. 2001. Differential functions of mPer1, mPer2, and mPer3 in the SCN circadian clock. Neuron 30, 525-536. Bhattacharjee, A., Richards, W. G., Staunton, J., Li, C., Monti, S., Vasa, P., Ladd, C., Beheshti, J., Bueno, R., Gillette, M., Loda, M., Weber, G., Mark, E. J., Lander, E. S., Wong, W., Johnson, B. E., Golub, T. R., Sugarbaker, D. J. and Meyerson, M. 2001. Classification of human lung carcinomas by mRNA expression profiling reveals distinct adenocarcinoma subclasses. Proc. Natl. Acad. Sci. USA 98, 13790-13795. Cadenas, C., van de Sandt, L., Edlund, K., Lohr, M., Hellwig, B., Marchan, R., Schmidt, M., Rahnenfuhrer, J., Oster, H. and Hengstler, J. G. 2014. Loss of circadian clock gene expression is associated with tumor progression in breast cancer. Cell Cycle 13, 3282-3291. Cao, Q., Gery, S., Dashti, A., Yin, D., Zhou, Y., Gu, J. and Koeffler, H. P. 2009. A role for the clock gene per1 in prostate cancer. Cancer Res. 69, 7619-7625. Chen, B., Tan, Y., Liang, Y., Li, Y., Chen, L., Wu, S., Xu, W., Wang, Y., Zhao, W. and Wu, J. 2017. Per2 participates in AKT-mediated drug resistance in A549/DDP lung adenocarcinoma cells. Oncol. Lett. 13, 423-428.

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