STYK1/NOK—A Potential Radiotherapeutic Target and Biomarker for Gastric Cancer and Cervical Cancer

Abstract

This article introduced the STYK1/NOK, including its origin, chemical composition and biological function, and the expression of STYK1/NOK in various cancer cell lines was reviewed. Furthermore, our recent study showed that STYK1/NOK protein was also over expressed in gastric cancer and cervical cancer specimens, and STYK1/NOK expression increased after tumor cells were irradiated with γ ray. These results indicated that STYK1/NOK might be involved in the occurrence and progress of gastric cancer and cervical cancer, and contribute to the radioresistance of tumor cells. Thus, STYK1/NOK might be a potential therapeutic target and diagnostic marker for gastric cancer and cervical cancer.

Share and Cite:

L. Gao, X. Chen, Z. Ma and F. Li, "STYK1/NOK—A Potential Radiotherapeutic Target and Biomarker for Gastric Cancer and Cervical Cancer," Journal of Cancer Therapy, Vol. 4 No. 2, 2013, pp. 575-577. doi: 10.4236/jct.2013.42073.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] L. Liu, X. Z. Yu, T. S. Li, L. X. Song, P. L. Chen, T. L. Suo, Y. H. Li, S. D. Wang, Y. Chen, Y. M. Ren, S. P. Zhang, Z. J. Chang and X. Y. Fu, “A Novel Protein Tyrosine Kinase NOK That Shares Homology with PlateletDerived Growth Factor/Fibroblast Growth Factor Receptors Induces Tumorigenesis and Metastasis in Nude Mice,” Cancer Research, Vol. 64, No. 10, 2004, pp. 3491-3499. doi:10.1158/0008-5472.CAN-03-2106
[2] J. Li, F. Wu, F. Sheng, Y. J. Li, D. Jin, X. Ding and S. Zhang, “NOK/STYK1 Interacts with GSK-3β and Mediates Ser9 Phosphorylation through Activated Akt,” FEBS Letters, Vol. 586, No. 21, 2012, pp. 3787-3792. doi:10.1016/j.febslet.2012.09.011
[3] K. S. Kimbro, K. Duschene, M. Willard, J. A. Moore and S. Freeman, “A Novel Gene STYK1/NOK Is Upregulated in Estrogen Receptor-Alpha Negative Estrogen Receptor-Beta Positive Breast Cancer Cells Following Estrogen Treatment,” Molecular Biology Reports, Vol. 35, No. 1, 2008, pp. 23-27. doi:10.1007/s11033-006-9047-1
[4] T. Amachika, D. Kobayashi, R. Moriai, N. Tsuji and N. Watanabe, “Diagnostic Relevance of Overexpressed mRNA of Novel Oncogene with Kinase-Domain (NOK) in Lung Cancers,” Lung Cancer, Vol. 56, No. 3, 2007, pp. 337-340. doi:10.1016/j.lungcan.2007.01.002
[5] D. M. Roder, “The Epidemiology of Gastric Cancer,” Gastric Cancer, Vol. 5 Suppl 1, 2002, pp. 5-11.
[6] B. Zilberstein, C. E. Jacob and I. Cecconello, “Gastric Cancer Trends in Epidemiology,” Arquivos de Gastroenterologia, Vol. 49, No. 3, 2012, pp. 177-178. doi:10.1590/S0004-28032012000300001
[7] P. Correa, M. B. Piazuelo and M. C. Camargo, “The Future of Gastric Cancer Prevention,” Gastric Cancer, Vol. 7, No. 1, 2004, pp. 9-16. doi:10.1007/s10120-003-0265-0
[8] T. Nakajima, “Gastric Cancer Treatment Guidelines in Japan,” Gastric Cancer, Vol. 5, No. 1, 2002, pp. 1-5. doi:10.1007/s101200200000
[9] J. Schiedel, A. Blaukat, S. Li, et al., “Matuzumab Binding to EGFR Prevents the Confomational Rearrangement Required for Dimerization,” Cancer Cell, Vol. 13, No. 4, 2008, pp. 365-373.
[10] Y. Matsui, M. Inomata, M. Tojigamori, et al., “Suppression of Tumor Growth in Human Gastric Cancer with HER2 Overexpression by an Anli-HER2 Antibody in a Murine Model,” International Journal of Oncology, Vol. 27, No. 3, 2005, pp. 68l-685.
[11] K. Fujimoto-Ouchi, F. Sekiguchi, H. Yasuuno, et al., “Antitumor Activity of Trustuzumab in Combination with Chemothempy in Human Gastric Cancer Xenograft Models,” Cancer Chemotherapy and Pharmacology, Vol. 59, No. 6, 2007, pp. 795-805.
[12] S. Y. Kim, H. P. Kim, Y. J. Kim, et al., “Traastuzumab Inhibits the Growth of Human Gastric Cancer Cell Lines with HER2 Amplification Synergistically with HER2/ Neu Overexpression/Amplification,” International Journal of Oncology, Vol. 32, No. 1, 2008, pp. 89-95.
[13] X. Ye, C. Ji, Q. Huang, C. Cheng, R. Tang, J. Xu, L. Zeng, J. Dai, Q. Wu, S. Gu, Y. Xie and Y. Mao, “Isolation and Characterization of a Human Putative Receptor Protein Kinase cDNA STYK1,” Molecular Biology Reports, Vol. 30, No. 2, 2003, pp. 91-96. doi:10.1023/A:1023934017174
[14] S. Chung, K. Tamura, M. Furihata, M. Uemura, Y. Daigo, Y. Nasu, T. Miki, T. Shuin, T. Fujioka, Y. Nakamura and H. Nakagawa, “Overexpression of the Potential Kinase Serine/Threonine/Tyrosine Kinase 1 (STYK 1) in Castrationresistant Prostate Cancer,” Cancer Science, Vol. 100, No. 11, 2009, pp. 2109-2114. doi:10.1111/j.1349-7006.2009.01277.x
[15] X. Ding, Q. B. Jiang, R. Li, S. Chen and S. Zhang, “NOK/ STYK1 Has a Strong Tendency towards Forming Aggregates and Colocalises with Epidermal Growth Factor Receptor in Endosomes,” Biochemical and Biophysical Research Communications, Vol. 421, No. 3, 2009, pp. 468-473. doi:10.1016/j.bbrc.2012.04.016
[16] Y. H. Li, Y. Y. Wang, S. Zhong, Z. L. Rong, Y. M. Ren, Z. Y. Li, S. P. Zhang, Z. J. Chang and L. Liu, “Transmembrane Helix of Novel Oncogene with Kinase-Domain (NOK) Influences Its Oligomerization and Limits the Activation of RAS/MAPK Signaling,” Molecules and Cells, Vol. 27, No. 1, 2009, pp. 39-45. doi:10.1007/s10059-009-0003-5
[17] T. Kondoh, D. Kobayashi, N. Tsuji, K. Kuribayashi and N. Watanabe, “Overexpression of Serine Threonine Tyrosine Kinase 1/Novel Oncogene with Kinase Domain mRNA in Patients with Acute Leukemia,” Experimental Hematology, Vol. 37, No. 7, 2009, pp. 824-830. doi:10.1016/j.exphem.2009.04.010
[18] Y. H. Li, S. Zhong, Z. L. Rong, Y. M. Ren, Z. Y. Li, S. P. Zhang, Z. Chang and L. Liu, “The Carboxyl Terminal Tyrosine 417 Residue of NOK Has an Autoinhibitory Effect on NOK-Mediated Signaling Transductions,” Biochemical and Biophysical Research Communications, Vol. 356, No. 2, 2007, pp. 444-449. doi:10.1016/j.bbrc.2007.02.154
[19] R. Moriai, D. Kobayashi, T. Amachika, N. Tsuji and N. Watanabe, “Diagnostic Relevance of Overexpressed NOK mRNA in Breast Cancer,” Anticancer Research, Vol. 26, No. 6C, 2006, pp. 4969-4973.
[20] K. A. Jackson, G. Oprea, J. Handy and K. S. Kimbro, “Aberrant STYK1 Expression in Ovarian Cancer Tissues and Cell Lines,” Journal of Ovarian Research, Vol. 2, No. 1, 2009, pp. 15-22.
[21] Y.-H. Li, Y.-Y. Wang, S. Zhong, Z.-L. Rong, Y.-M. Ren, Z.-Y. Li, S.-P. Zhang, Z.-J. Chang and L. Liu, “Transmembrane Helix of Novel Oncogene with Kinase-Domain (NOK) Influences Its Oligomerization and Limits the Activation of RAS/MAPK Signaling,” Molecules and Cells, Vol. 27, No. 1, 2009, pp. 39-45.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.