Share This Article:

The Significance of the Expression of FBXO31 in Gastric Cancer

Abstract Full-Text HTML XML Download Download as PDF (Size:370KB) PP. 75-79
DOI: 10.4236/jct.2013.41A011    3,769 Downloads   5,483 Views   Citations

ABSTRACT

Loss of Heterozygosity (LOH) is commonly considered to be one of a reason when some genes lose their function. Numbers of tumor suppressor genes are existing on the LOH lesion and chromosome 16q24 had been reported as a LOH region in gastric cancer. Little is known about what kind of tumor suppressor genes locates around the position. F-box protein, (FBXO31) is a candidate tumor suppressor gene encoded in chromosome 16q24.3 and LOH of the gene was reported in breast cancer, hepatocellular carcinoma and ovarian cancer but the status of FBXO31 was not analyzed in gastric cancer so far. One hundred twenty-seven pairs of tumor and corresponding normal tissue specimens collected from gastric cancer patients who underwent gastrectomy. Total RNAs were extracted from those samples and the expression of FBXO31 was investigated using real time quantitative RT-PCR analysis. Patients were classified into FBXO31 high expression group and low expression group. Clinicopahological factors were compared between the two groups and importance of FBXO31 was investigated. The standardized expression of FBXO31 was not significantly different between tumor (0.43 ± 0.46) and the corresponding 0.49 ± 0.55 in normal tissue (p = 0.39). Two years survival rate was 77% in FBXO31 high expression group and 54% in low expression group however the chance of survival rate of high expression group was dropped in 5 years (Wilcoxon p = 0.01). Clinicopathological factors were compared between the two groups and peritoneal dissemination was observed significantly higher in FBXO31 low expression group than did in high expression group (p = 0.0398). In order to predict existence of peritoneal dissemination of gastric cancer before surgery, FBXO31 may become a favorite marker for the low risk of peritoneal dissemination.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

T. Sudo, R. Kogo, N. Nishida, K. Takahahi, G. Sawada, M. Ishibashi, J. Kurashige, R. Uchi, T. Matsumura, H. Ueo, K. Mima, S. Akiyoshi, K. Sugimachi, K. Shibata, H. Fujita, K. Shirouzu, M. Mori and K. Mimori, "The Significance of the Expression of FBXO31 in Gastric Cancer," Journal of Cancer Therapy, Vol. 4 No. 1A, 2013, pp. 75-79. doi: 10.4236/jct.2013.41A011.

References

[1] P. Pisani, D. M. Parkin, F. Bray and J. Ferlay, “Estimates of the Worldwide Mortality from 25 Cancers in 1990,” International Journal of Cancer, Vol. 83, No. 1, 1999, pp. 18-29.
[2] M. Sasako, T. Sano, S. Yamamoto, Y. Kurokawa, A. Nashimoto, A. Kurita, et al., “D2 Lymphadenectomy Alone or with Para-Aortic Nodal Dissection for Gastric Cancer,” The New England Journal of Medicine, Vol. 359, No. 5, 2008, pp. 453-462. doi:10.1056/NEJMoa0707035
[3] S. Sakuramoto, M. Sasako, T. Yamaguchi, T. Kinoshita, M. Fujii, A. Nashimoto, et al., “Adjuvant Chemotherapy for Gastric Cancer with S-1, an Oral Fluoropyrimidine,” The New England Journal of Medicine, Vol. 357, No. 18, 2007, pp. 1810-1820. doi:10.1056/NEJMoa072252
[4] D. S. Arici, E. Tuncer, H. Ozer, G. Simek and A. Koyuncu, “Expression of Retinoblastoma and Cyclin D1 in Gastric Carcinoma,” Neoplasma, Vol. 56, No. 1, 2009, pp. 63-67. doi:10.4149/neo_2009_01_63
[5] Y. Hirata, S. Maeda, Y. Mitsuno, M. Akanuma, Y. Yamaji, K. Ogura, et al., “Helicobacter Pylori Activates the Cyclin D1 Gene through Mitogen-Activated Protein Kinase Pathway in Gastric Cancer Cells,” Infection and Immunity, Vol. 69, No. 6, 2001, pp. 3965-3971. doi:10.1128/IAI.69.6.3965-3971.2001
[6] M. K. Santra, N. Wajapeyee and M. R. Green, “F-Box Protein FBXO31 Mediates Cyclin D1 Degradation to Induce G1 Arrest after DNA Damage,” Nature, Vol. 459, No. 7247, 2009, pp. 722-725. doi:10.1038/nature08011
[7] R. Kumar, P. M. Neilsen, J. Crawford, R. McKirdy, J. Lee, J. A. Powell, et al., “FBXO31 Is the Chromosome 16q24.3 Senescence Gene, a Candidate Breast Tumor Suppressor, and a Component of an SCF Complex,” Cancer Research, Vol. 65, No. 24, 2005, pp. 11304-11313. doi:10.1158/0008-5472.CAN-05-0936
[8] V. Launonen, A. Mannermaa, F. Stenback, V.-M. Kosma, U. Puistola, P. Huusko, et al., “Loss of Heterozygosity at Chromosomes 3, 6, 8, 11, 16, and 17 in Ovarian Cancer: Correlation to Clinicopathological Variables,” Cancer Genetics and Cytogenetics, Vol. 122, No. 1, 2000, pp. 49-54. doi:10.1016/S0165-4608(00)00279-X
[9] H. L. Huang, W. L. Zheng, R. Zhao, B. Zhang and W. L. Ma, “FBXO31 Is Down-Regulated and May Function as a Tumor Suppressor in Hepatocellular Carcinoma,” Oncology Reports, Vol. 24, No. 3, 2010, pp. 715-720.
[10] P. Harkonen, A. P. Kyllonen, S. Nordling and P. Vihko, “Loss of Heterozygosity in Chromosomal Region 16q24.3 Associated with Progression of Prostate Cancer,” The Prostate, Vol. 62, No. 3, 2005, pp. 267-274. doi:10.1002/pros.20147
[11] Y. Mori, M. Matsunaga, T. Abe, S. Fukushige, K. Miura, M. Sunamura, et al., “Chromosome Band 16q24 Is Frequently Deleted in Human Gastric Cancer,” British Journal of Cancer, Vol. 80, No. 9, 1999, pp. 556-562. doi:10.1038/sj.bjc.6690391
[12] M. Mori, K. Mimori, H. Inoue, G. F. Barnard, K. Tsuji, S. Nanbara, et al., “Detection of Cancer Micrometastases in Lymph Nodes by Reverse Transcriptase-Polymerase Chain Reaction,” Cancer Research, Vol. 55, No. 15, 1995, pp. 3417-3420.
[13] T. Utsunomiya, H. Inoue, K. Taguchi, M. Shimada, K. Sugimachi and M. Mori, “G Protein Gamma 7 Expression as a New Clinicopathological Marker in Patients with Intrahepatic Cholangiocarcinoma,” Archives of Surgery, Vol. 137, No. 3, 2002, pp. 181-185.
[14] K. Ogawa, T. Utsunomiya, K. Mimori, Y. Tanaka, F. Tanaka, H. Inoue, et al., “Clinical Significance of Elongation Factor-1 Delta mRNA Expression in Oesophageal Carcinoma,” British Journal of Cancer, Vol. 91, No. 22, 2004, pp. 282-286. doi:10.1038/sj.bjc.6601941
[15] I. Bièche, P. Onody, I. Laurendeau, M. Olivi, D. Vidaud, R. Lidereau and M. Vidaud, “Real-Time Reverse Transcription-PCR Assay for Future Management of ERBB2-Based Clinical Applications,” Clinical Chemistry, Vol. 45, No. 8, 1999, pp. 1148-1156.
[16] P. Schraml, J. Kononen, L. Bubendorf, H. Moch, H. Bissig, A. Nocito, et al., “Tissue Microarrays for Gene Amplification Surveys in Many Different Tumor Types,” Clinical Cancer Research, Vol. 5, No. 8, 1999, pp. 1966-1975.
[17] G. K. Anagnostopoulos, D. Stefanou, E. Arkoumani, J. Karagiannis, K. Paraskeva, L. Chalkley, et al., “Immunohistochemical Expression of Cell-Cycle Proteins in Gastric Precancerous Lesions,” Journal of Gastroenterology and Hepatology, Vol. 23, No. 4, 2008, pp. 626-631. doi:10.1111/j.1440-1746.2007.05219.x
[18] K. Wang, J. Kan, S. T. Yuen, S. T. Shi, K. M. Chu, S. Law, et al., “Exome Sequencing Identifies Frequent Mutation of ARID1A in Molecular Subtypes of Gastric Cancer,” Nature Genetics, Vol. 43, No. 12, 2011, pp. 1219-1223. doi:10.1038/ng.982

  
comments powered by Disqus

Copyright © 2019 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.