Estrogen receptor 1 gene as a tumor suppressor gene in hepatocellular carcinoma detected by triple-combination array analysis

  • Authors:
    • Mitsuhiro Hishida
    • Shuji Nomoto
    • Yoshikuni Inokawa
    • Masamichi Hayashi
    • Mitsuro Kanda
    • Yukiyasu Okamura
    • Yoko Nishikawa
    • Chie Tanaka
    • Daisuke Kobayashi
    • Suguru Yamada
    • Goro Nakayama
    • Tsutomu Fujii
    • Hiroyuki Sugimoto
    • Masahiko Koike
    • Michitaka Fujiwara
    • Shin Takeda
    • Yasuhiro Kodera
  • View Affiliations

  • Published online on: May 20, 2013     https://doi.org/10.3892/ijo.2013.1951
  • Pages: 88-94
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Hepatocellular carcinoma (HCC) is one of the top five causes of cancer-related deaths worldwide. Recent developments in the treatment of HCC remain insufficient to cure unresectable disease or to prevent HCC. Consistent efforts are, therefore, needed to deepen understanding of pathogenesis of the disease. Genome-wide gene expression profile analyses can now detect various candidate genes that are modified by HCC. We have developed a new technique to identify tumor suppressor genes, triple-combination array analysis, which combines gene expression profiles, single nucleotide polymorphism and methylation arrays to identify genes with altered expression. Using HCC tissue samples, triple-combination array analysis was performed to identify a candidate tumor suppressor gene. Subsequently, samples from 48 HCC patients were subjected to quantitative polymerase chain reaction (qPCR) and methylation-specific PCR to further elucidate clinical relevance of the gene. Estrogen receptor 1 (ESR1) was detected as a candidate tumor suppressor gene. Of the 48 clinical samples, 40 (83.3%) showed ESR1 promoter hypermethylation. In 24 (50%) HCC samples, the expression levels of the ESR1 gene was decreased by >90%. The decreased expression was significantly related to high liver damage score, pathological invasion of the intrahepatic portal vein, the size of tumor (>3 cm in diameter) and hepatitis B virus infection. The present study represents another example that triple-combination array is a convenient technique for detecting genes with altered expression in disease. The ESR1 gene was identified as a candidate tumor suppressor gene in HCC and further validation is warranted.
View Figures
View References

Related Articles

Journal Cover

July 2013
Volume 43 Issue 1

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Hishida M, Nomoto S, Inokawa Y, Hayashi M, Kanda M, Okamura Y, Nishikawa Y, Tanaka C, Kobayashi D, Yamada S, Yamada S, et al: Estrogen receptor 1 gene as a tumor suppressor gene in hepatocellular carcinoma detected by triple-combination array analysis. Int J Oncol 43: 88-94, 2013
APA
Hishida, M., Nomoto, S., Inokawa, Y., Hayashi, M., Kanda, M., Okamura, Y. ... Kodera, Y. (2013). Estrogen receptor 1 gene as a tumor suppressor gene in hepatocellular carcinoma detected by triple-combination array analysis. International Journal of Oncology, 43, 88-94. https://doi.org/10.3892/ijo.2013.1951
MLA
Hishida, M., Nomoto, S., Inokawa, Y., Hayashi, M., Kanda, M., Okamura, Y., Nishikawa, Y., Tanaka, C., Kobayashi, D., Yamada, S., Nakayama, G., Fujii, T., Sugimoto, H., Koike, M., Fujiwara, M., Takeda, S., Kodera, Y."Estrogen receptor 1 gene as a tumor suppressor gene in hepatocellular carcinoma detected by triple-combination array analysis". International Journal of Oncology 43.1 (2013): 88-94.
Chicago
Hishida, M., Nomoto, S., Inokawa, Y., Hayashi, M., Kanda, M., Okamura, Y., Nishikawa, Y., Tanaka, C., Kobayashi, D., Yamada, S., Nakayama, G., Fujii, T., Sugimoto, H., Koike, M., Fujiwara, M., Takeda, S., Kodera, Y."Estrogen receptor 1 gene as a tumor suppressor gene in hepatocellular carcinoma detected by triple-combination array analysis". International Journal of Oncology 43, no. 1 (2013): 88-94. https://doi.org/10.3892/ijo.2013.1951