Reciprocal expressions of cyclin E and cyclin D1 in hepatocellular carcinoma

Yu Jin Jung, Kee Ho Lee, Dong Wook Choi, Chul Ju Han, Sook Hyang Jeong, Keun Cheol Kim, Jong Won Oh, Taek Kyu Park, Chang Min Kim

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Deregulation of the cell cycle by overexpression of G1 cyclins, cyclin E and cyclin D1 genes, has been demonstrated to be a prerequisite for the development of human cancer. Recently, cyclin E is proposed to be sufficient for the progression of the G1 cell cycle without cyclin D1. Here we show that the proposed model system was specifically present in human hepatocellular carcinoma (HCC) unlike other human cancers. Of 31 HCC tissues analyzed, 21 (67.7%) exhibited an overexpression of cyclin E protein. In contrast to cyclin E gene expression, cyclin D1 expression was strongly downregulated in 19 (61.2%) HCCs. Interestingly, 65% of HCC tissues with overexpression of the cyclin E gene exhibited downregulation of cyclin D1, suggesting reciprocal deregulation of these cyclins in the G1 progression of the cell cycle. Southern blot analysis proved the amplification of cyclin E gene in HCC with a high level of overexpression. The present findings suggest that the reciprocal deregulation of cyclin E lacking cyclin D1 expression might play a role in G1 progression and the development of HCC.

Original languageEnglish
Pages (from-to)57-63
Number of pages7
JournalCancer Letters
Volume168
Issue number1
DOIs
Publication statusPublished - 2001 Jul 10

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Cyclin E
Cyclin D1
Hepatocellular Carcinoma
Cyclin G1
Cell Cycle
Down-Regulation
bcl-1 Genes
Human Development
Southern Blotting
Genes
Neoplasms
Gene Expression

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Jung, Y. J., Lee, K. H., Choi, D. W., Han, C. J., Jeong, S. H., Kim, K. C., ... Kim, C. M. (2001). Reciprocal expressions of cyclin E and cyclin D1 in hepatocellular carcinoma. Cancer Letters, 168(1), 57-63. https://doi.org/10.1016/S0304-3835(01)00403-7
Jung, Yu Jin ; Lee, Kee Ho ; Choi, Dong Wook ; Han, Chul Ju ; Jeong, Sook Hyang ; Kim, Keun Cheol ; Oh, Jong Won ; Park, Taek Kyu ; Kim, Chang Min. / Reciprocal expressions of cyclin E and cyclin D1 in hepatocellular carcinoma. In: Cancer Letters. 2001 ; Vol. 168, No. 1. pp. 57-63.
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Jung, YJ, Lee, KH, Choi, DW, Han, CJ, Jeong, SH, Kim, KC, Oh, JW, Park, TK & Kim, CM 2001, 'Reciprocal expressions of cyclin E and cyclin D1 in hepatocellular carcinoma', Cancer Letters, vol. 168, no. 1, pp. 57-63. https://doi.org/10.1016/S0304-3835(01)00403-7

Reciprocal expressions of cyclin E and cyclin D1 in hepatocellular carcinoma. / Jung, Yu Jin; Lee, Kee Ho; Choi, Dong Wook; Han, Chul Ju; Jeong, Sook Hyang; Kim, Keun Cheol; Oh, Jong Won; Park, Taek Kyu; Kim, Chang Min.

In: Cancer Letters, Vol. 168, No. 1, 10.07.2001, p. 57-63.

Research output: Contribution to journalArticle

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AU - Choi, Dong Wook

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AU - Jeong, Sook Hyang

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AU - Oh, Jong Won

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AU - Kim, Chang Min

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AB - Deregulation of the cell cycle by overexpression of G1 cyclins, cyclin E and cyclin D1 genes, has been demonstrated to be a prerequisite for the development of human cancer. Recently, cyclin E is proposed to be sufficient for the progression of the G1 cell cycle without cyclin D1. Here we show that the proposed model system was specifically present in human hepatocellular carcinoma (HCC) unlike other human cancers. Of 31 HCC tissues analyzed, 21 (67.7%) exhibited an overexpression of cyclin E protein. In contrast to cyclin E gene expression, cyclin D1 expression was strongly downregulated in 19 (61.2%) HCCs. Interestingly, 65% of HCC tissues with overexpression of the cyclin E gene exhibited downregulation of cyclin D1, suggesting reciprocal deregulation of these cyclins in the G1 progression of the cell cycle. Southern blot analysis proved the amplification of cyclin E gene in HCC with a high level of overexpression. The present findings suggest that the reciprocal deregulation of cyclin E lacking cyclin D1 expression might play a role in G1 progression and the development of HCC.

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