SOCS-3 is associated with vascular invasion and overall survival in hepatocellular carcinoma

被引:19
作者
Yang, Sheau-Fang [1 ,2 ]
Yeh, Yao-Tsung [3 ]
Wang, Shen-Nien [4 ]
Hung, Sz-Chi [5 ]
Chen, Wan-Tzu [1 ]
Huang, Chu-Ho [1 ]
Chai, Chee-Yin [1 ,2 ]
机构
[1] Kaohsiung Med Univ Hosp, Dept Pathol, Kaohsiung 807, Taiwan
[2] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Pathol, Kaohsiung, Taiwan
[3] Fooyin Univ, Dept Med Technol, Kaohsiung, Taiwan
[4] Kaohsiung Med Univ Hosp, Dept Surg, Div Hepatobiliary Surg, Kaohsiung 807, Taiwan
[5] St Joseph Hosp, Dept Obstet & Gynecol, Kaohsiung, Taiwan
关键词
SOCS-3; hepatocellular carcinoma; vascular invasion; survival;
D O I
10.1080/00313020802320432
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Aims: Alteration of the suppressor of cytokine signalling-3 (SOCS-3) has been observed in certain human cancers. However, the clinical role of this short-lived protein in hepatocellular carcinoma (HCC) is not well established. Therefore, we aimed to explore the potential role of SOCS-3 proteins in HCC. Methods: Paraffin embedded sections from 87 HCC patients were included in this study. The expression patterns of SOCS-3 proteins were analysed using immunohistochemistry and the results were correlated with clinicopathological characteristics and overall survival of the HCC patients. Results: The SOCS-3 expression of HCC lesions and the adjacent non-tumourous liver tissues was significantly correlated (p = 0.035), while the SOCS-3 expression in HCC lesions was significantly and positively correlated with vascular invasion and histological grading (p = 0.034 and 0.032, respectively). The Kaplan-Meier survival curve showed that the HCC patients with high SOCS-3 expression were associated with a poor overall survival rate in the HCC subgroup with positive vascular invasion (p = 0.014). Furthermore, a multivariate Cox regression model showed that SOCS-3 expression was also a significant determinant of the overall survival for HCC (p = 0.006). Conclusions: Our results indicate that altered SOCS-3 expression is associated with the overall survival in a subset of HCC patients with positive vascular invasion. Constitutive and altered SOCS-3 expression may have potential roles in a subset of HCC patients.
引用
收藏
页码:558 / 563
页数:6
相关论文
共 36 条
  • [1] Autoregulation of pituitary corticotroph SOCS-3 expression: Characterization of the murine SOCS-3 promoter
    Auernhammer, CJ
    Bousquet, C
    Melmed, S
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (12) : 6964 - 6969
  • [2] Constitutive SOCS-3 expression protects T-cell lymphoma against growth inhibition by IFNα
    Brender, C
    Lovato, P
    Sommer, VH
    Woetmann, A
    Mathiesen, AM
    Geisler, C
    Wasik, M
    Odum, N
    [J]. LEUKEMIA, 2005, 19 (02) : 209 - 213
  • [3] Feng DY, 2001, WORLD J GASTROENTERO, V7, P33
  • [4] SOCS-1, a negative regulator of cytokine signaling, is frequently silenced by methylation in multiple myeloma
    Galm, O
    Yoshikawa, H
    Esteller, M
    Osieka, R
    Herman, JG
    [J]. BLOOD, 2003, 101 (07) : 2784 - 2788
  • [5] Harvat BL, 1996, CELL GROWTH DIFFER, V7, P289
  • [6] SOCS-3 is frequently silenced by hypermethylation and suppresses cell growth in human lung cancer
    He, B
    You, L
    Uematsu, K
    Zang, KL
    Xu, ZD
    Lee, AY
    Costello, JF
    McCormick, F
    Jablons, DM
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (24) : 14133 - 14138
  • [7] Negative regulators of cytokine signal transduction
    Hilton, DJ
    [J]. CELLULAR AND MOLECULAR LIFE SCIENCES, 1999, 55 (12) : 1568 - 1577
  • [8] HIROHASHI S, 2000, WHO CLASSIFICATION T, P159
  • [9] Are SOCS suppressors, regulators, and degraders?
    Johnston, JA
    [J]. JOURNAL OF LEUKOCYTE BIOLOGY, 2004, 75 (05) : 743 - 748
  • [10] Hepatitis C virus down-regulates insulin receptor substrates 1 and 2 through up-regulation of suppressor of cytokine signaling 3
    Kawaguchi, T
    Yoshida, T
    Harada, M
    Hisamoto, T
    Nagao, Y
    Ide, T
    Taniguchi, E
    Kumemura, H
    Hanada, S
    Maeyama, M
    Baba, S
    Koga, H
    Kumashiro, R
    Ueno, T
    Ogata, H
    Yoshimura, A
    Sata, M
    [J]. AMERICAN JOURNAL OF PATHOLOGY, 2004, 165 (05) : 1499 - 1508