Expression of phosphorylated-STAT3 and osteopontin and their correlation in melanoma

  • Yan Wu (吴艳)
  • Ping Jiang (蒋苹)
  • Yun Lin (林云)
  • Siyuan Chen (陈思远)
  • Nengxing Lin (林能兴)
  • Jiawen Li (李家文)
Article

Summary

The expressions of p-STAT3 and osteopontin in 22 cases of normal nevi and 43 cases of malignant melanoma were immunohistochemically detected, and the correlation between p-STAT3 and osteopontin in malignant melanoma and the correlations of p-STAT3 (or osteopontin) with invasion, metastasis and thickness of malignant melanoma were examined. The results showed p-STAT3 was expressed in 2 of 22 cases of normal nevi and 30 of 43 cases of malignant melanoma, while osteopontin was expressed in 3 cases of normal nevi and 29 cases of malignant melanoma. The expressions of p-STAT3 and osteopontin in melanoma were significantly higher than that in benign nevi. There existed significant correlations between the expression of p-STAT3 and that of osteopontin in melanoma. Furthermore, the expression rates of p-STAT3 were significantly higher in invasive or metastatic melanomas than that their non-invasive or non-metastatic counterparts, and the expression rates of osteopontin were significantly higher in invasive melanomas than that in non-invasive ones. It is concluded that p-STAT3 and osteopontin may play important roles in the pathogenesis of malignant melanoma.

Key words

p-STAT3 osteopontin malignant melanoma invasion metastasis tumor thickness 

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References

  1. 1.
    Li Y, Mc Clay EF. Systemic chemotherapy for the treatment of metastatic melanoma. Semin Oncol, 2002,29: 413–426PubMedCrossRefGoogle Scholar
  2. 2.
    Suiqing C, Min Z, Lirong C. Overexpression of phosphorylated-STAT3 correlated with the invasion and metastasis of cutaneous squamous cell carcinoma. J Dermatol, 2005,32:354–360PubMedGoogle Scholar
  3. 3.
    Yang SF, Yuan SS, Yeh YT, et al. The role of p-STAT3 (ser727) revealed by its association with Ki-67 in cervical intraepithelial neoplasia. Gynecol Oncol, 2005, 98:446–452PubMedCrossRefGoogle Scholar
  4. 4.
    Yang SF, Wang SN, Wu CF, et al. Altered p-STAT3 (tyr705) expression is associated with histological grading and intratumour microvessel density in hepatocellular carcinoma. J Clin Pathol, 2007,60:642–648PubMedCrossRefGoogle Scholar
  5. 5.
    Coppola D, Szabo M, Boulware D, et al. Correlation of osteopontin protein expression and pathological stage across a wide variety of tumor histologies. Clin Cancer Res, 2004,10:184–190PubMedCrossRefGoogle Scholar
  6. 6.
    Wai PY, Kuo PC. The role of Osteopontin in tumor metastasis. J Surg Res, 2004,121:228–241PubMedCrossRefGoogle Scholar
  7. 7.
    Denhardt DT, Mistretta D, Chambers AF, et al. Transcriptional regulation of osteopontin and the metastatic phenotype: evidence for a Ras-activated enhancer in the human OPN promoter. Clin Exp Metastasis, 2003,20:77–84PubMedCrossRefGoogle Scholar
  8. 8.
    Balch CM, Buzaid AC, Soong SJ, et al. Final version of the American Joint Committee on Cancer system for cutaneous melanoma. J Clin Oncol, 2001,19:3635–3648PubMedGoogle Scholar
  9. 9.
    Horvath CM. STAT proteins and transcriptional responses to extracellular signals. TIBS, 2000,25:496–502PubMedGoogle Scholar
  10. 10.
    Heimberger AB, Priebe W. Small molecular inhibitors of p-STAT3: novel agents for treatment of primary and metastatic CNS cancers. Recent Pat CNS Drug Discov, 2008, 3:179–188PubMedCrossRefGoogle Scholar
  11. 11.
    Kortylewski M, Jove R, Yu H. Targeting STAT3 affects melanoma on multiple fronts. Cancer and Metastasis Reviews, 2005,24:315–327PubMedCrossRefGoogle Scholar
  12. 12.
    Chakraborty G, Jain S, Behera R, et al. The multifaceted roles of osteopontin in cell signaling, tumor progression and angiogenesis. Curr Mol Med, 2006, 6:819–830PubMedCrossRefGoogle Scholar
  13. 13.
    Senger DR, Perruzzi CA, Papadopoulos A. Elevated expression of secreted phosphoprotein I (osteopontin, 2ar) as a consequence of neoplastic transformation. Anticancer Res, 1989,9(5):1291–1299PubMedGoogle Scholar
  14. 14.
    Philip S, Bulbule A, Kundu GC. Osteopontin stimulates tumor growth and activation of promatrix metalloproteinase-2 through nuclear factor-k B-mediated induction of membrane type I matrix metalloproteinase in murine melanoma cells. J Biol Chem, 2001,276:44926–44935PubMedCrossRefGoogle Scholar
  15. 15.
    Rangaswami H, Kundu GC. Osteopontin stimulates melanoma growth and lung metastasis through NIK/MEKK1-dependent MMP-9 activation pathways. Oncol Rep, 2007,18:909–915PubMedGoogle Scholar
  16. 16.
    Shijubo N, Uede T, Kon S, et al. Vascular endothelial growth factor and osteopontin in tumor biology. Crit Rev Oncog, 2000,11(2):135–146PubMedGoogle Scholar
  17. 17.
    Xie TX, Wei D, Liu M, et al. Stat3 activation regulates the expression of matrix metalloproteinase-2 and tumor invasion and metastasis. Oncogene, 2004,23:3550–3560PubMedCrossRefGoogle Scholar
  18. 18.
    Satoshi L, Cynthia DB, Gary EG, et al. Inhibition of Src kinase activity by ad-mda7 suppresses vascular endothelial growth factor expression in prostate carcinoma cells. Mol Ther, 2005,12:707–715CrossRefGoogle Scholar
  19. 19.
    Senger DR, Ledbetter SR, Claffey KP, et al. Stimulation of endo-thelial cell migration by vascular permeability fac-tor/vascular endothelial growth factor through cooperative mechanisms involving the avh3 integrin, osteopontin, and thrombin. Am J Pathol, 1996,149:293–305PubMedGoogle Scholar
  20. 20.
    Chakraborty G, Jain S, Kundu GC. Osteopontin promotes vascular endothelial growth factor-dependent breast tumor growth and angiogenesis via autocrine and paracrine mechanisms. Cancer Res, 2008,68(1):152–161PubMedCrossRefGoogle Scholar

Copyright information

© Huazhong University of Science and Technology and Springer-Verlag GmbH 2009

Authors and Affiliations

  • Yan Wu (吴艳)
    • 1
  • Ping Jiang (蒋苹)
    • 1
  • Yun Lin (林云)
    • 1
  • Siyuan Chen (陈思远)
    • 1
  • Nengxing Lin (林能兴)
    • 1
  • Jiawen Li (李家文)
    • 1
  1. 1.Department of Dermatology, Union Hospital, Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

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