Expression of the cellular adhesion molecule E-cadherin is reduced or absent in high-grade prostate cancer.
Expression of the cellular adhesion molecule E-cadherin is reduced or absent in high-grade prostate cancer.
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发表时间：
1992-09
期刊：
影响因子：
11.2
通讯作者：
R. Umbas;J. Schalken;T. Aalders;B. Carter;H. Karthaus;H. Schaafsma;F. Debruyne;W. Isaacs
中科院分区：
文献类型：
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作者：
R. Umbas;J. Schalken;T. Aalders;B. Carter;H. Karthaus;H. Schaafsma;F. Debruyne;W. Isaacs
e -钙粘蛋白是一种依赖Ca（2+）的细胞粘附分子，通过介导同型、亲同型细胞间相互作用，在正常生长发育中起重要作用。最近的研究表明，e -钙粘蛋白可能在肿瘤进展中也很重要，特别是作为一种侵袭抑制因子。我们之前已经证明大鼠前列腺癌细胞的侵袭性表型与E-cadherin的表达降低有关（m.j. Bussemakers, r.j. A. Van Moorselaar, l.a. Giroldi， T. Ichikawa, j.t. Isaacs， F. m.j. Debruyne， J. A. Schalken，癌症杂志，52:2916-2922,1992）。这是特别有趣的，因为人类e -钙粘蛋白基因定位的位点经常涉及前列腺癌的等位基因丢失（B. S. Carter， C. M. Ewing， W. S. Ward， B. F. Treiger， T. W. Aalders， J. A. Schalken， J. I. Epstein和W. B. Isaacs, Proc. Natl）。学会科学。美国，87:8751-8755,1990；王晓明，王晓明，王晓明，中华医学杂志，21(3):387 - 398,1991)。e -钙粘蛋白功能受损可能与该蛋白的异常表达有关。因此，我们通过免疫组化分析了E-cadherin在人前列腺组织非恶性和恶性标本中的原位表达。在92例原发性或转移性前列腺癌的肿瘤样本中，与正常前列腺相比，46例E-cadherin染色减少或缺失，而正常前列腺的E-cadherin染色一致呈强阳性。E-cadherin表达降低与肿瘤分化程度降低有统计学意义。此外，在组织学上相似的群体中，某些肿瘤可以通过e -cadherin阴性和阳性细胞混合群体的存在来区分。与具有广泛局部进展或前列腺癌转移沉积的肿瘤相比，临床定位的肿瘤中E-cadherin染色异常的肿瘤百分比增加，这表明E-cadherin的缺失与肿瘤进展之间存在相关性。综上所述，这些发现表明进一步探索e -钙粘蛋白作为人类前列腺癌的候选侵袭抑制分子是有必要的。
E-cadherin is a Ca(2+)-dependent cell adhesion molecule which plays an important role in normal growth and development via mediation of homotypic, homophilic cell-cell interaction. Recent studies suggest that E-cadherin may be important in neoplastic progression as well, particularly as a suppressor of invasion. We have previously demonstrated that the invasive phenotype of rat prostate cancer cells is associated with the decreased expression of E-cadherin (M. J. G. Bussemakers, R. J. A. Van Moorselaar, L. A. Giroldi, T. Ichikawa, J. T. Isaacs, F. M. J. Debruyne, and J. A. Schalken, Cancer Res., 52:2916-2922, 1992). This is of particular interest, since the locus to which the human E-cadherin gene is mapped is frequently involved in allelic loss in prostate cancer (B. S. Carter, C. M. Ewing, W. S. Ward, B. F. Treiger, T. W. Aalders, J. A. Schalken, J. I. Epstein, and W. B. Isaacs, Proc. Natl. Acad. Sci. USA, 87:8751-8755, 1990; U. S. Bergerheim, K. Kunimi, V. P. Collins, and P. Ekman, Genes, Chromosomes Cancer, 3: 215-220, 1991). Impaired E-cadherin function is likely to be associated with aberrant expression of the protein. We therefore analyzed E-cadherin expression in situ by immunohistochemistry in nonmalignant and malignant specimens of human prostatic tissue. Of 92 tumor samples of either primary or metastatic deposits of prostate cancer, 46 had reduced or absent E-cadherin staining when compared to nomalignant prostate, which uniformly stained strongly positive. There was a statistically significant correlation between the decreased expression of E-cadherin and loss of tumor differentiation. Additionally, certain tumors within a histologically similar group could be distinguished by the presence of mixed populations of E-cadherin-negative and -positive cells. The percentage of tumors with aberrant E-cadherin staining increased when clinically localized tumors were compared to either tumors with extensive local progression or metastatic deposits of prostate cancer, suggesting a correlation between loss of E-cadherin and tumor progression. Taken together, these findings suggest that further exploration of E-cadherin as a candidate invasion suppressor molecule in human prostate cancer is warranted.