Kruzelock R P, Cuevas B D, Wiener J R, Xu F J, Yu Y, Cabeza-Arvelaiz Y, Pershouse M, Lovell M M, Killary A M, Mills G B, Bast R C
Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas, TX 77030, USA.
Oncogene. 2000 Dec 14;19(54):6277-85. doi: 10.1038/sj.onc.1204013.
The identity of many tumor suppressor genes important in epithelial ovarian cancer tumorigenesis remains unknown. In an effort to localize a novel tumor suppressor on chromosome 22, a psv2neo tagged human chromosome 22 was transferred into the malignant epithelial ovarian cancer cell line, SKOv-3, by microcell-mediated chromosome transfer. Complete suppression of the transformed phenotype was observed in 16 of 18 individual microcell hybrid clones as evidenced by the complete abrogation of cell growth under anchorage-independent conditions. In vitro doubling times were also dramatically reduced, as was the ability to form subcutaneous tumors in CD1 nu/nu mice. Only one polymorphic marker, D22S429, segregated with decreased transformation and tumorigenic potential, suggesting that an unrecognized tumor suppressor may localize to chromosome 22q11-q12. These data provide functional support for the presence of a novel tumor suppressor locus (or loci) on chromosome 22 that is important in ovarian cancer tumorigenesis.
许多在上皮性卵巢癌发生过程中起重要作用的肿瘤抑制基因的身份仍然未知。为了在22号染色体上定位一个新的肿瘤抑制基因，通过微细胞介导的染色体转移，将一个psv2neo标记的人22号染色体转入恶性上皮性卵巢癌细胞系SKOv-3。在18个单独的微细胞杂交克隆中，有16个观察到转化表型完全受到抑制，这在非锚定依赖条件下细胞生长完全被消除得到证明。体外倍增时间也显著缩短，在CD1 nu/nu小鼠中形成皮下肿瘤的能力也是如此。只有一个多态性标记D22S429与转化和致瘤潜力降低相关联，这表明一个未被识别的肿瘤抑制基因可能定位于22号染色体的q11-q12区域。这些数据为22号染色体上存在一个对卵巢癌发生至关重要的新肿瘤抑制基因座（或多个基因座）提供了功能支持。
