Veronese M L, Bullrich F, Negrini M, Croce C M
Jefferson Cancer Center, Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Cancer Res. 1996 Feb 15;56(4):728-32.
Very little is known about the molecular and genetic mechanisms involved in prostate cancer. Previous studies have shown frequent loss of heterozygosity (40%) at chromosomal regions 8p, 10q, and 16q, suggesting the presence of tumor suppressor genes in these regions. The LNCaP cell line, established from a metastatic lesion of human prostatic adenocarcinoma, carries a t(6;16)(p21;q22) translocation. To determine whether this translocation involved genes important in the process of malignant transformation, we cloned and sequenced the t(6;16) breakpoint of this cell line. Sequence analysis showed that the breakpoint is within the haptoglobin gene cluster on chromosome 16, and that, on chromosome 6, the break occurs within a novel gene, tpc, similar to the prokaryotic S10 ribosomal protein gene. The translocation results in the production of a fusion transcript, tpc/hpr.
关于前列腺癌所涉及的分子和遗传机制，人们了解甚少。先前的研究表明，在染色体区域8p、10q和16q存在频繁的杂合性缺失（40%），这表明这些区域存在肿瘤抑制基因。LNCaP细胞系源自人前列腺腺癌的转移病灶，携带t(6;16)(p21;q22)易位。为了确定这种易位是否涉及在恶性转化过程中起重要作用的基因，我们克隆并测序了该细胞系的t(6;16)断点。序列分析表明，断点位于16号染色体上的触珠蛋白基因簇内，而在6号染色体上，断点发生在一个与原核生物S10核糖体蛋白基因相似的新基因tpc内。这种易位导致产生一种融合转录本tpc/hpr。
