CHROMOSOMAL ANALYSIS OF HUMAN PROSTATIC ADENOCARCINOMA CELL-LINES

Abstract

Karyological analyses of cell lines derived from metastatic and primary prostatic carcinoma were carried out by Q[quinacrine]-, C[constitutive heterochromatin]- and sequential banding techniques. The metastatic line, PC-3, isolated from a [human] bone marrow specimen, is an established epithelial line which is tumorigenic in nude, athymic mice and forms colonies in semisolid agar suspension. A subline, PC-3/M, was isolated from a PC-3-induced mouse tumor. Karyotypic analysis of PC-3 by Q- and C-banding showed the cells to be aneuploid at all culture passage levels. The modal chromosome number shifted from 62 to 55 between the 5th and 50th passages. PC-3 has a unique karyotype. Chromosomes 2, 3, 5, 15 and Y were always absent. At least 11 different marker chromosomes were observed. The subline, PC-3/M, had a similar karyotype and retained the parental PC-3 markers. PC-3/M had a more restricted chromosomal frequency distribution range. Nearly 73% of the PC-3/M cells examined had 60 or 61 chromosomes in contrast to the wide distribution seen in PC-3. Silver staining for nucleolus organizer regions indicated that the number of functional nucleolus organizer regions in PC-3 was proportional to the number of acrocentric chromosomes. Banding analysis of PC-5-PI isolated from primary prostatic adenocarcinoma indicated that this line also has a characteristic karyotype with 28% pseudodiploid and 72% pseudotetraploid components. All metaphases examined were partially trisomic in chromosome 9 and lacked a demonstrable Y chromosome. The overall karyological patterns of PC-3, PC-3/M and PC-5-PI as well as their marker chromosomes clearly distinguish these lines from other cancer lines including HeLa [human cervical carcinoma cells]. This is important since the authenticity of other putative prostatic cancer cell lines has been disputed. These cell lines provide a useful model for investigation of genetic changes in prostatic cancer as well as differences between primary and metastatic forms of the disease.