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First published online 21 March 2006
doi: 10.1242/jcs.02871

Journal of Cell Science 119, 1477-1482 (2006)
Published by The Company of Biologists 2006
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Research Article

Genetic instability and divergence of clonal populations in colon cancer cells in vitro

Laia Masramon1, Elisenda Vendrell1, Gemma Tarafa2, Gabriel Capellà2, Rosa Miró3, Maria Ribas1 and Miguel A. Peinado1,*

1 IDIBELL-Institut de Recerca Oncològica, L'Hospitalet, 08907 Barcelona, Spain
2 IDIBELL-Institut Català d'Oncologia, L'Hospitalet, 08907 Barcelona, Spain
3 Departament de Biologia Cellular, Fisiologia i Immunologia, Institut de Biotecnologia i Biomedicina, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain

* Author for correspondence (e-mail: mpeinado{at}iro.es)

Accepted 4 January 2006

The accumulation of multiple chromosomal abnormalities is a characteristic of the majority of colorectal cancers and has been attributed to an underlying chromosomal instability. Genetic instability is considered to have a key role in the generation of genetic and phenotypic heterogeneity in cancer cells. To shed light on the dynamics of chromosomal instability in colon cancer cells, we have analyzed genetic divergence in clonal and subclonal derivates of chromosomally unstable (SW480) and stable (HCT116, LoVo) cell lines. Conventional G-banding karyotyping and arbitrarily primed PCR (AP-PCR) fingerprinting were used to calculate genetic distances among clones and parental cells, and to trace tree-type phylogenies among individual cells and clonal cell populations. SW480 cells showed enhanced karyotypic heterogeneity in clones as compared with parental cells. Moreover, genetic clonal divergence was also increased after two consecutive episodes of single-cell cloning, demonstrating that the homogeneity induced by the bottleneck of cloning is disrupted by genetic instability during clonal expansion and, as a consequence, heterogeneity is restored. These results demonstrate genetic drift in clonal populations originated from isolated cells. The generated cell heterogeneity coupled with selection provides the grounds for the reported feasibility of pre-neoplastic and neoplastic cells to generate new phenotypic variants with increased evolutionary potential.

Key words: Colorectal cancer, Genomic instability, Tumor progression




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