Cytogenetic Characterization of Two Colon Cell Lines by Using Conventional G-Banding, Comparative Genomic Hybridization, and Whole Chromosome Painting

Masramon, Laia; Ribas, M.; Cifuentes, P.; Arribas, Rosa; García, Francisca; Egozcue, J.; Peinado, Miguel A.; Miró, Rosa

doi:10.1016/s0165-4608(00)00219-3

Cited by 54 publications

(42 citation statements)

References 23 publications

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“…Thus the question remains as to the origin and continuity of the abnormal centriole. It has been reported that HCT116 cells show relatively normal karyotypes (Masramon et al, 2000;Roschke et al, 2002). We have also confirmed stable karyotypes of the HCT116 cell lines used in the current study (our unpublished results), suggesting that the formation of γ-tubulin-specific structures in 5-10% of the total cell population might not be due to karyotype diversity.…”

Section: Abnormal Centrosomes In Cancer Cellssupporting

confidence: 90%

γ-Tubulin-containing abnormal centrioles are induced by insufficient Plk4 in human HCT116 colorectal cancer cells

Kuriyama

Bettencourt-Dias

Hoffmann

et al. 2009

Journal of Cell Science

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1 essential for initiation of centriole biogenesis, is not associated with the γ-tubulin-specific abnormal centrosomes. The amount of Plk4 at each centrosome was less in cells with abnormal centrosomes than cells without γ-tubulin-specific abnormal centrosomes. In addition, the formation of abnormal structures was abolished by expression of exogenous Plk4, but not SAS6 and Cep135/Bld10p, which are downstream regulators required for the organization of nine-triplet microtubules. These results suggest that HCT116 cells fail to organize the ninefold symmetry of centrioles due to insufficient Plk4.

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Section: Abnormal Centrosomes In Cancer Cellssupporting

confidence: 90%

γ-Tubulin-containing abnormal centrioles are induced by insufficient Plk4 in human HCT116 colorectal cancer cells

Kuriyama

Bettencourt-Dias

Hoffmann

et al. 2009

Journal of Cell Science

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“…33 When we compared our results to those published in the same CRC cell lines using SKY, 15,27,28 we obtained the same results using both multicolor karyotyping techniques. By comparing karyotypes of these cell lines previously analyzed by G banding carried out in our laboratory, 9,24 we confirmed that M-FISH techniques allow easy characterization of clones, avoiding misidentifications of chromosome markers and allowing us to follow them along clone generations or in vitro culture passages.…”

Section: Discussionsupporting

confidence: 68%

“…Molecular, G-banding and CGH analyses were previously performed in our laboratory by Masramon et al 24 M-FISH results of HCT116, LoVo and DLD-1 46,XY,dup(2)(p14p22) [17],der(6)t(6;11)(p23;??) [17],der (16)…”

Section: Cell Lines Of the Mis Pathwaymentioning

confidence: 99%

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Genetic evolution in colon cancer KM12 cells and metastatic derivates

Camps

Morales

Prat

et al. 2004

Intl Journal of Cancer

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So far, CRC cell lines have contributed to descriptions of 2 patterns of genetic instability, affecting either microsatellite sequences or chromosome number and structure. Often, these patterns are mutually exclusive; while near-diploid karyotypes usually appear with MSI and chromosomal stability, near-triploid or tetraploid cells display a high degree of CIN and are stable at the microsatellite level. In the present study, we describe the genomic instability pattern of KM12 CRC cells. KM12C and derived cell lines with different metastatic properties were analyzed by conventional cytogenetics, CGH and M-FISH. Results were compared to 5 cell lines usually used as model of MSI and CIN. Concordance between our results and previously published SKY data are also reviewed. Interestingly, the poorly metastatic KM12C cell line displayed a near-diploid karyotype with high levels of structural chromosome instability and microsatellite instability. Most carcinomas show highly complex karyotypes, suggesting that one of the tumor-development events may be related to genomic instability. 1,2 Up to now, MSI has been the only type of genomic instability well characterized in a minority of tumors (about 15% of sporadic CRCs). These tumors show a deficiency in mismatch repair genes with a replication error phenotype and a stable near-diploid karyotype. 3-7 chromosome instability has been described in some CRC cell lines, resulting in numerical changes 8 (CIN) or structural rearrangements. 9 Often, these patterns are mutually exclusive; while near-diploid karyotypes usually appear with MSI and chromosome instability, near-triploid or tetraploid cells display a high degree of CIN and are stable at the microsatellite level.It has been postulated that primary alterations in solid tumors consist of submicroscopic mutations, whereas unbalanced chromosomal rearrangements, whether numerical or structural, are secondary events and most likely associated with selective pressures during tumor progression. 10 A previous report demonstrated clonal chromosomal aberrations in 87% of CRC tumors analyzed. 11 The most frequent numerical changes were, in order of decreasing frequency, ϩ7, -18, -14, ϩ13. Gain of chromosome 8q and loss of 8p, loss of 17p and gain of 17q as well as loss of the entire chromosome 22 are also unbalanced rearrangements that have been reported. 11 Based on cytogenetic alterations, Dutrillaux 12 proposed 3 different evolutionary pathways: monosomic-type tumors undergo structural rearrangements resulting in gains and losses of different chromosome arms and show a relatively high rate of endoreduplication, leading to the formation of hypotetraploid clones that evolve to near-triploid cells; trisomic cells are characterized by tumors with a progressive increase in chromosome number but accompanied by a scarce number of rearrangements; tumors that display a near-normal karyotype and MSI were grouped into the normal type. Unbalanced chromosomal abnormalities would be secondary events and most likely associated with selective pre...

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“…In HCT116 there is a third copy located on an abnormal chromosome 18 that contains a small segment of chromosome 17q fused to the telomeric end of 18p (ref. 23). Fig.…”

Section: Disruption Of Fdxr By Targeted Homologous Recombinationmentioning

confidence: 99%

Ferredoxin reductase affects p53-dependent, 5-fluorouracil–induced apoptosis in colorectal cancer cells

Hwang

Bunz

et al. 2001

Nat Med

384

251

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Loss of p53 gene function, which occurs in most colon cancer cells, has been shown to abolish the apoptotic response to 5-fluorouracil (5-FU). To identify genes downstream of p53 that might mediate these effects, we assessed global patterns of gene expression following 5-FU treatment of isogenic cells differing only in their p53 status. The gene encoding mitochondrial ferredoxin reductase (protein, FR; gene, FDXR) was one of the few genes significantly induced by p53 after 5-FU treatment. The FR protein was localized to mitochondria and suppressed the growth of colon cancer cells when over-expressed. Targeted disruption of the FDXR gene in human colon cancer cells showed that it was essential for viability, and partial disruption of the gene resulted in decreased sensitivity to 5-FU-induced apoptosis. These data, coupled with the effects of pharmacologic inhibitors of reactive oxygen species, indicate that FR contributes to p53-mediated apoptosis through the generation of oxidative stress in mitochondria.5-fluorouracil (5-FU) has been in clinical use for several decades and is still the most effective adjuvant therapy for patients with colon cancer. Metabolically, it acts by blocking the enzyme thymidylate synthase and by inhibiting both RNA and DNA synthesis. Like most chemotherapeutic agents, 5-FU induces marked apoptosis in sensitive cells. However, the molecular mechanisms underlying this apoptosis are only beginning to be elucidated.Several studies have suggested a correlation between inactivation of p53 and resistance to 5-FU, both in patients and in experimental systems 1,2 . For example, a profound resistance to 5-FU-induced apoptosis was observed in a human colon cancer cell line with a targeted disruption of the p53 gene (Trp53) 3 . Such observations support a genetic basis for 5-FU chemosensitivity and indicate that isogenic cells differing only in p53 status represent a useful system for studying chemosensitivity in vitro.© 2001 Nature Publishing Group Correspondence should be addressed to B.V.; vogelbe@welch.jhu.edu. Supplementary information is available on the Nature Medicine website (http://medicine.nature.com/supplementary_info/). NIH Public Access NIH-PA Author ManuscriptThe mechanisms through which p53 induces apoptosis are the focus of much current research [4][5][6][7] . Several studies have implicated mitochondria-derived reactive oxygen species (ROS) in the process [8][9][10][11] . Though pro-apoptotic members of the Bcl-2 family of proteins have been shown to be induced by p53 and affect mitochondrial permeability, the molecular mechanisms responsible for the formation of mitochondrial ROS remain unclear 12,13 .In an effort to gain further insight into this process, we examined global patterns of gene expression using the serial analysis of gene expression (SAGE) approach 14 . We were particularly interested in finding p53-induced genes that encode mitochondrial proteins with the potential to directly stimulate ROS production. Here we identify mammalian ferredoxin reductase (FR) ...

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Cytogenetic Characterization of Two Colon Cell Lines by Using Conventional G-Banding, Comparative Genomic Hybridization, and Whole Chromosome Painting

Cited by 54 publications

References 23 publications

γ-Tubulin-containing abnormal centrioles are induced by insufficient Plk4 in human HCT116 colorectal cancer cells

γ-Tubulin-containing abnormal centrioles are induced by insufficient Plk4 in human HCT116 colorectal cancer cells

Genetic evolution in colon cancer KM12 cells and metastatic derivates

Ferredoxin reductase affects p53-dependent, 5-fluorouracil–induced apoptosis in colorectal cancer cells

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