Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines.
The LNCaP and C4-2B cell lines form an excellent preclinical model to study the development of metastatic castration-resistant prostate cancer, since C4-2B cells were derived from a bone metastasis that grew in nude mice after inoculation with the LNCaP-derived, castration-resistant C4-2 cells. Exom...
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0090002&type=printable |
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| author | Lien Spans Christine Helsen Liesbeth Clinckemalie Thomas Van den Broeck Stefan Prekovic Steven Joniau Evelyne Lerut Frank Claessens |
| author_facet | Lien Spans Christine Helsen Liesbeth Clinckemalie Thomas Van den Broeck Stefan Prekovic Steven Joniau Evelyne Lerut Frank Claessens |
| author_sort | Lien Spans |
| collection | DOAJ |
| description | The LNCaP and C4-2B cell lines form an excellent preclinical model to study the development of metastatic castration-resistant prostate cancer, since C4-2B cells were derived from a bone metastasis that grew in nude mice after inoculation with the LNCaP-derived, castration-resistant C4-2 cells. Exome sequencing detected 2188 and 3840 mutations in LNCaP and C4-2B cells, respectively, of which 1784 were found in both cell lines. Surprisingly, the parental LNCaP cells have over 400 mutations that were not found in the C4-2B genome. More than half of the mutations found in the exomes were confirmed by analyzing the RNA-seq data, and we observed that the expressed genes are more prone to mutations than non-expressed genes. The transcriptomes also revealed that 457 genes show increased expression and 246 genes show decreased expression in C4-2B compared to LNCaP cells. By combining the list of C4-2B-specific mutations with the list of differentially expressed genes, we detected important changes in the focal adhesion and ECM-receptor interaction pathways. Integration of these pathways converges on the myosin light chain kinase gene (MLCK) which might contribute to the metastatic potential of C4-2B cells. In conclusion, we provide extensive databases for mutated genes and differentially expressed genes in the LNCaP and C4-2B prostate cancer cell lines. These can be useful for other researchers using these cell models. |
| format | Article |
| id | doaj-art-f407d6d88355473c928d441a2da2ba0c |
| institution | OA Journals |
| issn | 1932-6203 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-f407d6d88355473c928d441a2da2ba0c2025-08-20T02:15:28ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e9000210.1371/journal.pone.0090002Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines.Lien SpansChristine HelsenLiesbeth ClinckemalieThomas Van den BroeckStefan PrekovicSteven JoniauEvelyne LerutFrank ClaessensThe LNCaP and C4-2B cell lines form an excellent preclinical model to study the development of metastatic castration-resistant prostate cancer, since C4-2B cells were derived from a bone metastasis that grew in nude mice after inoculation with the LNCaP-derived, castration-resistant C4-2 cells. Exome sequencing detected 2188 and 3840 mutations in LNCaP and C4-2B cells, respectively, of which 1784 were found in both cell lines. Surprisingly, the parental LNCaP cells have over 400 mutations that were not found in the C4-2B genome. More than half of the mutations found in the exomes were confirmed by analyzing the RNA-seq data, and we observed that the expressed genes are more prone to mutations than non-expressed genes. The transcriptomes also revealed that 457 genes show increased expression and 246 genes show decreased expression in C4-2B compared to LNCaP cells. By combining the list of C4-2B-specific mutations with the list of differentially expressed genes, we detected important changes in the focal adhesion and ECM-receptor interaction pathways. Integration of these pathways converges on the myosin light chain kinase gene (MLCK) which might contribute to the metastatic potential of C4-2B cells. In conclusion, we provide extensive databases for mutated genes and differentially expressed genes in the LNCaP and C4-2B prostate cancer cell lines. These can be useful for other researchers using these cell models.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0090002&type=printable |
| spellingShingle | Lien Spans Christine Helsen Liesbeth Clinckemalie Thomas Van den Broeck Stefan Prekovic Steven Joniau Evelyne Lerut Frank Claessens Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines. PLoS ONE |
| title | Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines. |
| title_full | Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines. |
| title_fullStr | Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines. |
| title_full_unstemmed | Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines. |
| title_short | Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines. |
| title_sort | comparative genomic and transcriptomic analyses of lncap and c4 2b prostate cancer cell lines |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0090002&type=printable |
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