Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA296510 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2473064_1.fastq.gz | Fastqsanger.gz | |||
| SRR2473064_2.fastq.gz | Fastqsanger.gz | |||
| SRR2473065_1.fastq.gz | Fastqsanger.gz | |||
| SRR2473065_2.fastq.gz | Fastqsanger.gz | |||
| SRR2473066_1.fastq.gz | Fastqsanger.gz |
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Project description:The complexity and heterogeneity of cancer cells are under-represented by the current experimental models which revolve around primary tumor cells, cancer cell lines, and rodent models. We used the transformed cell model in our studies. IMR90 and BJ fibroblast cells were transformed by three oncogenic genetic factors, SV40 Large-T antigen, H-Ras and human telomerase (hTERT). These transformed cells can grow under anchorage independent conditions, are self-sufficient in growth signals, have decreased sensitivity to apoptosis, and showed recurrent chromosomal abnormalities. Further characterization of transformed cells through cell cycle profiling and mass spectrometry analysis also revealed an increased fraction in the G2/M phase, and an up-regulation of Ku70. Furthermore, transformed cells exhibited increased telomerase activity that was not accountable by hTERT overexpression alone. Microarray results revealed that hTERT overexpression promoted cell migration and the initiation of DNA damage responses; two cellular processes that are important in cancer progression. Collectively, these data imply that IMR90 transformed cell model is an invaluable tool for cancer studies. Our results in the systematic study of this model helped us identify possible early events in cancer transformation and reveal the extra-telomeric effects of telomerase in cell migration and DNA damage initiation. IMR90 and BJ fibroblast cells were transformed by three oncogenic genetic factors, SV40 Large-T antigen, H-Ras and human telomerase (hTERT). Through microarray analysis, gene expression of transformed cells were compared against control cells.
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Project description:HoxC5 and Pbx4 repress hTERT to limit telomerase activity
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Project description:The complexity and heterogeneity of cancer cells are under-represented by the current experimental models which revolve around primary tumor cells, cancer cell lines, and rodent models. We used the transformed cell model in our studies. IMR90 and BJ fibroblast cells were transformed by three oncogenic genetic factors, SV40 Large-T antigen, H-Ras and human telomerase (hTERT). These transformed cells can grow under anchorage independent conditions, are self-sufficient in growth signals, have decreased sensitivity to apoptosis, and showed recurrent chromosomal abnormalities. Further characterization of transformed cells through cell cycle profiling and mass spectrometry analysis also revealed an increased fraction in the G2/M phase, and an up-regulation of Ku70. Furthermore, transformed cells exhibited increased telomerase activity that was not accountable by hTERT overexpression alone. Microarray results revealed that hTERT overexpression promoted cell migration and the initiation of DNA damage responses; two cellular processes that are important in cancer progression. Collectively, these data imply that IMR90 transformed cell model is an invaluable tool for cancer studies. Our results in the systematic study of this model helped us identify possible early events in cancer transformation and reveal the extra-telomeric effects of telomerase in cell migration and DNA damage initiation.
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Project description:Telomere length control is critical for cellular lifespan and tumor suppression. Telomerase is activated in the inner cell mass of the developing blastocyst to reset telomere reserves and its subsequent silencing in differentiated cells leads to gradual telomere shortening. Here, we report that transcriptional control through cis-regulatory elements minimally impact telomerase regulation as a function of pluripotency. Instead, developmental control of telomerase is largely driven by an alternative splicing event, centered around hTERT exon-2. Skipping of exon-2 triggers hTERT mRNA decay in differentiated cells. Conversely, its retention in pluripotent cells promotes telomerase accumulation. Our study also identifies SON as a regulator of exon-2 alternative splicing and we report a patient with insufficient telomerase and short telomeres and harboring a SON mutation. In summary, our study highlights a critical role for hTERT alternative splicing in the developmental regulation of telomerase and implicates defective splicing in telomere biology disorders.
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