Responsiveness of hypomethylated and control tumor cells to canonical Wnt-signalling
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA974092 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24653336_1.fastq.gz | Fastqsanger.gz | |||
| SRR24653336_2.fastq.gz | Fastqsanger.gz | |||
| SRR24653337_1.fastq.gz | Fastqsanger.gz | |||
| SRR24653337_2.fastq.gz | Fastqsanger.gz | |||
| SRR24653338_1.fastq.gz | Fastqsanger.gz |
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Project description:Hypothesis and proof of concept:
Our hypothesis is that increase in cellular iron import proteins (TfR1, DMT1) occur early in the adenoma-carcinoma sequence through mutations in APC and lead to cellular iron loading. As demonstrated in our previous work the effects of this iron loading is to mediate increased Wnt signalling resulting in c-myc induction. This in turn serves to increase the expression of iron import proteins (TfR1, DMT1) and decrease the expression of iron export (ferroportin [FPN]) and storage (ferritin) proteins. Such a hypothesis explains how Wnt signalling controls iron metabolism and ensures that there is adequate cellular iron for ATP generation and cellular proliferation.
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