Cornell University researchers report they have discovered direct genetic evidence that a family of genes, called MicroRNA-34 (miR-34), are bona fide tumor suppressors.
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It is well accepted that mutations of the p53 gene have been implicated in half of all cancers. Research in mice has revealed how interplay between genes p53 and miR-34 (MicroRNA-34) jointly inhibits another cancer-causing gene called MET. In absence of p53 and miR-34, MET overexpresses a receptor protein and promotes unregulated cell growth and metastasis.
In mice that had both miR-34 and p53 silenced concurrently, cancerous lesions formed in a proximal part of the prostrate ducts, in a compartment known to contain prostate stem cells. The early lesions that developed when p53 was silenced alone occurred in a distal part of the ducts, away from the compartment where the stem cell pool is located. This suggested there was another mechanism involved when p53 and miR-34 were jointly silenced.
These findings suggest that drug therapies that target and suppress MET could be especially successful in cancers where both p53 and miR-34 are deficient. This is the first time this mechanism has been proven in a mouse model, said Alexander Nikitin, a professor of pathology in Cornell's Department of Biomedical Sciences. "These results indicated that together miR-34 and p53 regulate the prostate stem cell compartments," said Nikitin.