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Chemical disruption to key interaction shown to limit metastasis in test mice

June 14, 2017

"A considerable amount of research has been dedicated to identifying novel E2F- regulated genes, but a clear role for E2Fs in cancer progression and metastasis had not been established," explained Chellappan. "We find that the Rb-E2F pathway contributes to the expression of many genes involved in different aspects of cancer, and that targeting this pathway might fight metastatic disease."

Their study found that a mouse model of non small cell lung cancer metastasis being treated with RRD-251 had "significantly less metastasis to the lung and surrounding areas." They concluded that disrupting the Rb-Raf-1 interaction using RRD-251 could inhibit the regulatory function of E2Fs as an activator of gene promoters that are related to tumor growth and metastases.

"There is a possibility that E2F might indirectly regulate tumor metastasis as a consequence of its activating these genes," suggested Chellappan. "Taken together, our studies link the Rb-E2F cell cycle regulatory pathway to advanced stages of cancer development and metastasis."

Although further studies are underway, their work suggests that disrupting Rb-Raf-1 interaction can prevent cancer cell proliferation, cell vascular growth (angiogenesis), tumor growth, and the metastatic colonization of organs.

"This approach appears to be a fruitful avenue to combat metastatic disease," concluded Chellappan.

Source: H. Lee Moffitt Cancer Center & Research Institute