Posts Tagged ‘breast cancer’

More speech gives fewer malignant breast tumours!

October 25, 2014

Who would have thought the ability to develop speech may be linked to the malignancy of breast cancer cells.

A new paper in Cell Stem Cell apparently shows that “silencing the Speech Gene FOXP2 Causes Breast Cancer Cells to Metastasize”Forkhead box protein P2 (FOXP2) is a protein that in humans is encoded by the FOXP2 gene and which is thought to enable speech and language development in the brain. It is also known to affect tissue development. While Neanderthals had the physical capability for speech it is not known if they had the FOXP2 gene. The new paper reports that suppressing the FOXP2 gene leads to more breast cancer cells turning malignant.

Perhaps the ability to talk is a survival factor for women?

The number of genes may be finite and limited but they are expert not only at multi-tasking but also in working in very many different “teams” with other genes.

Beth Israel Press Release:

It is an intricate network of activity that enables breast cancer cells to move from the primary breast tumor and set up new growths in other parts of the body, a process known as metastasis.

Now a research team led by investigators at Beth Israel Deaconess Medical Center (BIDMC) has identified an unexpected link between a transcription factor known to regulate speech and language development and metastatic colonization of breast cancer.

Currently described online in Cell Stem Cell, the new findings demonstrate that, when silenced, the FOXP2 transcription factor, otherwise known as the speech gene, endows breast cancer cells with a number of malignant traits and properties that enable them to survive – and thrive. …

…….. FOXP2 has primarily been implicated in regulating speech and language development and several reports have described functions for this protein in developmental neurogenesis. Additional reports have also linked FOXP2 to tissue development, such as the lung.

“We were curious and wanted to find out the business of FOXP2 in breast cancer,” he adds. “Surprisingly, we found that its suppression in the tumor cells was sufficient to expand cancer stem cell traits and caused the cancer cells to metastasize much more vigorously.”

These findings agreed with similar results in which the authors determined that miR-199a upregulation and FOXP2 repression are prominent features of aggressive clinical breast cancers and represent independent prognostic parameters for overall patient survival.

“We are one step closer to understanding how cells in the tumor microenvironment, such as MSCs, promote the malignancy of neighboring cancer cells,” says Karnoub. “We’re now more closely investigating FOXP2’s potential role as a metastasis suppressor that needs to be downregulated for metastasis to take place.”


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