Instability of TIAM1 Protein Spreads Lung Cancer

The routine maintenance processes in a cell detect and remove faulty and worn out cell parts so they can be broken down and recycled. A protein called TIAM1 controls the links by which the cells are bound together. In lung cancer cells where the cell maintenance goes wrong, too many TIAM1 links are scrapped off.

"This important research shows for the first time how lung cancer cells sever ties with their neighbours and start to spread around the body, by hijacking the cells' recycling process and sending it into overdrive. Targeting this flaw could help stop lung cancer from spreading," said Dr. Angeliki Malliri, Lead researcher, Cancer Research UK Manchester Institute.

Dr. Malliri and colleagues found that an over-abundance of a protein called HUWE1, which controls the disposal of TIAM1 is the reason for the breaking of too many TIAM1 ties.

HUWE1 has already been linked to tumor formation, but this is the first study to suggest it may also have a role in cell "junction disassembly, migration and invasion."

The team concludes that their results show that "HUWE1 stimulates human lung cancer cell invasion through regulating TIAM1 stability."

Nell Barrie, senior science information manager at Cancer Research UK, said: "Early-stage research like this is essential to find treatments which could one day block cancer spread - which would be a game changer."

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The chances of successful treatment and lower the chance of spreading is possible in lung cancer when it is diagnosed at an earlier stage.

Lung cancer, also known as carcinoma of the lung or pulmonary carcinoma, is a malignant lung tumor characterized by uncontrolled cell growth in tissues of the lung.

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Lung cancer is the second most common cancer in both men and women. Lung cancer accounts for about 13% of all new cancers. About 224,210 new cases of lung cancer and an estimated 159,260 deaths from lung cancer are the estimates for the year 2014 of American Cancer Society for lung cancer in the United States.

Source-Medindia