Biologists look to “age” cancerous cells

Scientists at the Moscow Lomonosov State University (MSU) have  studied interdependence  between the biological mechanisms responsible for premature and natural ageing. To do so, they looked into cells’ nuclear membranes. Based on the results of the study, the researchers are hoping to develop a compound that would thwart the proliferation of cancerous cells in the human body. 

The nuclear membrane is multilayered and, in addition to the outer and inner membranes, has an interior layer called nuclear lamina. The lamina is a network of proteins, with lamin A being the most important of them all. The lamina performs a range of functions, including the distribution of chromosomes, the regulation of gene structure, and the protection of genetic material against mechanical damage. Sometimes lamin A faces mutation in its protein genes; the Hutchinson-Gilford progeria syndrome (premature aging), one of the key mutations, draws the most attention. 

As cancer develops and cancerous cells spread in metastases, the lamin A gene “turns off” oftentimes. It’s a lamin A deficit that is believed to help cancerous cells easily permeate narrow intercellular space. 

The MSU researchers found that removing lamin A increases the plasticity of the nucleus and the agility of cells, while substituting a normal lamin A with a mutated one (responsible for premature ageing) leads to a reverse effect, with the nuclear membrane getting more rigid, thus slowing cancerous cells’ permeation considerably. 

The MSU team is currently looking for the best possible inhibitors of the enzyme that is responsible for transforming the immature prelamin A into a mature normal protein. The scientists hope the inhibitors would enhance broader cancer therapies and help rein in metastases.

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