A scientist analyses samples in the laboratory. / ALEJANDRO GARCÍA (EFE)

Spanish scientists discover a gene that could slow cancer development

The Plk1 gene, considered for decades to promote tumours, may also slow down the development of cancer

EUROPA PRESS MADRID.

The Plk1 gene considered for decades to promote tumours may also have the opposite function: to slow down the development of cancer. This is the finding of researchers from the Spanish National Cancer Research Centre (CNIO) and the German Cancer Research Centre (DKFZ), in a study published in the journal Nature Communications.

"The role of Plk1 as a target for potential drugs must now be reviewed since, depending on the type of tumour to be treated, it may or may not be of interest to inhibit it," said the researchers. They have discovered that Plk1 expression in breast tumours can determine different prognoses depending on the subtype of tumour.

The Plk1 gene is "essential" for the division and proliferation of tumour cells. "It has been known for years that Plk1 is overexpressed in a wide variety of tumour types and, on occasions, this overexpression is associated with a poor prognosis (when a gene is overexpressed, there is an excess of the protein produced by that gene in the cell)," researchers said.

Plk1 has for decades been considered an oncogene, a gene that promotes tumour development. However, this had never been formally demonstrated. "Until now, no experiment had been designed to show that Plk1 overexpression does indeed contribute to tumour development," the researchers said.

But in studies the joint team "found that Plk1 not only does not act as an oncogene, but surprisingly, it acts as a tumour suppressor," said Guillermo de Cárcer, one of the principal CNIO scientists.

The researchers consulted breast cancer databases in search of a relationship between Plk1 expression and patient prognosis. They confirmed that "Plk1 expression can result in a very different prognosis depending on the tumour subtype," de Cárcer said. In Her2-positive tumours, the study found that Plk1 expression confers a better prognosis; however, in patients with oestrogen receptor-positive (ER+) tumours, the opposite is true.

The fact that Plk1 acts as a tumour suppressor "may call into question therapeutic strategies based on Plk1 inhibition," said Marcos Malumbres, head of the Cell Division and Cancer Group at the CNIO, but he added that Plk1 inhibition "is still a valid and useful option".

"The fact that Plk1 is a tumour suppressor rather than an oncogene does not imply that Plk1 inhibitors are not effective against cancer. Many essential components of cell proliferation can be used as anti-cancer targets despite not having oncogenic activity, due to the addiction of cancer cells to specific cellular processes such as cell division," Malumbres said.