A new study gives hope for improved treatment of prostate cancer, the second most diagnosed cancer, and the fifth leading cause of cancer death, among men worldwide.

In fact, one of the researchers behind the find has gone so far as to say the discovery could “stop the progression of implicated cancers in their track”.

In 2020, almost 1.5 million people were diagnosed with the disease, and nearly 400,000 people died from it.

Scientists have now figured out how one of the main drivers of prostate cancer, the enzyme Protein Serine Kinase H1 (PSKH1), can be switched on, and off.

The new Australian-led study could help develop better, more targeted therapeutic approaches to treat cancer.

“Tumours form because cells ignore normal signals that tell them it’s time to stop growing, or that it’s time to die,” Dr John Scott of the Monash Institute of Pharmaceutical Sciences, joint senior author of the study published in the journal PNAS, said.

“When a signalling molecule, such as PSKH1, interacts with certain proteins on a cell surface, this binding triggers a chain of events that can amplify the cell activity and lead to the formation of tumours.”

Calmodulin binds to PSKH1 (in grey) to ‘switch on’ its activity. Reticulocalbin binds to PSKH1 to ‘switch off’ its activity. Photo: WEHI

PSKH1 overactivity is associated with tumour progression and metastasis (spread) in prostate cancer. It is also linked to lung and kidney cancers.

How it does this has been unclear until now.

Scott and collaborators found that PSKH1 becomes active when it binds to a protein called Calmodulin, which triggers the cascade of signals that promote tumour formation.

But when PSKH1 binds to a protein called Reticulocalbin, this activity is switched off.

“Now that we know more about the proteins driving the ‘on’ and ‘off’ status of PSKH1, we can start to develop new drugs that target this molecule,” Scott said.

Joint senior author of the study, Professor James Murphy of WEHI, agree. The information “opens a whole new world of potential when it comes to developing new drugs”, he said.

“Switching off PSKH1 essentially means being able to stop the progression of implicated cancers in their track,” Murphy said.

“From here, our goal is to explore how we can start to develop new effective therapies, with less side effects.”

This article first appeared in Cosmos. Read the original here