UQ invents test to track how medicines ‘hitchhike’ on cholesterol

Technology developed by PhD scholar Raluca Ghebosu and Associate Professor Joy Wolfram has been designed to assess how different medicines bind to cholesterol particles in our bloodstream.

Ms Ghebosu said mapping this cholesterol ‘hitchhiking’ is crucial to establishing how long medicines remain active, which organs they travel to and, ultimately, how effective they are.

“The problem is that this process requires costly, complex, and time-consuming techniques,” Ms Ghebosu said.

“All are significant barriers to what could be a crucial breakthrough in medicine.

“Our test seeks to simplify the mapping process while also making it much cheaper to get answers.”

The new test, named lipoprotein association fluorometry (LAF), was developed at UQ’s Australian Institute for Bioengineering and Nanotechnology (AIBN) under the mentorship of Associate Professor Wolfram from the AIBN and the UQ School of Chemical Engineering.

Ms Ghebosu said LAF works by using a fluorescent signal to detect when a ‘molecular handshake’ occurs between cholesterol particles and test agents such as medicines.

Crucially, each test is low cost and delivers results in an hour instead of a week.

“By predicting cholesterol binding to various synthetic nanoparticles - as well as polymers, proteins, peptides, and small molecules - we are better placed to uncover information beneficial to drug development,” Ms Ghebosu said.

New insights on cancer progression

As well as measuring how medicines bind to cholesterol, Ms Ghebosu said the LAF also showed how cancer cells could be exploiting the same hitchhiking system.

The technology revealed that tiny messenger particles released by cancer cells - called extracellular vesicles (EVs) – display a particular affinity for latching onto “bad” cholesterol particles. 

Previous studies have shown that these messenger particles help cancers grow and spread, meaning the binding patterns of these particles with cholesterol could open up new inquiries on how to slow or stop the disease.

“Cholesterol is essential for normal body function, but EVs released by cancer cells may be hijacking this system,” Ms Ghebosu said.

Ms Ghebosu said their team had already used the LAF technology to show EVs released by metastatic or ‘super-spreading,’ cancer cells were much better at binding to bad cholesterol compared to those from healthy cells and less aggressive cancer cells.

Associate Professor Wolfram said the binding patterns revealed by LAF could advance our understanding of biological processes and inform future medical applications.

“Ultimately, this raises the possibility that cholesterol may contribute to the spread of cancer through EV binding,” Associate Professor Wolfram said.

“Thankfully, our technique can also be used to explore therapies that help block this binding and assess whether this could slow cancer progression.”

Collaboration and acknowledgements