The discovery means researchers may have found a clearer direction for treatment.

A team of researchers at UC San Diego School of Medicine has discovered an enzyme called MICAL2 promotes tumor growth and spread in pancreatic ductal adenocarcinomas (PDAC), the most common form of pancreatic cancer.

The findings, published Jan 2 in the journal Cancer Research, suggest that MICAL2 could be a promising target for PDAC drug therapies, according to senior author Dr. Andrew Lowy, UCSD School of Medicine professor and division chief of surgical oncology and UCSD Moores Cancer Center associate clinical director for surgery.

Pancreatic cancer kills 50,000 people annually, according to the National Cancer Institute; there are few effective treatment options for the disease.

Normally, MICAL2 plays an important role in cell migration and morphology. But when UCSD researchers measured gene expression in PDAC tumor cells, they found an excessive amount of the enzyme was being produced compared with non-diseased cells.

This marked the first time MICAL2 has been experimentally linked to pancreatic cancer.

Additionally, the team found that PDAC patients undergoing tumor-removal surgery with low MICAL2 expression in their tumor cells survived about twice as long as those whose tumor cells produced more of the enzyme, suggesting that MICAL2 may be involved in progressing the disease to an advanced stage.

The team also discovered MICAL2 expression promotes tumor cell division, migration and the invasion of healthy tissue.

“Pancreatic cancer has the highest mortality rate of any common cancer and thus current treatments are woefully inadequate,” Lowy said in a press release. 

“We believe it will be possible to target MICAL2 with drugs as it is an enzyme in a class of proteins against which inhibiting drugs have been successfully made to treat other human diseases.”

The team is now working to identify candidate drugs that would block MICAL2 function in pancreatic cancer. 

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