The small non-coding molecule miR-194 may promote the spread of prostate cancer by blocking the anticancer protein SOCS2, a study says.
The finding provides new insight into the molecular mechanisms driving metastasis — or the spread of — prostate cancer. Gene expression is the translation of information encoded in a gene into protein or RNA structures that operate in a cell.
The research, “MicroRNA-194 Promotes Prostate Cancer Metastasis By Inhibiting SOCS2,” was published in the journal Cancer Research.
“Prostate cancers only kill men after they have spread or ‘metastasized’ from the prostate. The identification of markers that accurately predict, at an early stage, prostate tumors that are likely to metastasize could guide the urgency and aggressiveness of treatment — and this could save lives,” Luke Selth, senior author of the study, said in a news release. Seth is a senior research fellow at the University of Adelaide’s Dame Roma Mitchell Cancer Research Laboratories and a member of the Freemasons Foundation Center for Men’s Health.
MicroRNAs, or simply miRs, are small RNA molecules that block the expression of certain proteins, acting as regulators of gene expression.
Blood levels of miR-194 have been suggested as a biomarker of whether prostate cancer will recur after surgery, but the exact role of the molecule remained elusive until recently.
Now researchers have found that increased levels of miR-194 in prostate tissue are associated with disease aggressiveness and a poor outcome. Using human prostate cancer cells, the team discovered that enhanced expression of miR-194 promoted migration of tumor cells. On the other hand, inhibiting miR-194 activity suppressed cancer cells’ ability to migrate.
Further laboratory experiments indicated that miR-194 inhibits SOCS2, a protein that suppresses the spread of tumor cells. Indeed, low levels of SOCS2 were strongly associated with disease recurrence and spread.
“In previous work, we had found that a high level of miR-194 in a patient’s blood was associated with rapid relapse of prostate cancer following surgical removal of the tumor,” Selth said. “This new work explains why miR-194 is associated with a poor outcome, and in the process reveals a completely novel pathway regulating prostate cancer metastasis.”
Measuring miR-194 in blood samples of patients with prostate cancer may become a valuable test to determine the risk of metastasis, the researchers said. Patients with increased levels of the molecule could receive more aggressive therapy to decrease the risk of the disease spreading to other organs. The team is now testing this idea in a larger group of patients.
MiR-194 could also be a good avenue for a prostate-cancer treatment, the researchers said.
“There are currently no drugs that effectively inhibit the spread of prostate cancer,” Selth said. “We propose that inhibiting miR-194 could reduce rates of metastasis in patients with aggressive disease, but the development of a drug to achieve this goal is still a long way off.”