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One Specific MicroRNA Appears To Promote Tumor Growth And Cancer Spread

Researchers at have determined that the overexpression of microRNA-155 (miR-155), a short, single strand of ribonucleic acid encoded by the miR-155 host gene, promotes the growth of blood vessels in tumors, tumor inflammation, and metastasis. As a , miR-155 could potentially provide a new avenue of treatment when targeted with drugs to suppress its activity.

The study was published in a recent online issue of Oncogene.

MiR-155, which plays an important role in various physiological and pathological processes, is considered an indicator of poor prognosis for patients when it is overexpressed. Controlling miR-155 expression could inhibit malignant growth, said the researchers.

“Our study shows that miR-155 is a driver of new blood vessel growth in tumors,” said study lead author , M.D., Ph.D., senior member of the Cancer Biology and Evolution Program at Moffitt. “It also plays a critical role in metastasis, especially in triple-negative breast cancer. This makes miR-155 both a prognostic marker and a potential therapeutic drug target.”

According to the researchers, several studies show that miR-155 is frequently increased in various human malignancies, including breast, lung, pancreatic and colon cancers. It also regulates a number of cell processes, including growth, survival, migration and invasion. Their study demonstrates that miR-155 promotes new blood vessel growth in breast cancer by targeting a natural tumor suppressor called VHL, part of an important cancer pathway for a cascade of events.

“Further studies could provide insight into the role of miR-155 in inflammation that leads to tumor progression,” noted the researchers, who found elevated miR-155 in triple-negative breast cancer, a form of breast cancer that does not express the genes for estrogen, progesterone and human epidermal growth factor receptors.

“Our findings are important for a number of reasons,” Cheng said. “We have shown that miR-155 targets and downregulates the tumor suppressor VHL and that miR-155 contributes to and spread. This makes miR-155 a critical therapeutic target in breast cancer.”


The study was funded by federal grants CA14343, CA15308 and CA137041.
H. Lee Moffitt Cancer Center & Research Institute