Scientists of Memorial Sloan-Kettering Cancer Center revealed a handful of tiny ribonucleic acid (RNA) molecules that halts the spread of breast cancer to the lungs and bone.
MicroRNAs are known to stall the activity of entire sets of genes linked to cancer metastasis, which is a process that is responsible for the majority of cancer-related deaths.
AdvertisementThese "microRNAs" essentially play the role of brakes in the proliferation of cancer. When they are missing, that allows the disease to spread freely, and when they are restored, however, the cancer cells lose some of their ability to metastasize, the Memorial Sloan-Kettering Cancer Center scientists report.
The work has implications both for predicting which cancers are aggressive and establishing new targets for drug therapy down the line, said study's lead author Sohail Tavazoie, MD, PhD, a postdoctoral fellow in the Oncology-Hematology Fellowship program at MSKCC.
For the study, the researchers examined human breast cancer cells with strong metastatic ability and found that the cells had lost large numbers of three different microRNA molecules.
On the other hand, when researchers put those molecules back into human breast cancer tumours in mice, the tumours lost their ability to spread.
Besides, the researchers studied breast cancer patients and found that those with tumours that had lost these molecules were much more likely to suffer from cancer metastasis to the lung and bone.
"The identification of molecules that inhibit a cell's metastatic potential may help guide clinical decision-making in the future by enabling oncologists to more accurately identify patients at highest risk for metastatic relapse," Nature quoted Tavazoie, as saying.
The team further inspected one of these microRNAs, called miR-335, and discovered that miR-335 works by suppressing certain genes that are associated with human metastasis, predominantly SOX4, which acts as a transcription factor (meaning that it regulates a group of genes responsible for cell development and migration), and tenascin-C, which functions outside the cell in what is called the extra-cellular matrix and is implicated in cell migration.
"We now have a better understanding of the role this molecular pathway plays as a suppressor of breast cancer's ability to spread to the lung and bone, and we have identified the genes involved in that process," said Joan Massagué, PhD, Chair of the Cancer Biology and Genetics Program at MSKCC, a Howard Hughes Medical Institute Investigator, and the study's senior author.
"These findings may enhance our ability to come up with more effective drugs to prevent or treat cancer metastasis," he added.
The study appears in the January 10, 2008, issue of Nature.
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