Abstract
A wide variety of cancer types have been linked to the misregulation of long non-coding RNA (lncRNA) genes. Now, a team from Cold Spring Harbor Laboratory (CSHL) showed that a particular lncRNA, Mammary Tumor-Associated RNA 25 (MaTAR25), plays a role in mammary tumor cell proliferation, migration, and invasion, both in vitro and in vivo. In animal experiments, the growth of metastatic tumors was reduced by a molecule designed to target that RNA and trigger its destruction. The work demonstrates that the lncRNA represents a potential therapeutic target to alter breast cancer progression.
Experiments by Kung-Chi Chang, a graduate student in the CSHL Lab of David Spector, Ph.D., indicated that MaTAR25 contributes to cancer's progression by accelerating the growth of cancer cells as well as their ability to migrate and invade tissue. These effects may be due to changes in the activity of the Tensin1 gene, which the team found is one of MaTAR25's targets.
The team also identified LINC01271 as the human ortholog of MaTAR25, and importantly, they found that high levels of an analogous RNA called LINC01271 are associated with more aggressive disease in patients' breast tumors. The findings demonstrate that LINC01271 represents a potential therapeutic target to alter breast cancer progression. The team is now investigating whether an antisense oligonucleotide that targets LINC01271 can interfere with tumor growth and metastases in patient-derived breast cancer models.
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