Researchers have found a set of long non-coding RNAs (lncRNAs) – RNA molecules with no protein-coding capacity – that participate in the metastatic process of ovarian cancer cells.
Inhibiting one of these molecules, called DNM3OS, reduced migration and invasion, suggesting that targeting lncRNAs might be a viable approach for treating ovarian cancer.
The study, “Decoding critical long non-coding RNA in ovarian cancer epithelial-to-mesenchymal transition,” was published in the journal Nature Communications.
Metastasis, which refers to the spread of cancer cells, is a common occurrence in patients with ovarian cancer and occurs in as many as 80 percent of patients. Metastasis is dependent on the ability of cancer cells to undergo a process called epithelial-to-mesenchymal transition (EMT), which allows cells to detach from other cancer cells and enter circulation.
Recent studies have suggested that lncRNAs are involved in the metastatic process. These molecules are known to regulate gene expression, though the exact mechanism by which this occurs is unknown. Researchers set out to determine whether lncRNAs were involved in ovarian cancer metastasis, and if so, which ones were involved.
After conducting a bioinformatics analysis of more than 700 ovarian cancer molecular profiles, the team found three lncRNAs whose levels were significantly higher in aggressive ovarian cancer samples. The lncRNAs, called DNM3OS, MEG3, and MIAT, regulate genes involved in ovarian cancer EMT.
Interestingly, only DNM3OS levels were significantly associated with worse overall survival.
“Overexpression of one of the lncRNAs, DNM30S, was significantly correlated with worse overall ovarian cancer patient survival,” Christine Eischen, an investigator at the Sidney Kimmel Cancer Center at Thomas Jefferson University and lead author of the study, said in a press release.
This finding prompted researchers to further investigate the role of DNM3OS. They used a technique that eliminates specific RNA molecules without affecting the genome to significantly reduce DNM3OS levels. This led to altered expression of genes and pathways linked to EMT, as well as a reduction in the EMT process, cell migration, and invasion.
Therefore, the authors concluded, “our results elucidate lncRNA that regulate EMT and demonstrate DNM3OS specifically contributes to EMT in ovarian cancer.”
Future work in this lab will focus on determining the role of lncRNAs in ovarian cancer. Researchers hope to one day translate their findings into a treatment that can be used to decrease the rate of ovarian cancer metastasis.
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