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Key takeaways: MicroRNA (miRNA) is a post-transcriptional modifier of RNA. Although it’s only about 22 molecules long, its impacts on gene expression are profound. Recent research has established that miRNA manipulation by mesothelioma facilitates the characteristics of the cancer: immunosuppression, unregulated cellular growth, no cell cycle checkpoints, among others. Because gene therapy is already being used to treat mesothelioma—and the mechanisms would be similar to miRNA treatments—maybe miRNA treatments can be implemented in order to stop the cancer at its source.
RNA carries genetic information, like DNA does. Unlike DNA, it only has one strand (compared to DNA’s double-helix shape) and can be found within the whole cell—not just tightly wrapped
up in chromosome-form, like DNA. There are different types of RNA, depending on their function, structure, and general location within the cell. In the case of microRNA (miRNA), they have about 22 nucleotides—which are the subunits of both DNA and RNA—and can be found in different compartments of the cell and directly outside the cell’s membrane. For genes to be expressed, they are “copied” from DNA into RNA in a process called transcription. This transcripted RNA leaves the cell’s nucleus to travel to the ribosomes, which convert RNA into proteins in a process called translation. This is the central dogma of biology: transcription → translation → proteins. miRNA modifies RNA after transcription, so before the RNA is translated into chains of proteins. This means that miRNA can affect genetic expression without imparting any changes on DNA; instead, miRNA turns “on” and “off” different segments of RNA. This can result in some genes being amplified while others being silenced—all thanks to tiny segments of miRNA.
Even beyond mesothelioma, researchers have established that miRNA contributes to the upregulation and downregulation of genes in instances of cancer. For instance, immunosuppression is characteristic of most cancers. If immune function was intact, then its antitumor functions would’ve killed the cancerous cells—so, cancer cells seek to disrupt this anti-tumor immunity by way of miRNA manipulation. miRNA plays an active role in regulating the characteristics of mesothelioma: immunosuppression, abnormal cell growth, lack of programmed cell death, abnormal vasculature, etc. Because it’s been established as associated with mesothelioma, it can serve as a target for new therapies. Gene therapy, which replaces cancer-mediating genes with healthy genes, is already being implemented as a treatment option for mesothelioma patients. What about miRNA therapy?
miRNA levels can be easily quantified: they can be accessed through urine, blood, and other non-invasive tests. This makes them an excellent tool for differentiating between mesothelioma and other similar diseases, even though research is still exploring the “trademarks” of mesothelioma miRNA presentation. miRNA mimics—which are drugs that have the same molecules as RNA, so they mimic the functions of the miRNA they’re replacing—are currently being investigated as a therapeutic option for mesothelioma. When mesothelioma changes miRNA efficacy—so that miRNA can no longer promote normal cell cycle checkpoints and immune function—these effects seem to be reversible, so long as the impacted segments of miRNA are replaced. Although this is still a new avenue of mesothelioma research, it’s exciting: it’s noninvasive, targets the source of the cancer rather than just killing the cells, and provides insight about the development of mesothelioma at the micro-level.
If you or a loved one has been diagnosed with mesothelioma, please call The Halpern Law Firm at 1 (855)-304-3227. We are here to help you navigate the legal process of filing a claim to receive compensation for your cancer diagnosis. We help mesothelioma victims and their families in Pennsylvania.
Sources:
https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2020.00105/full
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020748/
https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2018.00650/full