Could RNA Interference be the Key to Shutting Down Cancer?

Each individual cancer cell displays a multitude of genetic mutations. Among the hundreds of these potentially hazardous mutations, scientists believe that the alteration of one to twelve could be enough to render a caner cell impotent and effectively shut it down within the body. The method currently being proposed to achieve this potentially landmark procedure is known as RNA interference.

RNA interference is a naturally occurring cellular phenomenon. In normal cell division, DNA must be transported from the nucleus to the ribosomes. However, RNA can disrupt this path by intercepting small snippets of genetic material en route. This unique type of RNA is specifically referred to as short interfering RNA (siRNA).

As Dr. Daniel Anderson of the David H. Koch Institute for Integrative Cancer Research at MIT explains, this method of interference “offers the potential to turn off essentially any gene in the cell.”

To bring this new theory of cancer treatment into practice, two factors must be addressed. The first is identifying which specific cancer mutations to target for interference. On the top of the list for researchers are those genes that cause cancer cells to divide and replicate quickly. In some cases, such genes have already been identified. However, it should be noted that different kinds of cancer might require different targets for RNA interference.

The second factor that needs to be addressed is finding a way to safely deliver siRNA to cancer cells without overly affecting healthy tissues. According to Steven Dowdy of the University of California, San Diego, delivery of this siRNA is the “number one hurdle” associated with RNA interference treatment.

Presently, the leading candidate for delivery of siRNA is via a fatty molecule called a lipidoid. With RNAi hidden within the lipidoid, the molecule can slip into a cell’s membrane and allow the RNA to go to work. Researchers at MIT have already shown that such a process can be effective in shutting off specific genes within the livers of mice. They have also made progress in reducing ovarian cancer tumor growth in mice via the procedure.

A number of additional steps are required before lipidoid transmission is ready for clinical trials. Most notably, is the fact that lipidoid molecules are fairly large in comparison to RNA data. As a result, the transmission could be hindered.

Another issue is the potential for the lipidoid to enter a normal cell. If such a scenario occurs, the DNA of a healthy cell could be abnormally damaged. To address this issue, scientists are toying with the idea of engineering lipidoids that are peppered with specific proteins. These proteins serve as a homing device of sorts by being drawn to binding proteins present on the exterior of cancer cells.

Currently, experts on the subject such as Dr. Dowdy believe patient-specific RNA interference could be readily available within ten to 20 years. As he sees it, future patients will have their tumors genetically sequenced to discover which cancer-causing genes have been activated. Once this information is known, a specific siRNA treatment can be implemented to effectively shut off the cancer’s ability to proliferate.


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