Cancer pain delivers a message. A vile, biting message to patients that life itself is seeping through their fingers. A disheartening, damning message to medical specialists that even their powers are limited. It thrusts itself as a physical manifestation of the unseen, of your interiors being eaten away. It is common to mistaken pain as merely pain neurons being stuck in the ‘on’ position, but it is much more complex than that: pain that develops from an acute injury is actually the result of hyperactivation of the peripheral pain neurons responsible for inflammation. Previously thought of as merely bystanders, these pain neurons have been revealed to actively participate in the progression of the carcinogens. With cancer pain being one of the most intense and difficult brands of pain to treat, further research is warranted more than ever.
My project this summer in the Ji lab branches off of my mentor’s ongoing project on the role of STING, a protein that activates interferons, in suppressing pain and reducing neuroinflammation. STING holds a central role in the innate immunity–it produces a protective response by inducing mediators such as cytokines or chemokines. These molecules can then either produce or suppress neuroinflammation. One of the most important mediators that STING activates is type I interferons, which are proteins that boost the immune system in fending off viruses or cancer. As a result, activating STING has potential to not only decrease tumor growth but also dampen neuroinflammation, the underlying etiology of pain.
My mentor and I have been running experiments on mice to not only affirm the role of STING in producing interferons that decrease sustained pain but to also eliminate the possibility that other mechanisms are contributing to this effect. Mice that experience chronic pain have a heightened ability to feel pain from that stimuli that wouldn’t induce pain in normal conditions. To determine the exact threshold where these mice are first able to sense pain, I have been conducting a test called the Von Frey assay. A factor that can lead to false signs of pain in mice is anxiety, so I have also been conducting an open field test to track the movement of mice and then analyze signs of anxiety, ultimately to show that these mice are not any more anxious than normal. So far, the hypothesis that activating STING decreases pain has been supported, but further experiments are necessary to identify the exact mechanism by which STING is able to do so.