Bitter taste receptors inside cancer cells have been found to be activated in the presence of anti-cancer drugs. Shutting these receptors down could make the cells more susceptible to drug treatment and help us fight the disease more effectively.
You already know that the human tongue has taste receptors on it that respond to bitter flavors. While that helps some of us love and others loathe tastes like super-dark chocolate or black coffee, the evolutionary purpose of these receptors is to keep us from eating things that could harm or kill us.
What you may not have realized though is that there are other biological structures that also have bitter taste receptors.
They’ve been found in lung cells where they cause muscles to relax and therefore have been studied as a potential treatment for asthma and COPD. They exist in our intestines where they’ve been found to affect the aging process. And they’ve been found in oral and neck cancer cells with one study finding that their activation using the common anesthetic, lidocaine, caused the cells to die off.
Now researchers from Japan’s Okayama University of Science have found another way bitter taste receptors function in cancer cells. They discovered that the receptors, known as TAS2Rs, become activated when cancer cells encounter drugs meant to harm them. Their activation then triggers a drug pumping mechanism that prevents build-up inside the cell. This allows the cells to become drug resistant and difficult to kill using chemotherapy.
In tests, the team found that the cells became highly active and experienced rapid growth in the face of the anticancer drug, doxorubicin. But the scientists also discovered that inhibiting the TAS2R receptors made the cells more receptive to the drug’s effects. They propose that in further research, the role the bitter taste receptors play in pumping out chemotherapeutic drugs be explored more deeply, as well as ways that harmless bitter taste blockers might make the cells more vulnerable to chemical treatments.
“Resistance to anticancer drugs is a significant obstacle in therapy and often leads to relapse and death,” they write in a study published in the journal, Scientific Reports. “Although more extensive studies are required to better understand the functional significance of TAS2Rs in cancer cells, we suggest that intracellular TAS2Rs act as chemosensory receptors that drive the excretion of toxic substances to develop multidrug resistance.
“Good medicine tastes bitter,” they conclude. “This ancient teaching will likely be verified in modern molecular biology in the near future.”
Source: Okayama University of Science via Phys.org
