Researchers have been able to ‘coax’ human breast cells to turn into harmless fat cells in a new proof-of-concept study in mice. Senior author Gerhard Christofori, a biochemist at the University of Basel, in Switzerland, as well as a team of other researchers published their findings in the journal Cancer Cell.
To accomplish this feat, the team exploited a weird pathway that metastasising cancer cells have. When we have a cut, or when a fetus is growing organs, our epithelium tissue can transform into a stem cell called mesenchyme and then reform into whatever cells our body needs to heal or in the case of a fetus, grow body parts. This process is called epithelial-mesenchymal transition (EMT) and it is essential for embryonic development.
Unfortunately, cancer can also use this process, and it’s counterpart, MET (mesenchymal‐to‐epithelial transition), to spread throughout the body and metastasise.
Christofori’s research centred around trying to stop cancer from using any of these two processes to spread throughout the body. The researchers treated mice with an aggressive form of human breast cancer with both a diabetic drug called rosiglitazone and a cancer treatment called trametinib. Both drugs are FDA-approved.
When cancer cells in the mice used one of the two processes to try and spread they changed from cancer into fat cells – a process called adipogenesis.
“The models used in this study have allowed the evaluation of disseminating cancer cell adipogenesis in the immediate tumour surroundings,” the team writes.
“The results indicate that in a patient-relevant setting combined therapy with rosiglitazone and trametinib specifically targets cancer cells with increased plasticity and induces their adipogenesis.”
Although not all cancer cells turned into fat using this method, the ones that underwent the process didn’t change back into cancer cells. The remaining cancer cells within the tumor were no longer able to proliferate unchecked.
“The breast cancer cells that underwent an EMT not only differentiated into fat cells, but also completely stopped proliferating,” Christofori said, as reported by Eureka Alert. “As far as we can tell from long-term culture experiments, the cancer cells-turned-fat cells remain fat cells and do not revert back to breast cancer cells,” he says.
According to Christofori, cells undergoing EMT or MET are in a highly changeable state, and this provides a window of opportunity for therapeutic targeting. The drugs also suppressed the growth of primary tumors in the mice and prevented the tumors from metastasizing throughout the animals’ bodies.
The researchers hypothesize that turning so many cancerous cells into fat cells could also deplete a tumor’s ability to fight off conventional chemotherapy. The group now plan to use their method in combination with existing chemotherapies and in other types of cancers.