Posted: Friday, September 30, 2022
Human chorion-derived mesenchymal stem cells appear to have an anticancer effect on cholangiocarcinoma cells, providing a potential opportunity for alternative cell therapy with or without conventional chemotherapy. The impact of this type of stem cells on cholangiocarcinoma cells was studied by Chairat Tantrawatpan, PhD, of Thammasat University, Thailand, and his colleagues. Their work was recently published in Scientific Reports.
“These results indicate, for the first time, that [human chorion derived–mesenchymal stem cells] release soluble factors that induce apoptosis of human cholangiocarcinoma cells,” concluded the authors.
Researchers used flow-cytometry analysis to characterize the surface antigens present on isolated mesenchymal stem cells derived from chorion tissue. They then used these stem cells to create a conditioned medium to expose to the cholangiocarcinoma cells. A variety of assays were used to assess the proliferation of three different cholangiocarcinoma cell lines incubated with increasing concentrations of chorion-derived mesenchymal stem cell–conditioned media Western blot analysis aided in understanding the role mesenchymal stem cells may play in modulating the JAK2/STAT3 pathway.
When incubated with CH-CM, the amount of surviving cholangiocarcinoma cells was dramatically decreased, from between 86.9% and 96.0% to 1.5% and 38.0% among the three tested cell lines. The apoptotic cell population was increased in a dose-dependent manner as well, from 0.3% to 2.4% up to 56.2% to 84.0% in the different cholangiocarcinoma lines. Researchers found that the mesenchymal stem cell–conditioned medium may have affected apoptosis of the cancer cells by inducing the loss of mitochondrial membrane potential and activating and regulating apoptosis-related proteins (including BAX, cleaved caspase-3, cleaved PARP, and BCL2). In addition, CH-CM seemed to suppress JAK2/STAT3 signaling in the cholangiocarcinoma cell lines. This inhibitory capability may be mediated through the inhibition of interleukin-6–induced JAK2/STAT3.
Disclosure: The study authors reported no conflicts of interest.