Researchers investigated the mechanism underneath MSC-reversed lung injury and fibrosis. They determined that coculture with MSC led to the inactivation of NF-κB signaling and therefore suppressed the hedgehog pathway in LPS-treated MLE-12 cells.
Xiao, K., He, W., Guan, W., Hou, F., Yan, P., Xu, J., Zhou, T., Liu, Y., & Xie, L. (2020). Mesenchymal stem cells reverse EMT process through blocking the activation of NF-κB and Hedgehog pathways in LPS-induced acute lung injury. Cell Death & Disease, 11(10), 1–17. https://doi.org/10.1038/s41419-020-03034-3Cite
In vitro and in vivo functional studies performed by silencing or overexpressing TET1 suggested that TET1 was able to suppress epithelial-mesenchymal transition and sensitize pancreatic ductal adenocarcinoma cells to 5FU and gemcitabine. RNA-seq, whole genome bisulfite sequencing and ChIP-seq were used to explore the TET1-associated pathway, and showed that TET1 promoted the transcription of CHL1 by binding and demethylating the CHL1 promoter, which consequently inhibits the Hedgehog pathway.
DHCR24 knockdown reduced whereas DHCR24 overexpression enhanced breast cancer stem‐like cell populations such as mammosphere and aldehyde dehydrogenase positive cell numbers. In addition, DHCR24 overexpression increased the expression of the Hedgehog pathway regulated genes.