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.
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Li, H., Jiang, W., Liu, X.-N., Yuan, L.-Y., Li, T.-J., Li, S., Xu, S.-S., Zhang, W.-H., Gao, H.-L., Han, X., Wang, W.-Q., Wu, C.-T., Yu, X.-J., Xu, H.-X., & Liu, L. (2020). TET1 downregulates epithelial-mesenchymal transition and chemoresistance in PDAC by demethylating CHL1 to inhibit the Hedgehog signaling pathway. Oncogene, 1–14. https://doi.org/10.1038/s41388-020-01407-8 Cite
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.
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Researchers investigated whether itraconazole induced autophagy-mediated cell death of colon cancer cells through the Hedgehog signaling pathway.
[Cell Death & Disease]
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