our present study revealed that KMT2A epigenetically promotes cancer progression by targeting CTSZ which has specific functions in cancer invasion and metastasis.
expression of cathepsin B and X was detected in stromal cells and cancer cells throughout the glioblastoma (GBM) sections whereas cathepsin K expression was more restricted to arteriole-rich regions in the GBM sections. Metabolic mapping showed that cathepsin B but not cathepsin K is active in GSC niches.
we evaluated the involvement of cathepsin B and X in the TGF-b1 signaling pathway one of the key signaling mechanisms triggering epithelial-mesenchymal transition in cancer. In MCF-7 cells the expression of cathepsin B was shown to depend on their activation with TGF-b1 while for cathepsin X a TGF-b1 independent mechanism of induction during EMT is indicated.
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