PMC:4330249 / 25089-25832 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4330249","sourcedb":"PMC","sourceid":"4330249","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4330249","text":"Fig. 3 Detailed scheme of the growth factor signalling pathways targeted by nimbolide in cancer cells. Nimbolide strongly inhibits IGF-IR and also affects downstream signalling via the MAPK (ERK) and PI3K/Akt. Transcription factors like NF-κB, c-Myc, and β-catenin consequently cannot be activated, thus modulating target gene expression. As most of the target genes are implicated in cell cycle regulation and proliferation, the cancer cells are finally blocked in cell cycle progression. ERK, extracellularsignal-regulated kinase; IGF-IR, insulin-like growth factor 1 receptor; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor kappa B; PI3K, phosphoinositide 3-kinase; PTEN, phosphatase tensin homolog deleted on chromosome 10.","tracks":[]}