Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation.
Fernando J VellosoAlexandre R CamposMari C SogayarRicardo G CorreaPublished in: BMC genomics (2019)
Our proteomic analyses shed new light on the molecular pathways that may be modulating tumorigenesis via NOD1 and NOD2 signaling in TNBC. Up- and downregulation of several proteins associated to inflammation and stress response pathways may promote activation of protein degradation systems, as well as modulate cell-cycle and cellular adhesion proteins. Altogether, these signals seem to be modulating cellular proliferation and migration via NF-κB, PI3K/Akt/mTOR and MAPK signaling pathways. Further investigation of altered proteins in these pathways may provide more insights on relevant targets, possibly enabling the immunomodulation of tumorigenesis in the aggressive TNBC phenotype.
Keyphrases
- signaling pathway
- cell cycle
- cell proliferation
- induced apoptosis
- pi k akt
- cell cycle arrest
- oxidative stress
- innate immune
- epithelial mesenchymal transition
- single cell
- genome wide
- cystic fibrosis
- candida albicans
- cell death
- nuclear factor
- pseudomonas aeruginosa
- dna methylation
- staphylococcus aureus
- small molecule
- lps induced
- amino acid