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Phosphorylation of NFATC1 at PIM1 target sites is essential for its ability to promote prostate cancer cell migration and invasion.

Sini K EerolaNiina M SantioSanni RinnePetri KouvonenGarry L CorthalsMauro ScaravilliGiovanni ScalaAngela SerraDario GrecoPekka RuusuvuoriLeena LatonenEeva-Marja RainioTapio VisakorpiPäivi J Koskinen
Published in: Cell communication and signaling : CCS (2019)
Based on our data, phosphorylation of PIM1 target sites stimulates NFATC1 activity and enhances its ability to promote prostate cancer cell migration and invasion. Therefore, inhibition of the interplay between PIM kinases and NFATC1 may have therapeutic implications for patients with metastatic forms of cancer.
Keyphrases
  • prostate cancer
  • benign prostatic hyperplasia
  • papillary thyroid
  • protein kinase
  • electronic health record
  • big data
  • squamous cell carcinoma