Figure 1From: A mechanistic role for the chromatin modulator, NAP1L1, in pancreatic neuroendocrine neoplasm proliferation and metastasesEffect of NAP1L1 silencing. Effect of NAP1L1 silencing on p57Kip2 and menin expression as well as on the mTOR pathway in BON cells. An effective NAP1L1 knockdown (approximately 3-fold, *p < 0.001) increased p57Kip2 protein (A) and mRNA (B) (#p < 0.01), while menin was increased at protein level only (A and B). The ERK pathway was unaffected in NAP1L1-silenced cells, while total mTOR as well as phosphorylated mTOR decreased in NAP1L1 silenced BON cells (C). The mTOR downstream effectors eukaryotic initiation factor 4E-binding protein (4E-BP1) and S6 kinase (S6K1) also showed less protein expression and decreased phosphorylation when NAP1L1 was absent (D and E) (*p < 0.05). MRNA levels of the two ribosomal proteins RPS24 and RPL28, as a measure of mTOR activity, were also decreased in NAP1L1 knockdown cells (*p < 0.05), indicating that NAP1L1 may promote mTOR signaling (F). 4E-BP1, lower band. Mean ± standard error of mean (SEM).Back to article page