Coexpression of Notch1 and NF-κB signaling pathway components in human cervical cancer progression

Notch-1 associates with IKKα and regulates IKK activity in cervical cancer cells

“…In all these cases, Notch-1, -2 and -4 were clearly expressed, with a mostly diffuse cytoplasmic pattern, whereas Notch-3 was negative. Notch-1 data are consistent with previous observations (Zagouras et al, 1995;Daniel et al, 1997;Ramdass et al, 2006). In an independent set of 22 samples from University of Southern California, we did not find a statistically significant difference in the number of cases showing strong Notch-1 staining (7/11 normal, 6/11 cancers).…”

“…Immunohistochemistry data of 352 patients (Ramdass et al, 2006) indicate that activation of Notch signaling, as determined by expression levels of intracellular Notch-1, HES1, CDK9 and Jagged-1, is observed in the majority of cervical cancer, and is accompanied by activation of the nuclear factor-kappa B (NF-kB) pathway, as determined by nuclear staining for p50 and p65 and expression of NF-kB target genes. Constitutive activation of NF-kB with nuclear accumulation of p50 and p65 with cervical cancer progression has been described (Nair et al, 2003;Prusty et al, 2005).…”

Notch1 regulates the functional contribution of RhoC to cervical carcinoma progression

“…Dysregulated Notch signalling has been implicated in other tumours including mammary and cervical cancer (Zagouras et al, 1995;Daniel et al, 1997;Politi et al, 2004). Cervical carcinoma, the second most prevalent cancer in women, is initiated and sustained in part by the presence of high-risk human papillomavirus oncogene expression (zur Hausen, 2002), and has an aberrant expression of Notch1, its ligand Jagged1 and downstream target Hes1 (Ramdass et al, 2007).…”

The role of Notch signaling in human cervical cancer: implications for solid tumors

“…This was interpreted as a tumor-suppressive role for Notch signaling in conjunction with the notion that Notch1 is actually downregulated during tumor progression. A later study on an extremely large series of clinical samples did not reveal any evidence of downregulation per se (Ramdass et al, 2007). In contrast the data broadly supported a persistent activation of the pathway in a ligand-dependent manner along with crosstalk with the nuclear factor (NF)-kB pathway.…”