The peptidyl-prolyl isomerase Pin1 is correlated with the progression of cervical cancer via regulating numerous oncogenic and tumor suppressor pathways. p65 is a crucial regulator of tumorigenesis that is regulated by Pin1, and p65 signaling suppression can enhance the antitumor efficacy of doxorubicin (DOX).
On the whole, the synchronous co‑expression of Id‑1 and nuclear NF‑κB p65 has a prominent role in cervical cancer, suggesting a combined analysis of Id‑1 and NF‑κB may help to predict malignant properties and prognosis.
We found both the membrane expression of CFTR and nuclear translocation of NF-κB p65 were progressively increased from normal cervical tissue, cervical intraepithelial neoplasm, to cervical cancer (overall R² = 0.74, P < 0.001).
Features of Notch1 activation as measured by intracellular Notch1, high levels of Jagged1, Hes1 and Cdk9 were paralleled by nuclear translocation of both NF-kappaB p50 and p65 with target gene expression (IkappaB-alpha, Bcl-2, and CyclinD1) in human cervical cancer sections.