Synchronous co-expression of Id-1 and nuclear NF-κB p65 promotes cervical cancer progression and malignancy, and is associated with a poor prognosis and chemosensitivity

Although inhibitor of differentiation 1 (Id-1) and NF-kappa B have been shown have play a role in tumorigenesis, their mechanisms and exact roles in cervical cancer have not yet been addressed. This study aimed to investigate the clinical significance of Id-1 and NF-kappa B p65 in cervical cancer and to elucidate their roles in malignant properties. Paraffin-embedded cervical tissue specimens (n=85) were collected for immunohistochemistry and survival analysis. Targeting Id-1 with lentivirus in vitro allowed the examination of the NF-kappa B signaling pathway and cell survival. The results demonstrated the elevated co-expression of Id-1 and nuclear NF-kappa B p65 was more frequently associated with aggressive cervical cancer behavior and poorer clinical outcomes. Targeting Id-1 with short hairpin RNA or Id-1 overexpression lentivirus in SiHa cells demonstrated that Id-1 is associated with nuclear NF-kappa B p65 expression and cell survival capacity. The physical interaction between Id-1 and NF-kappa B p65 was validated in SiHa cells. Moreover, the survival-promoting or chemoresistant effects of Id-1 may be attributed to the subsequent activation of NF-kappa B signaling. On the whole, the synchronous co-expression of Id-1 and nuclear NF-kappa B p65 has a prominent role in cervical cancer, suggesting a combined analysis of Id-1 and NF-kappa B may help to predict malignant properties and prognosis. Aside from NF-kappa B, Id-1 may also be developed as a promising therapeutic strategy for cervical cancer.