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‑κB 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‑κB 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‑κB signaling pathway and cell survival. The results demonstrated the elevated co‑expression of Id‑1 and nuclear NF‑κB 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‑κB p65 expression and cell survival capacity. The physical interaction between Id‑1 and NF‑κB 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‑κB signaling. 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. Aside from NF‑κB, Id‑1 may also be developed as a promising therapeutic strategy for cervical cancer.

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