IL-1β promotes cervical cancer through activating NF-κB/CCL-2.

Cervical cancer is a malignancy with high morbidity and mortality among women. Interleukin (IL)-1β, chemokine (C-C motif) ligand 2 (CCL-2), and activation of NF-κB have been proven to be closely related to the progression of various tumors. However, their role in cervical cancer remains unclear. Cell proliferation, migration, and invasion were detected using MTT, wound healing, and transwell assays. Western blotting and qRT-PCR were used to measure expression of target genes. IL-1β greatly promoted the release of CCL-2 from HeLa cells. Activation of NF-κB and phosphorylated NF-κB (p65) nuclear translocation were accelerated by IL-1β. TPCA-1, a blocker of NF-κB, significantly inhibited the release of CCL-2 from HeLa cells. TPCA-1 markedly reversed the promotional effect of IL-1β on viability of HeLa cells. IL-1β increased the cell migration, proliferation, and invasion of HeLa cells through targeting the NF-κB/CCL-2 pathway. IL-1β/NF-κB/CCL-2 might be a promising treatment target for cervical cancer treatment and prevention.