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

Area of Science:

• Oncology
• Immunology
• Molecular Biology

Background:

• Cervical cancer presents a significant global health burden with high morbidity and mortality.
• Interleukin-1β (IL-1β), chemokine (C-C motif) ligand 2 (CCL-2), and NF-κB pathway activation are implicated in various cancers, but their specific roles in cervical cancer are not fully understood.

Purpose of the Study:

• To investigate the role of IL-1β, CCL-2, and NF-κB activation in cervical cancer progression.
• To elucidate the molecular mechanisms by which IL-1β influences cervical cancer cell behavior.

Main Methods:

• Cell viability, migration, and invasion were assessed using MTT, wound healing, and Transwell assays, respectively.
• Gene and protein expression levels were quantified using quantitative real-time PCR (qRT-PCR) and Western blotting.
• The effect of NF-κB inhibition was evaluated using TPCA-1, a specific NF-κB blocker.

Main Results:

• IL-1β significantly enhanced the release of CCL-2 from HeLa cervical cancer cells.
• IL-1β promoted NF-κB activation, evidenced by increased phosphorylation and nuclear translocation of NF-κB (p65).
• Inhibition of NF-κB with TPCA-1 suppressed IL-1β-induced CCL-2 release and reversed the promotional effects of IL-1β on cell viability, migration, and invasion.

Conclusions:

• IL-1β drives cervical cancer cell proliferation, migration, and invasion by activating the NF-κB/CCL-2 signaling pathway.
• The IL-1β/NF-κB/CCL-2 axis represents a potential therapeutic target for cervical cancer treatment and prevention.