Mechanistic studies suggested that canonical TGF-β/Smad signaling pathway is involved in CLC-3-induced gastric cancer cells proliferation, migration and invasion.
The purpose of this study was to evaluate whether ClC-3 influences the migration and invasion of cervical squamous cell carcinoma cells and its possible mechanisms.
Furthermore, higher expression of CLC-3 was correlated with deeper tumor invasion (P = 0.006) and increased lymph node metastasis (P = 0.016), and knockdown of CLC-3 inhibited cell proliferation and migration in vitro.
Silencing endogenous CLC-3 with ShCLC-3 adenovirus significantly decreases volume-regulated chloride currents, inhibits the nuclear translocation of p65 subunit of Nuclear Factor-κB (NF-κB), decreases transcriptional activity of NF-κB, reduces MMP-3 and MMP-9 expression and decreases glioma cell migration and invasion.