Effect of TLR4 on the growth of SiHa human cervical cancer cells via the MyD88-TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways.

The present study aimed to investigate the effect of Toll-like receptor 4 (TLR4) on SiHa human cervical cancer cells and its potential molecular biological mechanisms. The expression of TLR4 following treatment with lipopolysaccharide (LPS) in in SiHa cervical cancer cells was detected by quantitative polymerase chain reaction (qPCR). LPS-induced cell proliferation and apoptosis were detected by MTT assay as well as staining with propidium iodide (PI) and Annexin V/PI double staining. qPCR was performed to analyze the expression levels of tumor necrosis factor receptor-associated factor 6 (TRAF6) and transforming growth factor-activated kinase 1 (TAK1) genes. Western blot analysis was performed to analyze the expression of myeloid differentiation 88 (MyD88), nuclear factor-κB (NF-κB), cyclin D1 and signal transducer and activator of transcription 3 (STAT3) proteins. In the present study, it was revealed that TLR4 expression in SiHa cervical cancer cells may be upregulated by LPS. Additionally, LPS was able to increase the proliferation of SiHa cells. However, LPS treatment did not have an effect on apoptosis of the cells. In addition, the MyD88-TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways were induced in SiHa cells by LPS. These results suggested the effect of LPS and TLR4 on proliferation of SiHa human cervical cancer cells via the MyD88-TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways.