The Influence Of TLR4 High Expression On The Function Of HPV Infected Cervical Carcinoma Cell

Cervical carcinoma is one of the most common gynecological malignancies, and HPV persistent infection was the main pathogenic factors of cervical carcinoma. Human TLR proteins, the family of innate immune recognition receptors, play an important role in defense of infections. Current evidence suggests that TLR4, which is a member of TLRs, are expressed not only on immune cells but also on many cancer cells, especially inflammation-related cancers. Chronic inflammation mediated by TLR4 may regulate tumor microenvironment to influence the initiation and development of cancer. However, the researches on the correlation between TLR4 and HPV infection cervical carcinoma are still few, in particular, the biological function of TLR4 and its signaling pathway on cervical carcinoma remains unclear.Thus, by taking the human cervical carcinoma cell line, C33A (HPV negative) and SiHa (HPV-16 positive), we try to detect the TLR4 gene differential expression between these two cell line firstly. Furtherly, try to investigate the effect of TLR4 high expression on cell cycle, cell apoptosis resistance, cell migration, cell metabasis and cell reproduction in cervical carcinoma cell line C33A and SiHa. For the aim to explore the relationship between TLR4 and HPV infection cervical carcinoma, to provide more theoretics basis to the research of cervical carcinoma.Our results were as follows:1. The TLR4 mRNA expression was detected by RT-PCR. It was found that TLR4 mRNA expression was much higher in HPV-16 positive SiHa than that in HPV negative C33A.2. The cell growth and reproduction were measured by MTS. It showed that high TLR4 expression could promote cell growth.3. The apoptosis detection was detected by flow cytometry using Annex V-FITC/PI apoptosis detection kit. It gave the result of that the TLR4 might promote the SiHa cell to anti-apoptosis.4. The cell migration was investigated by scarification test and trabswell,We found a stronger migration and metabasis ability in HPV-16 infected SiHa.5. The cell cycle measuring was detected by flow cytometry. It implied that HPV-16 infection could make G0/G1、G1/S cell cycle arrest.Above results indicated that HPV-16 infection SiHa and no-HPV infection C33A behave differently as to cell cycle arrest, anti-apoptosis effect and migration ability to some extent. Such differences might be induced by both HPV-16 infection and TLR4 high expression.