Expression of Toll-like receptor 4 in cervical cell lines and cervical lesions and its relation to HPV16 infection.
10.3969/j.issn.1672-7347.2013.11.005
- Author:
Qiaozhi LI
1
,
2
;
Hasimu AYSHAMGUL
;
Yan JIANG
;
Yanhong LIU
;
Guancheng LI
Author Information
1. Department of Pathology, Xinjiang Medical University, Urumqi 830011
2. Cancer Research Institute, Central South University, Changsha 410078, China.
- Publication Type:Journal Article
- MeSH:
Carcinoma, Squamous Cell;
metabolism;
virology;
Cell Line, Tumor;
Cervical Intraepithelial Neoplasia;
metabolism;
virology;
Female;
Human papillomavirus 16;
Humans;
Immunohistochemistry;
Lymphatic Metastasis;
Oncogene Proteins, Viral;
metabolism;
Papillomavirus Infections;
metabolism;
RNA, Messenger;
Repressor Proteins;
metabolism;
Toll-Like Receptor 4;
metabolism;
Up-Regulation;
Uterine Cervical Neoplasms;
metabolism;
virology
- From:
Journal of Central South University(Medical Sciences)
2013;38(11):1110-1116
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the relation between human papillomavirus (HPV16) infection and expression of Toll-like receptor 4 (TLR4) in cervical cell lines and cervical lesion tissues and to investigate the effect of TLR4 on cervical cancer progression.
METHODS:Expression of HPV16 E6 mRNA was detected by RT-PCR. Western blot and immunohistochemistry were used to detect the expression of TLR4 in H8, SiHa, Caski cell lines and formalin-fixed and paraffin-embedded cervical tissue specimens with cervicitis, cervical intraepithelial neoplasia (CIN) and cervical squamous cell carcinama (CSCC). DNA was extracted from paraffin-embedded cervical cancer tissues and HPV16 genes were detected.
RESULTS:The differentiation expression of HPV16 E6 mRNA and TLR4 in SiHa and Caski was significantly higher than that of normal cervical cell H8 (P<0.05). The positive expression rates of TLR4 and HPV16 in chronic cervicitis, CIN, and cervical cancer were 32.0%, 59.4%, and 77.8% (P<0.01) and 8.0%, 48.4%, and 81.0% (P<0.01), respectively. Up-regulation of TLR4 was correlated with tumor differentiation (P<0.01), but not with FIGO stages or lymph node metastasis (P>0.05). The expression of TLR4 was significantly correlated with HPV16 infection in CIN and CSCC (r=0.303, P<0.05, r=0.633, P<0.05).
CONCLUSION:High expression of TLR4 may play important roles in the development and progression of CIN and CSCC, and the expression of TLR4 can be up-regulated by HPV16 infection.
