Keywords
E6
beta catenin
vimentin
smooth muscle alpha-actin
EMT
EGFR / PI3K / AkT / mTOR pathway
How to Cite
Abstract
Introduction: The invasion and metastasis of carcinomas are regulated by different signaling pathways, some of which (Wnt/beta catenin, TGFβ-R) regulate the epithelial-mesenchymal transition EMT). In cervical cancer, the E6 protein of the high-risk human papillomavirus (HPV) destabilizes adherent junctions, the first step in the invasive process.
Objectives: a) To investigate EMT in cervical cancer and b) to study the expression of beta-catenin during the neoplastic transformation process, in relation to E6 protein expression.
Materials and methods: Surgical specimens from various cervical cancers were used and immunohistochemistry was performed with antibodies to Beta catenin, Vimentin, Alpha smooth Muscle Actin (αSMA) and E6 from HPV 16/18. Results: Beta catenin showed a peripheral (membranous) pattern in the upper 2/3 of Low grade Squamous Intraepithelial Lesion (LSIL) (12/12) and a cytoplasmic one in the lower 1/3. Negative in adenocarcinoma (Adenok) (15/15) and Squamous carcinoma (25/25). Vimentin and αSMA were negative in all lesions. All pathological epithelial cells were positive for HPV 16/18: adenocarcinoma in situ (AIS) 6/6, Adenok (11/11), Squamous carcinoma (9/9).
Conclusion: The Wnt / beta catenin pathway and EMT are not activated in cervical cancers. The HPV E6 protein destabilizes adherent joints and triggers invasive processes. Probably, the EGFR / PI3K / AkT / mTOR pathway w