Loss of E-cadherin Activates EGFR-MEK/ERK Signaling, Promoting Cervical Cancer Progression

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Authors: Hee Yun ; Gwan Hee Han ; Daniel J Wee ; Doo-Byung Chay ; Joon-Yong Chung ; Jae-Hoon Kim ; Hanbyoul Cho

MeSH: Antigens, CD / genetics ; Antigens, CD / metabolism ; Cadherins* / genetics ; Cadherins* / metabolism ; Cell Line, Tumor ; Cell Proliferation ; Disease Progression* ; ErbB Receptors* / genetics ; ErbB Receptors* / metabolism ; Female ; Humans ; MAP Kinase Signaling System* ; Middle Aged ; Prognosis ; Uterine Cervical Neoplasms* / genetics ; Uterine Cervical Neoplasms* / metabolism ; Uterine Cervical Neoplasms* / pathology

Keywords: E-cadherin ; EGFR-MEK/ERK pathway ; biomarkers ; cervical cancer ; pERK1/2 signaling

Abstract: Background/aim: This study investigated the relationship between E-cadherin down-regulation and enhanced pERK1/2 signaling in cervical cancer, evaluated their combined prognostic impact, and explored potential therapeutic targets.

Materials and methods: We analyzed 188 cervical cancer specimens and 300 normal cervical tissue samples using tissue microarray and immunohistochemistry. Small interfering RNA transfection and western blotting were used to study molecular interactions in cervical cancer cell lines.

Results: We observed a significant inverse correlation between E-cadherin and pERK1/2 expression, as well as poor disease-free survival and overall survival. Additionally, molecular analysis indicated that E-cadherin silencing enhanced ERK signaling and promoted cancer cell proliferation.

Conclusion: The findings suggest that E-cadherin and pERK1/2 are crucial biomarkers for cervical cancer prognosis and their interaction provides a potential target for therapeutic interventions. Further studies are recommended to explore these pathways in the clinical setting.