CEACAM6 Promotes The Proliferation And Migration Of Renal Cancer Cells Through The ERK/AKT Signaling Pathway

Background: Carcinoembryonic antigen related cell adhesion molecule 6(CEACAM6)is a versatile glycoprotein and a member of the CEACAM family.Studies suggest that it serves as a diagnostic and prognostic biomarker in some malignancies.In addition,it is involved in tumorigenesis by stimulating proliferation,suppressing apoptosis,facilitating migration and invasion,promoting angiogenesis,and inducing drug resistance.However,its role in renal cell carcinoma(RCC)remains unknown.In the present study,we demonstrated the oncogenic effects of CEACAM6 in RCC.Methods: CEACAM6 expression was detected by quantitative real-time PCR,immunohistochemical staining and western blot in cc RCC tumor tissues and cell lines.Survival analysis was performed using the data of TCGA database.Cell proliferation and migration were detected by CCK-8 and transwell assays with the overexpression or silencing of CEACAM6.LY294002 was used to block the activation of PI3K/AKT pathway.Associated pathway proteins were detected by western blot.Results: CEACAM6 was upregulated in cc RCC cell lines and tumor tissues.Longer overall survival was observed in RCC patients with relatively low CEACAM6 levels.Furthermore,overexpression of CEACAM6 promoted the proliferation and migration of cc RCC cells.Conversely,sh RNA-mediated CEACAM6 depletion modulated those changes.Further investigation demonstrated that the ERK/AKT signaling pathway activation played a pivotal role.In addition,PI3K/AKT pathway blockade abrogated the effects of CEACAM6 overexpression.Conclusions: CEACAM6 is highly expressed in renal cancer tissues and cell lines,and its high expression is associated with poor survival,which may serve as a biomarker for the diagnosis and clinical prognosis of renal cancer.Abnormal high expression of CEACAM6 is a carcinogenic factor that promotes the development of renal cell carcinoma.The mechanism preliminarily confirms that CEACAM6 may play its role by activating ERK/AKT pathway to promote the proliferation and migration ability of renal cell carcinoma.