6533b859fe1ef96bd12b76bc

RESEARCH PRODUCT

sE-cadherin is upregulated in serum of patients with renal cell carcinoma and promotes tumor cell dissemination in vitro

Helge TaubertFelix K.-h. ChunTanja HüschChristian ThomasMeike SchneiderRoman A. BlahetaVerena LiebFrederike SchneiderEva JüngelAxel HaferkampIgor TsaurSven Wach

subject

AdultMaleUrologyPopulation030232 urology & nephrologymedicine.disease_cause03 medical and health sciences0302 clinical medicineDownregulation and upregulationRenal cell carcinomaBiomarkers TumorTumor Cells CulturedmedicineHumansNeoplasm InvasivenessProspective StudieseducationCarcinoma Renal CellAgedAged 80 and overeducation.field_of_studyCadherinCell growthbusiness.industryChemotaxisMiddle AgedCadherinsmedicine.diseaseKidney NeoplasmsUp-RegulationOncology030220 oncology & carcinogenesisCancer cellCancer researchFemaleCarcinogenesisbusiness

description

Abstract Introduction Cadherin family proteins are involved in the tumorigenesis of several malignancies. However, their significance in renal cell carcinoma (RCC) has not been extensively investigated. The current study investigates the potential of several cadherins to perform as biomarkers for tumor detection and exert functional RCC activity. Methods Pre- and postoperative concentrations of sE-cadherin, cadherin-6, N-cadherin, cadherin-11, cadherin-17, and cadherin-5 were measured in serum of patients undergoing surgery for RCC and correlated to clinical and histopathological parameters. Control serum was obtained from healthy volunteers. A498 and Caki-1 cells were incubated with sE-cadherin and assessed for cell growth, adhesion, and chemotaxis. Results sE-cadherin was significantly upregulated in RCC patients, as compared to controls, and discriminated them with striking accuracy (area under the curve value 0.83). Serum levels remained stable several days after surgery. Treating A498 and Caki-1 cancer cells with various concentrations of sE-cadherin attenuated cell growth and adhesion, while chemotaxis was augmented. Conclusions sE-cadherin is overexpressed in serum of RCC patients and provides a functional cellular switch from sessility to aggressive dissemination. While sE-cadherin is not tumor-specific and thus inappropriate for population-based screening, further studies are warranted to investigate its role in monitoring RCC and employing it as a therapeutic target.

https://doi.org/10.1016/j.urolonc.2019.03.001