Apolipoprotein C1 stimulates the malignant process of renal cell carcinoma via the Wnt3a signaling

Abstract

Background RCC is a clinically common tumor in the urinary system, showing an upward trend of both incidence and mortality. APOC1 has been identified as a vital regulator in tumor progression. This study aims to uncover the biological function of APOC1 in RCC process and the underlying mechanism. Methods Differential levels of APOC1 in RCC samples and controls in a downloaded TCGA profile and clinical samples collected in our center were detected by qRT-PCR. The prognostic value of APOC1 in RCC was assessed by depicting Kaplan-Meier survival curves. After transfection of sh-APOC1 or oe-APOC1, cell phenotypes were examined through CCK-8, colony formation, Transwell assay and flow cytometry. Subsequently, EMT-related genes influenced by APOC1 were determined by Western blot. The involvement of Wnt3a in APOC1-regulated malignant process of RCC was then examined through a series of rescue experiments. Finally, a xenograft model was generated in nude mice for clarifying the in vivo function of APOC1 in RCC process. Results APOC1 was upregulated in RCC samples. Notably, its level was correlated to overall survival of RCC patients, displaying a certain prognostic value. APOC1 was able to stimulate proliferative and metastatic abilities in RCC cells. Wnt3a signaling was identified to be involved in APOC1-mediated RCC process. Notably, Wnt3a was able to reverse the regulatory effects of APOC1 on RCC cell phenotypes. In vivo knockdown of APOC1 slowed down the growth of RCC. Conclusions APOC1 stimulates the malignant process of RCC via targeting the Wnt3a signaling.