Expression of apolipoprotein C1 in clear cell renal cell carcinoma: An oncogenic gene and a prognostic marker

• Published in: The Kaohsiung journal of medical sciences 2021-05, Vol.37 (5), p.419-426
• Main Authors: Wang, Hai‐Jun, Ma, Yong‐Xiang, Wang, Ai‐Hua, Jiang, Yuan‐Shun, Jiang, Xian‐Zhou
• Format: Article
• Language: English
• Subjects: Aged; Analysis; APOC1; Apolipoprotein C-I - biosynthesis; Apolipoproteins; Biomarkers; Biomarkers, Tumor - metabolism; Cancer; Cancer therapies; Carcinoma, Renal cell; Carcinoma, Renal Cell - diagnosis; Carcinoma, Renal Cell - metabolism; Cell Line, Tumor; Cell Proliferation; Cell Survival; clear cell renal cell carcinoma; Diabetes; Epithelial-Mesenchymal Transition; Female; Gender; Gene expression; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Genetic aspects; Humans; Kaplan-Meier Estimate; Kidney cancer; Kidney Neoplasms - diagnosis; Kidney Neoplasms - metabolism; Male; Medical prognosis; Metabolism; Middle Aged; Phenotype; Prognosis; prognostic; Regression Analysis; RNA, Small Interfering - metabolism; Statistical analysis; Up-Regulation; Variance analysis
• ISSN: 1607-551X; 2410-8650
• DOI: 10.1002/kjm2.12328

This study aimed to explore whether APOC1 expression has a function in the biological behavior of clear cell renal cell carcinoma (ccRCC) cells and its possible mechanism. Bioinformatics analysis of data TCGA and OnComine was conducted to explore the expression pattern and prognostic value of APOC1, as well as the relationship between APOC1 expression and clinical indicators. Loss‐ and gain‐ of APOC1 function assays were carried out to assess the biological functions of APOC1. Western blotting was applied to detect protein expression. We revealed that APOC1 was upregulated in ccRCC tissues. APOC1 expression was related to gender, grade, pathologic‐T, pathologic‐stage, and pathologic‐M in patients with ccRCC. Meanwhile, Kaplan–Meier analysis evidenced that the high APOC1 expression indicated unfavorable outcomes of ccRCC. Functional experiments in vitro revealed that upregulation of APOC1 in UT33A cells promoted cell proliferation, invasion, and migration, while downregulation of APOC1 in 786‐O cells had the opposite effect. Furthermore, epithelial mesenchymal transition (EMT) was activated in cells with upregulated APOC1 but inhibited in cells with down‐regulated APOC1. Collectively, our data suggested that APOC1 was overexpressed in ccRCC cells and promoted the malignant biological behaviors and EMT of ccRCC cells.