ArticleThe Kaohsiung journal of medical sciences2021
Expression of apolipoprotein C1 in clear cell renal cell carcinoma: An oncogenic gene and a prognostic marker.
Article in The Kaohsiung journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- The roles, signalling pathways and therapeutic implications of Apoc1 in cancer.Discover oncology · 2025Review
- APOC1 knockdown induces apoptosis and decreases angiogenesis in diffuse large B-cell lymphoma cells through blocking the PI3K/AKT/mTOR pathway.Biomolecules & biomedicine · 2025Article
- Downregulation of RNA binding protein 47 predicts low survival in patients and promotes the development of renal cell malignancies through RNA stability modification.Molecular biomedicine · 2023Article
- APOC1 promotes the progression of osteosarcoma by binding to MTCH2.Experimental and therapeutic medicine · 2023Article
- Apolipoprotein C1 promotes tumor progression in gastric cancer.Oncology research · 2023Article
- Decreased APOC1 expression inhibited cancer progression and was associated with better prognosis and immune microenvironment in esophageal cancer.American journal of cancer research · 2022Article
- Expression of apolipoprotein C1 in clear cell renal cell carcinoma: An oncogenic gene and a prognostic marker.The Kaohsiung journal of medical sciences · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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