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CLEC3B is downregulated and inhibits proliferation in clear cell renal cell carcinoma

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机构: [1]Medical Research Center, Beijing Chao‑Yang Hospital, Capital Medical University, Beijing 100020 [2]Department of Oncology, Beijing Chao‑Yang Hospital, Capital Medical University, Beijing 100020 [3]Department of Obstetrics and Gynecology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, P.R. China
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关键词: C-Type Lectin Domain Family 3 Member B downregulation copy number loss clear cell renal cell carcinoma proliferation

摘要:
Dysregulation of C-Type Lectin Domain Family 3 Member B (CLEC3B) in serum or tumor tissues has been reported in patients with various cancer types. However, the expression and function of CLEC3B in clear cell renal cell carcinoma (ccRCC) remain unknown. To examine the function of CLEC3B in ccRCC, The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were examined to determine the expression of CLEC3B at the transcriptional level and it was demonstrated that CLEC3B mRNA was significantly downregulated in ccRCC compared with normal tissues (P<0.0001 and P=0.0392 in TCGA and GEO databases, respectively). The downregulation of CLEC3B was further validated at the protein level in 78.9% of ccRCCs by immunohistochemistry. To investigate the potential genetic mechanism for CLEC3B downregulation in ccRCC, copy number analysis was performed by profiling the copy number variation data from the TCGA project and it was revealed that the copy number loss of CLEC3B was prevalent in up to 88.1% of patients with ccRCC. CLEC3B genetic deletion was coupled with the well-known genetic loss of the von Hippel-Lindau tumor suppressor, which is a characteristic oncogenic event during ccRCC carcinogenesis. The downregulation of CLEC3B was associated with tumor progression and predicted unfavorable prognostic outcomes in the TCGA cohort. Real-time cell analyzer system technology revealed that CLEC3B inhibited the proliferation of ccRCC cell lines in vitro and that the mitogen-activated protein kinase pathway may contribute to this process. CLEC3B demonstrated substantial positive associations with proliferation inhibitors, but inverse associations with proliferation inducers and markers in two large ccRCC cohorts, suggesting that CLEC3B was able to identify ccRCCs with a lower proliferation capacity. In conclusion, the results of the present study propose that CLEC3B is a promising target for therapeutic intervention in ccRCC.

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出版当年[2017]版:
大类 | 3 区 医学
小类 | 4 区 肿瘤学
最新[2023]版:
大类 | 3 区 医学
小类 | 4 区 肿瘤学
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出版当年[2016]版:
Q3 ONCOLOGY
最新[2023]版:
Q2 ONCOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2016版] 出版当年五年平均 出版前一年[2015版] 出版后一年[2017版]

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第一作者机构: [1]Medical Research Center, Beijing Chao‑Yang Hospital, Capital Medical University, Beijing 100020
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通讯机构: [1]Medical Research Center, Beijing Chao‑Yang Hospital, Capital Medical University, Beijing 100020 [2]Department of Oncology, Beijing Chao‑Yang Hospital, Capital Medical University, Beijing 100020 [*1]Department of Oncology, Beijing Chao‑Yang Hospital, Capital Medical University, 8 Gong Ti Nan Lu, Beijing 100020, P.R. China [*2]Medical Research Center, Beijing Chao‑Yang Hospital, Capital Medical University, 8 Gong Ti Nan Lu, Beijing 100020, P.R. China
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