High expression levels of CLEC4M indicate poor prognosis in patients with hepatocellular carcinoma.
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ABSTRACT: The identification of novel and accurate biomarkers is important to improve the prognosis of patients with hepatocellular carcinoma (HCC). C-Type lectin domain family 4 member M (CLEC4M) is involved in the progression of numerous cancer types. However, the clinical significance of CLEC4M in HCC is yet to be elucidated. The aim of the present study is to evaluate the involvement of CLEC4M in HCC progression. The expression level of CLEC4M was determined in tumor, and their corresponding adjacent non-tumor tissues derived from 88 patients with HCC, using immunohistochemistry, western blot and reverse transcription-quantitative PCR. The correlation between CLEC4M expression and certain clinicopathological characteristics was retrospectively analyzed. The results suggested that CLEC4M was specifically labeled in sinusoidal endothelial cells, in both HCC and non-tumor tissues. Moreover, the expression of CLEC4M in tumor tissues was significantly lower than that in non-tumor tissues (P<0.0001), which indicated its potential as a biomarker of the development of HCC. Subsequently, correlation analysis suggested that the relatively higher CLEC4M expression in HCC tissues was significantly associated with increased microvascular invasion (P=0.008), larger tumor size (P=0.018), absence of tumor encapsulation (P<0.0001) and lower tumor differentiation (P=0.019). Notably, patients with high CLEC4M expression levels in their tumor tissues experienced more frequent recurrence and shorter overall survival (OS) times compared with the low-expression group. Furthermore, CLEC4M expression in tumor tissues was identified as an independent and significant risk factor for recurrence-free survival and OS. The results of the present study suggest that CLEC4M may be a valuable biomarker for the prognosis of the patients with HCC, postoperatively.
SUBMITTER: Luo L
PROVIDER: S-EPMC7038977 | biostudies-literature | 2020 Mar
REPOSITORIES: biostudies-literature
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