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  • Title: Decreased expression of CLCA2 and the correlating with immune infiltrates in patients with cervical squamous cell carcinoma: A bioinformatics analysis.
    Author: Yang X, Cao JL, Yang FN, Li XF, Tao LM, Wang F.
    Journal: Taiwan J Obstet Gynecol; 2021 May; 60(3):480-486. PubMed ID: 33966732.
    Abstract:
    OBJECTIVE: Calcium-activated chloride channel 2 (CLCA2) is closely related to the invasion, metastasis, and prognosis of some common malignant tumors. The present study aimed to evaluate the role of CLCA2 in cervical squamous cell carcinoma (CESC) using bioinformatics analysis. MATERIALS AND METHODS: The mRNA sequencing data and the corresponding clinical data were obtained from Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA) database respectively. Then univariate analysis of variance was used to analyze the differential mRNA expression of CLCA2 between normal, cervical Intraepithelial neoplasia (CIN), and CESC tissues and clinicopathological characteristics. The Gene Expression Profiling Interactive Analysis (GEPIA) was used to assess the association between CLCA2 and Disease-Free Survival (DFS), overall survival (OS). The Gene Set Enrichment Analysis (GSEA) was used to explore the associated signaling pathways. The Tumor Immune Estimation Resource (TIMER) was used to predict the potential biological roles of CLCA2 in tumor-immune of CESC. RESULTS: CLCA2 expression was significantly decreased in CESC tissues compared with normal and CIN tissues (P < 0.05). Meanwhile, obese patients had lower levels of CLCA2 expression than normal-weight CESC patients (P < 0.05). However, there was no significant difference in the expression level of CLCA2 in patients with different T stage, lymph node status, metastasis, and FIGO stage in CC(P > 0.05). The survival analysis indicated that for DFS, CESC with high CLCA2 expression was associated with better prognoses compared with those with low expression levels (P < 0.05). But for the OS, there was no difference. GSEA revealed that 4 pathways exhibited significant differential enrichment in the CLCA2 high-expression phenotype, including the P53 signaling pathway, the ERBB signaling pathway, the NOTCH signaling pathway, and the ubiquitin-mediated proteolysis. The TIMER reveals the expression of CLCA2 showed a significant inverse association with the number of B cells, Macrophage cells, and Dendritic Cell infiltration. CONCLUSION: The present study indicates that CLCA2 expression may be a potential prognostic marker for patients with CESC.
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