Abstract
: Background Growing evidences have showed that mucins (MUCs) are linked to occurrence and progression of human cancers. However, a comprehensive study regarding the expression, diagnosis, prognosis and mechanism of MUCs in breast cancer remains absent. Methods: A series of in silico analyses were employed in this study. Results: After performing comprehensive analysis for MUCs, MUC14 was identified as the most potential regulator in breast cancer, with downregulated expression in both mRNA and protein levels and significant diagnostic and prognostic values in breast cancer. Mechanistic exploration revealed that a potential ncRNA-mRNA axis, involving LINC01128/LINC01140/SGMS1-AS1/LINC00667-miR-137/miR-429-BCL2, might be partially responsible for MUC14′s functions in breast cancer. Conclusions: Collectively, our study elucidated a key role of MUC14 in breast cancer and also provided some clues for explanation of the molecular action mechanism of MUC14 in breast cancer.
Highlights
Breast cancer, the most frequent cancer type in women worldwide, is one of the leading causes of cancer-related deaths in females [1,2]
Et al found that secretory MUC5AC promoted neoplastic progression by augmenting KLF4-mediated pancreatic cancer cell stemness [7]; Xu et al indicated that MUC1 was overexpressed in NSCLC and silence of MUC1 alleviated paclitaxel resistance of NSCLC [8]; Gao et al suggested that MUC12 enhanced RCC progression by regulating c-Jun/TGF-β signaling [9]; Tiemin et al found that MUC13 facilitated progression of intrahepatic cholangiocarcinoma via EGFR/PI3K/AKT pathways [10]
The expression differences of MUCs among various major stage in breast cancer were assessed using GEPIA database, and the results showed that only MUC16 and mucin 14 (MUC14) presented statistical significance (Table S1)
Summary
The most frequent cancer type in women worldwide, is one of the leading causes of cancer-related deaths in females [1,2]. Treatment regimens for breast cancer contain surgical resection, chemotherapy, radiotherapy, endocrine therapy and molecular target therapy [4]. Et al found that secretory MUC5AC promoted neoplastic progression by augmenting KLF4-mediated pancreatic cancer cell stemness [7]; Xu et al indicated that MUC1 was overexpressed in NSCLC and silence of MUC1 alleviated paclitaxel resistance of NSCLC [8]; Gao et al suggested that MUC12 enhanced RCC progression by regulating c-Jun/TGF-β signaling [9]; Tiemin et al found that MUC13 facilitated progression of intrahepatic cholangiocarcinoma via EGFR/PI3K/AKT pathways [10]. Dysregulated MUCs are reported to serve as potential biomarkers in multiple tumor types. Serum MUC3A is a potential diagnostic biomarker for extrahepatic cholangiocarcinoma [11]; high expression of MUC3A is associated with localized clear-cell renal cell carcinoma [12]; bone marrow MUC4 expression had significant prognostic value in acute myeloid leukaemia [13]
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