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Mucin 1 (MUC1) is a transmembrane glycoprotein involved in tumorigenesis of diverse cancers. However, the role of MUC1 in glioblastoma (GBM) has not yet been fully explored. In this study, the anticancer mechanism of  MUC1  suppression in GBM was investigated. The expression level of  MUC1  was analyzed in human glioma and paired normal brain tissues.  MUC1  was overexpressed in GBM and was negatively associated with overall survival. Moreover, we silenced  MUC1  to investigate its effect in GBM cell lines and found that knockdown of  MUC1  inhibited cell proliferation and resulted in cell cycle arrest at G1 phase.  MUC1  silencing decreased the phosphorylation of  RB1  and increased the expression of  CDKN1B . Gene set enrichment analysis showed that a series of genes related to cell cycle, telomere maintenance and transforming growth factor Beta (TGF-β) signaling in epithelial mesenchymal transition (EMT) were influenced by  MUC1  knockdown. Notably, the reduced  TERT  expression levels combined with impaired telomerase activity and the switching of telomere maintenance mechanism to alternative lengthening of telomeres (ALT) were observed after  MUC1  knockdown. Our results support the role of  MUC1  in oncological process in GBM which can be developed as a therapeutic target for cell cycle control and telomere maintenance mechanism.

Inhibition of MUC1 exerts cell-cycle arrest and telomerase suppression in glioblastoma cells