N-glycosylation of GSTO1 promotes cervical cancer migration and invasion through JAK/STAT3 pathway activation
- PMID: 40032681
- DOI: 10.1007/s10142-025-01565-6
N-glycosylation of GSTO1 promotes cervical cancer migration and invasion through JAK/STAT3 pathway activation
Abstract
Protein glycosylation is strongly associated with tumor progression. Glutathione S-transferase omega 1 (GSTO1) is a member of the glutathione S-transferase family. The significance of GSTO1 N-glycosylation in the progression of cervical cancer (CC) has remained elusive. In this study, we investigated the functional significance of GSTO1 N-glycosylation in CC progression. We employed immunohistochemistry to detect the relative expression of evaluating the link between GSTO1 in CC and benign tissues and the overall survival (OS) and progression-free survival (PFS) in CC patients.In vitro and in vivo experiments to detect CC cell proliferation or metastatic ability after GSTO1 downregulation. NetNGly1.0 Server database predicts potential N-glycosylation modification sites of GSTO1 (Asn55, Asn135, Asn190). Investigating GSTO1 N-glycosylation's function in cellular migration, invasion and epithelial-mesenchymal transition (EMT), we mutated the N-glycosylation sites of GSTO1 through lentivirus-based insertional mutagenesis. Detection of signalling pathways associated with N-glycosylation-modified GSTO1 by enrichment analysis and Western blot. Compared to normal cervical tissue, CC tissue showed significantly higher GSTO1 expression. Further, high GSTO1 levels were a poor predictor of OS and PFS. Both cell and animal experiments suggested that down-regulation of GSTO1 inhibited cell proliferation and metastasis. Glycosylation modification of targeted mutant GSTO1 at positions 55, 135 and 190 significantly inhibits migration and invasion of CC cells. GSTO1 N-glycosylation fixed point mutation inhibits EMT process in CC cells. Mechanistically, N-glycosylated GSTO1 promoted the expression of JAK/STAT3 pathway related markers. GSTO1 N-glycosylation is associated with CC progression and may promote EMT via JAK/STAT3 signaling.
Keywords: Cervical cancer; EMT; GSTO1; JAK/STAT3; N-glycosylation.
© 2025. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Conflict of interest statement
Declarations. Ethics approval and consent to participate: This study was approved by the Medical Ethics Committee of the First Affiliated Hospital of Shihezi University (KJ2020-065–01 and A2020-115–01). Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.
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