Evidence map›Paper›PMID 40032681›Full record

ArticleFunctional & integrative genomics2025

N-glycosylation of GSTO1 promotes cervical cancer migration and invasion through JAK/STAT3 pathway activation.

Panpan Yu, Zouyu Zhao, Qianyu Sun, Bowen Diao, Chongfeng Sun, Yan Wang, Hui Qiao, Hong Li, Ping Yang

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Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Panpan YuFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Zouyu ZhaoFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Qianyu SunFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Bowen DiaoFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Chongfeng SunFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Yan WangFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Hui QiaoFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Hong LiFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China.
Ping YangFirst Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, China. pingy2018@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Glutathione TransferaseJanus KinasesSTAT3 Transcription FactorUterine Cervical NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGlycosylationHumansMiceNeoplasm InvasivenessSignal TransductionGlutathione TransferaseGSTO1 protein, humanJanus KinasesSTAT3 protein, humanSTAT3 Transcription FactorCervical cancerEMTGSTO1JAK/STAT3N-glycosylation

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.