ArticleTranslational lung cancer research2022
Targeting STT3A produces an anti-tumor effect in lung adenocarcinoma by blocking the MAPK and PI3K/AKT signaling pathway.
Article in Translational lung cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Expanding TheCellMap.org to visualize a genome-scale genetic interaction network for a human cell line.bioRxiv : the preprint server for biology · 2026Article
- NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis.Translational oncology · 2026Article
- Functional inactivation of oligosaccharyltransferase a isoform suppresses tumor metastasis.Glycobiology · 2025Article
- Integrated multi-omics analysis identifies key biomarkers associated with post-translational modifications and RNA methylation in clear cell renal cell carcinoma.Discover oncology · 2025Article
- Safety, Pharmacokinetics, Translational and Molecular Mechanistic Insights on the Prostate Cancer Recurrence Suppressor Pseurotin A.Molecules (Basel, Switzerland) · 2025Article
- A global genetic interaction map of a human cell reveals conserved principles of genetic networks.bioRxiv : the preprint server for biology · 2025Article
- ER stress-driven unfolded protein response fuels aging-related tumor aggressiveness in gliomas.Frontiers in molecular biosciences · 2025Article
- B3GNT5 is a novel marker correlated with malignant phenotype and poor outcome in pancreatic cancer.iScience · 2024Article
- The Glycosylation of Immune Checkpoints and Their Applications in Oncology.Pharmaceuticals (Basel, Switzerland) · 2022Review
- CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glycosylation is crucial for the stability and biological functions of proteins. The aberrant glycosylation of critical proteins plays an important role in multiple cancers, including lung adenocarcinoma (LUAD). STT3 oligosaccharyltransferase complex catalytic subunit A (STT3A) is a major isoform of N-linked glycosyltransferase that catalyzes the glycosylation of various proteins. However, the functions of STT3A in LUAD are still unclear. Methods: The expression profiles of STT3A were initially analyzed in public data sets and then validated by quantitative real-time polymerase chain reaction, Western blot and immunohistochemistry assays in clinical LUAD samples. The overall survival (OS) between patients with high and low STT3A expression was compared using a Kaplan-Meier curve with a log-rank analysis. STT3A was knocked-out using CRISPR/Cas9 and inhibited by NGI-1. Cell Counting Kit-8, colony formation assay, wound-healing, transwell assay, and flow cytometry were performed to assess the cellular functions of STT3A Results: The expression of STT3A was frequently upregulated in LUAD tissues than normal lung tissues. The high expression of STT3A was significantly associated with poor OS in LUAD patients. The knockout or inhibition of STT3A suppressed proliferation, migration, and invasion, and arrested the cell cycle of LUAD cell lines Conclusions: STT3A promotes LUAD progression via the MAPK and PI3K/AKT signaling pathways and could serve as a novel prognostic biomarker and potential therapeutic target for LUAD patients.
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