ArticleOncogene2025
SPTLC2 drives an EGFR-FAK-HBEGF signaling axis to promote ovarian cancer progression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Structure-guided discovery and evaluation of an EGFR L858R-targeting peptide with antiproliferative activity against ovarian cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- SPTLC2-driven sphingolipid reprogramming of neutrophils impairs anti-tumour immunity and drives liver cancer progression.Oncogene · 2026Article
- Prediction and mechanistic insights into drug-induced reproductive toxicity through integrated machine learning, FAERS-based signal comparison, and network toxicology analyses.Molecular diversity · 2026Article
- PLCD1 expression for early detection and prognosis in High-Grade serous ovarian cancer.BMC cancer · 2025Article
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- SRC and ERK Regulate the Turnover of Cytoskeletal Keratin Filaments.International journal of molecular sciences · 2025Article
- FAM49B suppresses ovarian cancer cell growth through regulating MAPK signaling.American journal of cancer research · 2025Article
- The DHODH inhibitor teriflunomide impedes cell proliferation and enhances chemosensitivity to daunorubicin (DNR) in T-cell acute lymphoblastic leukemia.Annals of hematology · 2024Article
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Authors and funding
10 authors.
Funding
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Abstract
The epidermal growth factor receptor (EGFR) signaling pathway is frequently associated with ovarian cancer (OC) progression. However, inhibition of EGFR signaling in OC patients achieved limited therapeutic effects, highlighting the need to define the mechanism of EGFR deregulation in OC development. Herein we showed that serine palmitoyltransferase long chain base subunit 2 (SPTLC2) acts as a positive regulator in the EGFR signaling pathway in OC. Phenotypically, depletion of SPTLC2 suppressed clonogenic growth and migration of OC cells in vitro and in ovo, as well as metastasis in OC xenograft models, whereas overexpression of SPTLC2 yielded opposite effects. Mechanistically, SPTLC2 drives an EGFR-FAK-HBEGF signaling axis via binding with EGFR. Notably, the serine palmitoyltransferase activity of SPTLC2 is critical for regulation of the EGFR-FAK-HBEGF signaling axis and activity in OC progression. Clinically, high SPTLC2 expression is associated with high-grade serous ovarian cancer and metastasis. Collectively, our findings establish an oncogenic role of SPTLC2 in OC growth and progression though upregulation of EGFR signaling and suggest that SPTLC2 represents a potential therapeutic target in EGFR-driven ovarian cancer patients.
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