ArticleJournal of gastrointestinal oncology2024
SPP1 promotes tumor progression in esophageal carcinoma by activating focal adhesion pathway.
Article in Journal of gastrointestinal oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells.Regenerative therapy · 2026Article
- Targeted suppression of SPP1 inhibits tumor invasion and metastasis in NRF2 hyperactivated cisplatin resistant HNSCC.Journal of translational medicine · 2026Article
- MAGNET: Multi-view graph autoencoder with cell-gene attention for cell interaction network reconstruction from spatial transcriptomics.PLoS computational biology · 2025Article
- Evaluating Potential Therapeutic Targets and Drug Repurposing Based on the Esophageal Cancer Subtypes.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Interactions between cancer-associated fibroblasts and the extracellular matrix in oesophageal cancer.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Identification of Schwann Cells in Human Intracranial Arteries: Potential Regulatory Role in Atherosclerotic Plaque Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Advances of aptamers in esophageal cancer diagnosis, treatment and drug delivery.Beilstein journal of nanotechnology · 2025Review
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3 authors.
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Abstract
Background: Recurrence and metastasis are the major obstacles affecting the therapeutic efficacy and clinical outcomes for patients with esophageal carcinoma (ESCA). Secreted phosphoprotein 1 (SPP1) is considered as a hub gene in ESCA and is negatively associated with disease-free survival (DFS) in ESCA. However, the exact roles and underlying mechanisms remain elusive. This study aims to examine the roles of SPP1 on ESCA, and elucidate the potential mechanisms. Methods: Bioinformatics were used to analyze the expression of SPP1 in ESCA tissues, and its relations with clinicopathological characteristics and clinical prognosis in patients with ESCA based on The Cancer Genome Atlas (TCGA) dataset. Loss-of-function was conducted to examine the roles of SPP1 on malignant behaviors of ESCA cells by cell counting kit-8 (CCK8), plate clone, wound healing, and transwell assays. Gene set enrichment analysis (GSEA) was conducted to screen the pathways associated with SPP1 in ESCA. Then, the enriched pathway and the underlying mechanism were elucidated by western blotting, cell adhesion, and cell spreading assays. Lastly, Y15 [a specific inhibitor of focal adhesion kinase (FAK)] was used to examine its potential to inhibit tumor growth in ESCA cells. Results: SPP1 was upregulated in ESCA tissues compared to the adjacent nontumorous tissues, which was closely associated with clinical stage, lymph node metastasis, histological subtype, and p53 mutation. A high expression of SPP1 indicated a poor clinical prognosis in patients with ESCA. The knockdown of SPP1 inhibited cell proliferative, migratory, and invasive capacities in ESCA cells. GSEA indicated that the focal adhesion pathway was closely related with SPP1 in ESCA. Further studies confirmed that the knockdown of SPP1 suppressed cell adhesion ability and reduced the expression of p-FAK and p-Erk in ESCA cells. In addition, Y15 inhibited FAK autophosphorylation and dramatically inhibited cell proliferation, migration, and invasion in ESCA cells. Conclusions: SPP1 promotes tumor progression in ESCA by activating FAK/Erk pathway, and FAK is a potential therapeutic target to overcome tumor recurrence and metastasis of ESCA.
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