ArticleScientific reports2025
CALCR interaction with ANTXR1 drives gastric tumor growth and metastasis via AKT signaling pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- GPCRs in CAR-T Cell Immunotherapy: Expanding the Target Landscape and Enhancing Therapeutic Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Integration of single-cell and bulk RNA sequencing data to identify liquid-liquid phase separation-related prognostic biomarkers in hepatocellular carcinoma.Scientific reports · 2025Article
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11 authors.
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Abstract
This study investigates the role of CALCR, a G-protein-coupled receptor, in gastric cancer (GC) progression and its interaction with ANTXR1. A total of 121 patients with gastric cancer were enrolled from the Department of General Surgery, Anyang Tumor Hospital, Anyang City, Henan Province, China. 218 tumor tissues and corresponding para-carcinoma tissues were collected from 109 patients, while adjacent tissues were retained from the remaining 12 cases. Kaplan-Meier analysis evaluated the prognostic value of m6A-related genes in GC. Immunohistochemistry (IHC) was conducted to evaluate CALCR expression. Quantitative real-time PCR (qRT-PCR), Western blot analysis, CCK-8 assays, flow cytometry and transwell assays were used to assess CALCR's role in cell proliferation, apoptosis, migration, and invasion. Co-immunoprecipitation experiments were performed to explore the interaction between CALCR and ANTXR1. Statistical analyses were conducted using SPSS 25.0 and GraphPad Prism 8.0, with p < 0.05 considered significant. IHC staining revealed that 53.2% (n = 58) of the tumor tissues exhibited high CALCR expression, compared to only 6.6% (n = 8) of the para-carcinoma tissues (p < 0.001). CALCR knockdown in GC cell lines significantly reduced proliferation (p < 0.01), increased apoptosis (p < 0.01), and inhibited migration and invasion (p < 0.001). In a nude mouse model, CALCR knockdown resulted in significantly reduced tumor growth and metastasis (p < 0.05). Co-immunoprecipitation showed that CALCR interacts with ANTXR1, leading to decreased AKT phosphorylation. CALCR is a crucial factor in GC progression, presenting a potential prognostic marker and therapeutic target. Targeting the CALCR-ANTXR1 axis and AKT pathway offers new avenues for GC treatment.
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