The therapeutic potential of targeting LYAR in gastric cancer.
2/5 보강
OpenAlex 토픽 ·
RNA regulation and disease
interferon and immune responses
Mitochondrial Function and Pathology
[AIM] To investigate the expression of Ly1 antibody-reactive clone (LYAR) in gastric cancer (GC) tissues and predict potential drugs targeting its sensitivity.
- 95% CI 0.89-1.51
APA
Kai Qin, Guoqiang Chen, et al. (2026). The therapeutic potential of targeting LYAR in gastric cancer.. Future science OA, 12(1), 2610163. https://doi.org/10.1080/20565623.2025.2610163
MLA
Kai Qin, et al.. "The therapeutic potential of targeting LYAR in gastric cancer.." Future science OA, vol. 12, no. 1, 2026, pp. 2610163.
PMID
41511857
Abstract
[AIM] To investigate the expression of Ly1 antibody-reactive clone (LYAR) in gastric cancer (GC) tissues and predict potential drugs targeting its sensitivity.
[METHODS] We assessed the standardized mean difference (SMD) of LYAR mRNA expression across 20 GC datasets (1,804 GC samples, 858 normal tissues) using multi-center high-throughput data, in-house immunohistochemistry, and CCLE cell expression data. Clinical and pathological relevance of LYAR was evaluated using metrics such as receiver operating characteristic curve, sensitivity, specificity, and likelihood ratios. Additionally, upstream transcriptional regulation and enrichment analyses were performed, and drug sensitivity analysis identified potential drugs for high LYAR expression.
[RESULTS] LYAR expression was significantly upregulated in GC (SMD: 1.20, 95% CI: 0.89-1.51). The area under the curve was 0.89 (95% CI: 0.86-0.92), with sensitivity 0.74 (95% CI: 0.66-0.81) and specificity 0.89 (95% CI: 0.82-0.94). MYC potentially enhances LYAR expression, promoting GC progression. High LYAR expression indicates sensitivity to AZD compounds.
[CONCLUSION] LYAR overexpression promotes GC progression and tumorigenesis, suggesting its potential as a therapeutic target.
[METHODS] We assessed the standardized mean difference (SMD) of LYAR mRNA expression across 20 GC datasets (1,804 GC samples, 858 normal tissues) using multi-center high-throughput data, in-house immunohistochemistry, and CCLE cell expression data. Clinical and pathological relevance of LYAR was evaluated using metrics such as receiver operating characteristic curve, sensitivity, specificity, and likelihood ratios. Additionally, upstream transcriptional regulation and enrichment analyses were performed, and drug sensitivity analysis identified potential drugs for high LYAR expression.
[RESULTS] LYAR expression was significantly upregulated in GC (SMD: 1.20, 95% CI: 0.89-1.51). The area under the curve was 0.89 (95% CI: 0.86-0.92), with sensitivity 0.74 (95% CI: 0.66-0.81) and specificity 0.89 (95% CI: 0.82-0.94). MYC potentially enhances LYAR expression, promoting GC progression. High LYAR expression indicates sensitivity to AZD compounds.
[CONCLUSION] LYAR overexpression promotes GC progression and tumorigenesis, suggesting its potential as a therapeutic target.
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