Correlation between ADGRV1 expression and clinical pathological and prognostic features in breast cancer

被引:0
作者
Lili Wang [1 ]
Jiadi He [2 ]
Jiaqing Chen [2 ]
Xueqing Zeng [2 ]
Wenjie Lu [2 ]
Yulan Qiu [2 ]
Meigong Zhong [3 ]
Qiuli Li [4 ]
Qisheng Long [5 ]
Liangliang Ren [2 ]
Xin Zhang [2 ]
Yuanzhi Lu [6 ]
机构
[1] Jiangmen Maternity and Child Health Care Hospital,Department of Clinical Pathology
[2] Jiangmen Central Hospital,Jiangmen Key Laboratory of Precision and Clinical Translation Medicine, Clinical Experimental Center, Jiangmen Engineering Technology Research Center of Clinical Biobank and Translational Research
[3] Jiangmen Maternity and Child Health Care Hospital,Department of Pharmacy
[4] Jiangmen Maternity and Child Health Care Hospital,Medical Genetics Center
[5] Jiangmen Maternity and Child Health Care Hospital,Department of Breast Surgery
[6] the First Affiliated Hospital of Jinan University,Department of Clinical Pathology
关键词
Breast cancer; ADGRV1; Methylation; Immune microenvironment; Prognosis; Drug sensitivity;
D O I
10.1038/s41598-025-04695-w
中图分类号
学科分类号
摘要
Breast cancer, a leading global health threat with rising incidence, demands precision medicine guided by molecular subtyping. ADGRV1, an adhesion G protein-coupled receptor gene implicated in tumorigenesis but unexplored in breast cancer, was investigated using TCGA data (1,231 cases) and a local cohort (408 cases). While ADGRV1 showed no differential expression between tumors and normal tissues (P = 0.210), it was significantly downregulated in basal-like subtypes (P < 0.001). The association between high ADGRV1 expression and poor prognosis remains significant in the overall cohort as well as within individual molecular subtype. Functional enrichment analyses linked ADGRV1 to ribosome suppression, ECM remodeling (positive ECM-receptor interaction), and immunosuppression (negative immune pathway regulation), suggesting its role in tumor metastasis. Drug sensitivity assays demonstrated ADGRV1-high tumors confer resistance to lapatinib, gemcitabine, and 5-fluorouracil, particularly in LumB subtypes. Mechanistically, copy number variations and promoter methylation (Pearson r =-0.45, P < 0.001) regulated ADGRV1 expression, with basal-like tumors showing hypermethylation-associated suppression. These findings position ADGRV1 as a prognostic biomarker and potential therapeutic target, highlighting its dual role in tumor microenvironment modulation and drug resistance.
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