乳腺癌（BC）是一种常见的癌症，其特征是具有高分子异质性。因此，了解其生物学特性并为具有不同分子特征的患者开发有效的治疗方法势在必行。钙敏感受体（CaSR）与多种人类癌症的多种调节功能有关。然而，其在BC进展中的潜在病理机制仍然难以捉摸。我们利用癌症基因组图谱和基因表达综合数据库来探讨CaSR在BC转移中的功能。基因本体分析、京都基因和基因组百科全书分析以及生物过程和细胞信号通路的基因集富集分析揭示了CaSR可以被激活或抑制。重要的是，定量逆转录酶-聚合酶链反应和蛋白质印迹用于验证 CaSR 的基因表达。进行伤口愈合和transwell实验来评估CaSR对BC细胞迁移的影响。我们证明转移性BC中CaSR的表达高于非转移性BC。这是首次利用数据库信息揭示BC中CaSR的生物学过程和分子机制。此外，正常乳腺上皮细胞中的CaSR表达明显低于BC细胞中的表达。西那卡塞（一种 CaSR 激动剂）激活 CaSR 显着增强了 BC 细胞的迁移，而 NPS-2143（一种 CaSR 拮抗剂）治疗则显着抑制了这些作用。生物信息学技术和实验证明了 CaSR 参与了 BC 转移。我们的研究结果为 BC 的受体治疗和分子发病机制提供了新的线索，并强调了 CaSR 促进 BC 转移的关键功能。

Breast cancer (BC) is a common cancer characterized by a high molecular heterogeneity. Therefore, understanding its biological properties and developing effective treatments for patients with different molecular features is imperative. Calcium-sensing receptor (CaSR) has been implicated in several regulatory functions in various types of human cancers. However, its underlying pathological mechanism in BC progression remains elusive.We utilized The Cancer Genome Atlas and Gene Expression Omnibus databases to explore the function of CaSR in the metastasis of BC. Gene ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis, and Gene Set Enrichment Analysis of biological processes and cell signaling pathways revealed that CaSR could be activated or inhibited. Importantly, quantitative reverse transcriptase-polymerase chain reaction and western blotting were used to verify the gene expression of the CaSR. Wound healing and transwell assays were conducted to assess the effect of CaSR on the migration of BC cells.We demonstrated that CaSR expression in metastatic BC was higher than that in non-metastatic BC. It is the first time that database information has been used to reveal the biological process and molecular mechanism of CaSR in BC. Moreover, the CaSR expression in normal breast epithelial cells was notably less compared to that in BC cells. The activation of CaSR by Cinacalcet (a CaSR agonist) significantly enhanced the migration of BC cells, whereas NPS-2143 (a CaSR antagonist) treatment dramatically inhibited these effects.Bioinformatics techniques and experiments demonstrated the involvement of CaSR in BC metastasis. Our findings shed new light on the receptor therapy and molecular pathogenesis of BC, and emphasize the crucial function of CaSR, facilitating the metastasis of BC.