乳腺癌转移是乳腺癌患者死亡的主要原因。本研究旨在探讨IGJ在乳腺癌侵袭和转移中的作用和潜在机制。利用癌症基因组图谱数据库分析了具有或不具有转移乳腺癌患者的差异基因表达谱；筛选出有显著表达和具有预后价值的靶基因多聚免疫球蛋白A和IgM连接链（JCHAIN，以下简称 IGJ）。利用逆转录‑定量PCR和Western blot分析检测了人乳腺癌配对组织和细胞系的IGJ表达水平。通过免疫组织化学法检测了乳腺癌配对组织中的IGJ差异表达。利用CCK‑8、侵袭和迁移实验以及体内和体外擦痕试验验证了IGJ在乳腺癌中的作用。通过基因集富集分析、京都基因和基因组百科全书分析、Western blot分析和免疫荧光实验进一步探索了IGJ在乳腺癌中的作用和机制。通过基因表达谱分析发现，与无转移乳腺癌患者相比，有转移乳腺癌患者IGJ的表达差异较小。IGJ的过表达与改善远处转移生存率和总生存率有关（OS）。COX多元回归分析表明，IGJ是乳腺癌患者OS和无复发生存的独立预后因子。与健康乳腺癌相邻组织和细胞系相比，乳腺癌组织和细胞系中的IGJ表达较低（P<0.05）。进一步分析显示，IGJ的过表达通过抑制上皮‑间质转化（EMT）的发生和p65的核转位来抑制乳腺癌细胞的增殖、侵袭和转移。最后的拯救实验表明，IGJ通过调节NF‑κB信号通路抑制乳腺癌细胞的增殖和转移。总体而言，本研究表明，IGJ通过抑制EMT的发生和NF‑κB信号通路抑制乳腺癌的侵袭和转移。这些发现可能为转移性乳腺癌的治疗提供新的生物标志物和潜在治疗靶点。

Breast cancer metastasis is the primary cause of mortality of patients with breast cancer. The present study aimed to explore the role and underlying mechanisms of IGJ in the invasion and metastasis of breast cancer. The Cancer Genome Atlas database was utilized to analyze the differential gene expression profiles in patients with breast cancer with or without metastasis; the target gene, joining chain of multimeric IgA and IgM (JCHAIN, also known as IGJ, as referred to herein), with significant expression and with prognostic value was screened. The expression levels of IGJ in human breast cancer paired tissues and cell lines were detected using reverse transcription‑quantitative PCR and western blot analysis. IGJ differential expression was detected in paired human breast cancer tissues using immunohistochemistry. The role of IGJ in breast cancer was verified using CCK‑8, invasion and migration assays, and scratch tests in vivo and in vitro. Further exploration of the role and mechanism of IGJ in breast cancer was conducted through Gene Set Enrichment Analysis, Kyoto Encyclopedia of Genes and Genomes analysis, western blot analysis and immunofluorescence experiments. Through the analysis of gene expression profiles, it was found that IGJ was poorly expressed in patients with breast cancer with metastasis compared to patients with non‑metastatic breast cancer. The overexpression of IGJ was associated with an improved distant metastasis‑free survival and overall survival (OS). COX multivariate regression analysis demonstrated that IGJ was an independent prognostic factor for the OS and relapse‑free survival of patients with breast cancer. In comparison to healthy breast cancer adjacent tissues and cell lines, IGJ was poorly expressed in breast cancer tissues and cell lines (P<0.05). Further analyses indicated that the overexpression of IGJ suppressed the proliferation, invasion and metastasis of breast cancer cells in vivo and in vitro by inhibiting the occurrence of epithelial‑to‑mesenchymal transition (EMT) and suppressing the nuclear translocation of p65. Finally, rescue experiments indicated that IGJ restricted the proliferation and metastasis of breast cancer cells by regulating the NF‑κB signaling pathway. On the whole, the present study demonstrates that IGJ suppresses the invasion and metastasis of breast cancer by inhibiting both the occurrence of EMT and the NF‑κB signaling pathway. These findings may provide novel biomarkers and potential therapeutic targets for the treatment of metastatic breast cancer.