肝内胆管癌（ICC）的发病率正在稳步上升，并且死亡率很高。收集临床样本检测ICC组织中HSPB8和BAG3的表达情况。培养 ICC 细胞，并用过表达或沉默特定基因的质粒转染，以研究基因表达改变对细胞功能的影响。 qPCR 和蛋白质印迹技术用于测量基因和蛋白质表达水平。进行伤口愈合测定以评估细胞迁移能力。 Transwell实验用于评估细胞侵袭能力。使用Co-IP来验证HSPB8和BAG3之间的绑定关系。通过构建转移性肿瘤模型验证了HSPB8和BAG3对体内肿瘤肺转移的影响。通过上述实验，我们发现ICC组织和细胞中HSPB8和BAG3的表达上调，且二者的表达量呈正相关。上调或下调BAG3的表达可促进或抑制ICC细胞的转移能力。此外，HSPB8-BAG3伴侣复合物通过激活自噬导致Filamin A的异常降解。 Filamin A 表达增加抑制 ICC 细胞的迁移和侵袭。 HSPB8和BAG3在体内的过表达促进了ICC细胞的肺转移能力。 HSPB8-BAG3 伴侣复合物通过调节 CASA 介导的 Filamin A 降解来促进 ICC 细胞迁移和侵袭，为增强 ICC 治疗策略提供见解。

The incidence of intrahepatic cholangiocarcinoma (ICC) is steadily rising, and it is associated with a high mortality rate. Clinical samples were collected to detect the expression of HSPB8 and BAG3 in ICC tissues. ICC cells were cultured and transfected with plasmids that overexpressed or silenced specific genes to investigate the impact of gene expression alterations on cell function. qPCR and Western blot techniques were utilized to measure gene and protein expression levels. A wound healing assay was conducted to assess cell migration ability. The Transwell assay was used to assess cell invasion ability. Co-IP was used to verify the binding relationship between HSPB8 and BAG3. The effects of HSPB8 and BAG3 on lung metastasis of tumors in vivo were verified by constructing a metastatic tumor model. Through the above experiments, we discovered that the expressions of HSPB8 and BAG3 were up-regulated in ICC tissues and cells, and their expressions were positively correlated. The metastatic ability of ICC cells could be promoted or inhibited by upregulating or downregulating the expression of BAG3. Furthermore, the HSPB8-BAG3 chaperone complex resulted in the abnormal degradation of Filamin A by activating autophagy. Increased expression of Filamin A inhibits the migration and invasion of ICC cells. Overexpression of HSPB8 and BAG3 in vivo promoted the lung metastasis ability of ICC cells. The HSPB8-BAG3 chaperone complex promotes ICC cell migration and invasion by regulating CASA-mediated degradation of Filamin A, offering insights for enhancing ICC therapeutic strategies.