趋化因子在肿瘤转移调控中具有重要作用，但胆囊癌中的相关研究较少。我们前期研究发现，趋化因子CXCL11在胆囊癌组织中表达量显著升高，功能学研究提示其可促进胆囊癌细胞的迁移和侵袭能力，并可介导FAK/PI3K/Akt信号通路的活化。进一步研究发现FAK蛋白可与CXCL11的特异性受体CXCR3相结合。上述研究结果提示CXCL11在胆囊癌转移调控中可能起重要作用，但目前尚无CXCL11在胆囊癌中的研究。据此我们提出假说：CXCL11与其受体CXCR3特异性结合后，通过招募并激活FAK蛋白而介导FAK/PI3K/Akt信号通路的活化，从而调控胆囊癌细胞的侵袭和转移。本课题将深入研究CXCL11在胆囊癌转移中的调控作用，揭示CXCL11介导FAK/PI3K/Akt信号通路活化的具体机制，为胆囊癌的靶向治疗提供新思路。

Chemokines play a crucial role in the regulation of tumor metastasis. However, the expression profiles and biological functions of chemokines in gallbladder cancer (GBC) remain largely unknown. Our previous study revealed that chemokine CXCL11 was overexpressed in GBC tissues. Functional studies indicated that CXCL11 not only enhanced the migrative and invasive capacities of GBC cells, but also activated FAK/PI3K/Akt signaling pathway. After exposure to CXCL11, FAK was found to bind to CXCR3, a specific receptor for CXCL11. These observations imply that CXCL11 might be critically involved in GBC metastasis. To date, the role of CXCL11 in GBC has not yet been elucidated. Based on these findings, we have proposed the hypothesis that through specifically binding to its receptor CXCR3, CXCL11 could activate FAK/PI3K/Akt signaling pathway by recruiting and activating FAK, thereby regulating the invasion and metastasis of GBC cells. The present study aims to investigate the regulatory role of CXCL11 in GBC metastasis and explore the underlying mechanism involved in CXCL11-mediated activation of FAK/PI3K/Akt signaling pathway, which may provide novel insights into the targeted therapy in GBCs.