门静脉癌栓（PVTT）是影响原发性肝癌预后的重要因素之一，研究门静脉癌栓的形成机制有助于研发新的干预治疗方案。血小板（platelet）作为血栓形成的核心因素，同样促进肿瘤癌栓的形成。我们前期研究发现，血小板数目是肝癌门静脉癌栓患者预后的独立风险因素，并且癌栓患者的血小板聚集能力和活化程度明显增加，癌栓细胞系CSQT-2可以直接触发血小板活化，诱导体外癌栓形成，敲除IV型胶原蛋白COL4可以抑制癌栓细胞与血小板的体外成栓作用。进一步研究发现干细胞因子KITLG可以影响CSQT-2细胞系中COL4的表达和体外成栓作用。小鼠PVTT发生进展模型则表明，KITLG或COL4敲低的CSQT-2细胞系诱导癌栓形成的能力明显减弱。本研究将进一步从分子、细胞、动物水平，探讨KITLG上调肝癌细胞COL4表达进而激活血小板促进癌栓形成的具体机制，从而为肝癌伴门静脉癌栓的诊断和治疗提供新的思路和药物靶点。

Portal vein tumor thrombus (PVTT) is one of the most important factors affecting the prognosis of hepatocellular carcinoma (HCC). Studying the formation mechanism of PVTT is helpful to develop new interventional treatment schemes. As the core factor of thrombosis, platelets can promote the formation of tumor thrombus during the development of tumors. However, the mechanism of liver cancer cells activating platelets and promoting PVTT is still blank. Our previous studies showed that the platelet count is an independent risk factor for the prognosis of patients with PVTT. The aggregation ability and activation degree of the platelets from patients with PVTT both increased significantly. Besides, the tumor thrombus cell line CSQT-2 can directly trigger platelet activation and tumor thrombosis in vitro. Knockdown of the type IV collagen COL4 can inhibit tumor thrombosis in vitro. Further studies showed that the stem cell factor KITLG can affect the expression of COL4 and tumor thrombosis. The mouse PVTT progression model showed that the ability of inducing tumor thrombus by KITLG or COL4 knockdown CSQT-2 cell lines was significantly reduced. Our study aims to further explore the mechanism of KITLG activating the platelets to promote the formation of PVTT by up-regulating the expression of COL4. All of these can provide new ideas and drug targets for the diagnosis and treatment of PVTT.