Department of Pathology, University of Iowa, Iowa City, IA 52242, USA.
Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA.
Cells. 2024 Mar 23;13(7):565. doi: 10.3390/cells13070565.
Leucine-rich repeat kinase 2 (LRRK2) is a serine-threonine protein kinase belonging to the ROCO protein family. Within the kinase domain of LRRK2, a point mutation known as LRRK2 G2019S has emerged as the most prevalent variant associated with Parkinson's disease. Recent clinical studies have indicated that G2019S carriers have an elevated risk of cancers, including colon cancer. Despite this observation, the underlying mechanisms linking LRRK2 G2019S to colon cancer remain elusive. In this study, employing a colitis-associated cancer (CAC) model and LRRK2 G2019S knock-in (KI) mouse model, we demonstrate that LRRK2 G2019S promotes the pathogenesis of colon cancer, characterized by increased tumor number and size in KI mice. Furthermore, LRRK2 G2019S enhances intestinal epithelial cell proliferation and inflammation within the tumor microenvironment. Mechanistically, KI mice exhibit heightened susceptibility to DSS-induced colitis, with inhibition of LRRK2 kinase activity ameliorating colitis severity and CAC progression. Our investigation also reveals that LRRK2 G2019S promotes inflammasome activation and exacerbates gut epithelium necrosis in the colitis model. Notably, GSDMD inhibitors attenuate colitis in LRRK2 G2019S KI mice. Taken together, our findings offer experimental evidence indicating that the gain-of-kinase activity in LRRK2 promotes colorectal tumorigenesis, suggesting LRRK2 as a potential therapeutic target in colon cancer patients exhibiting hyper LRRK2 kinase activity.
富含亮氨酸重复激酶 2(LRRK2)是一种丝氨酸/苏氨酸蛋白激酶,属于 ROCO 蛋白家族。在 LRRK2 的激酶结构域中,一种称为 LRRK2 G2019S 的点突变已成为与帕金森病最相关的常见变体。最近的临床研究表明,G2019S 携带者患癌症的风险增加,包括结肠癌。尽管有此观察结果,但将 LRRK2 G2019S 与结肠癌联系起来的潜在机制仍不清楚。在这项研究中,我们使用结肠炎相关癌症(CAC)模型和 LRRK2 G2019S 敲入(KI)小鼠模型,证明 LRRK2 G2019S 促进了结肠癌的发病机制,表现为 KI 小鼠中的肿瘤数量和大小增加。此外,LRRK2 G2019S 增强了肿瘤微环境中的肠上皮细胞增殖和炎症。在机制上,KI 小鼠对 DSS 诱导的结肠炎表现出更高的易感性,抑制 LRRK2 激酶活性可改善结肠炎的严重程度和 CAC 的进展。我们的研究还表明,LRRK2 G2019S 促进了炎症小体的激活,并加剧了结肠炎模型中的肠道上皮细胞坏死。值得注意的是,GSDMD 抑制剂可减轻 LRRK2 G2019S KI 小鼠的结肠炎。总之,我们的研究结果提供了实验证据,表明 LRRK2 的激酶活性获得促进了结直肠肿瘤的发生,这表明 LRRK2 可能是具有高 LRRK2 激酶活性的结肠癌患者的潜在治疗靶点。