背景：结直肠癌（CRC）仍然是一个重大的全球健康挑战，通常以晚期转移和预后不良为特征。 Runt 相关转录因子 1 (RUNX1) 在包括结直肠癌在内的多种癌症中发挥着癌基因和抑癌基因的双重作用。然而，RUNX1在CRC中的具体调控机制，特别是其直接作用，尚不完全清楚。目的：本研究旨在探讨 RUNX1 在 CRC 进展中的作用及其与作为潜在调控靶点的粘蛋白 13 (MUC13) 的相互作用。方法：与对照相比，分析 CRC 组织和细胞系中的 RUNX1 表达。进行体外和体内测定以评估 RUNX1 过表达和敲低对细胞行为的影响。进行 ChIP-seq 和 RNA-seq 分析来鉴定 RUNX1 靶标，重点是 MUC13。结果：RUNX1 表达在 CRC 组织和细胞中显着上调，与晚期病理特征和不良患者预后相关。 RUNX1过表达增强了CRC细胞的增殖、迁移、侵袭和G2/M期阻滞，而其敲除则具有相反的效果。 MUC13 被确定为 RUNX1 的直接转录靶标，其表达有助于 Wnt/β-catenin 信号通路的激活。 MUC13 的破坏部分逆转了 RUNX1 诱导的恶性表型。结论：RUNX1通过上调MUC13和激活Wnt/β-catenin通路促进CRC进展。该 RUNX1-MUC13 轴代表了治疗 CRC 的潜在治疗靶点。© 作者。

Background: Colorectal cancer (CRC) remains a significant global health challenge, often characterized by late-stage metastasis and poor prognosis. The Runt-related transcription factor 1 (RUNX1) plays a dual role as both an oncogene and a tumor suppressor in various cancers, including CRC. However, the specific regulatory mechanisms of RUNX1 in CRC, particularly its direct roles, are not fully understood. Objective: This study aimed to investigate the role of RUNX1 in CRC progression and its interaction with Mucin 13 (MUC13) as a potential regulatory target. Methods: RUNX1 expression was analyzed in CRC tissues and cell lines compared to controls. In vitro and in vivo assays were conducted to assess the effects of RUNX1 overexpression and knockdown on cell behavior. ChIP-seq and RNA-seq analyses were performed to identify RUNX1 targets, with a focus on MUC13. Results: RUNX1 expression was significantly upregulated in CRC tissues and cells, correlating with advanced pathological characteristics and poor patient outcomes. RUNX1 overexpression enhanced CRC cell proliferation, migration, invasion, and G2/M phase arrest, while its knockdown had the opposite effects. MUC13 was identified as a direct transcriptional target of RUNX1, with its expression contributing to the activation of the Wnt/β-catenin signaling pathway. Disruption of MUC13 partially reversed the malignant phenotypes induced by RUNX1. Conclusion: RUNX1 promotes CRC progression by upregulating MUC13 and activating the Wnt/β-catenin pathway. This RUNX1-MUC13 axis represents a potential therapeutic target for managing CRC.© The author(s).