Abstract: Colorectal cancer，one of the most prevalent malignancies globally with persistently high incidence and mortality rates，poses a significant threat to human health. However，its early detection rate remains relatively low，with many patients diagnosed at intermediate or advanced stages，resulting in suboptimal treatment outcomes and prognoses. Current research predominantly focuses on surgical interventions，while studies on cellular and molecular mechanisms remain limited. With the deepening research in tumor biology，the close relationship between inflammation and tumors has gradually been revealed. As a novel programmed cell death mechanism，cellular pyroptosis has attracted significant attention in tumor immunity and microenvironment regulation. This study systematically reviews the research progress on inflammatory carcinogenesis and cellular pyroptosis in colorectal cancer，analyzing their interaction mechanisms and the role of cellular pyroptosis in disease progression. The findings indicate that chronic inflammation regulates the transformation of undifferentiated cells into cancer stem cells through cytokines and growth factors，thereby constructing a procarcinogenic microenvironment. Cellular pyroptosis， triggered by inflammatory body activation and mediated by caspase family and gasdermin family proteins，exhibits dual effects：it promotes tumor cell death while influencing the tumor microenvironment through the release of cytokines such as IL-1β and IL-18. Targeting strategies for inflammatory carcinogenesis and cellular pyroptosis demonstrate therapeutic potential. This study provides theoretical foundations at the cellular and molecular levels to understand colorectal cancer pathogenesis，lays the groundwork for developing precision-targeted therapies，and facilitates the transition of colorectal cancer treatment from surgery-focused approaches to multi-mechanism combined interventions，ultimately improving patient prognosis.

Key words: Colorectal cancer, Pyroptosis, Inflammatory cancer transformation, Growth factors, Cell factor

摘要： 结直肠癌作为全球范围内发病率和死亡率均居高不下的恶性肿瘤之一，对人类健康构成了严重威胁。而且结直肠癌的早期诊断率相对较低，许多患者在确诊时已处于中晚期，治疗效果和预后均不理想。然而目前大多数结直肠癌的研究都还停留在外科层面，对于内部细胞和分子的作用机制研究较少。随着对肿瘤生物学的深入研究，炎症与肿瘤之间的密切联系逐渐被揭示，细胞焦亡作为新型程序性细胞死亡方式，在肿瘤免疫及微环境调控中备受关注。本研究系统梳理结直肠癌炎癌转化及细胞焦亡的研究进展，分析两者相互作用机制及细胞焦亡在疾病发展中的作用。研究发现，慢性炎症通过细胞因子、生长因子等调控未分化细胞向癌症干细胞转化，构建促癌微环境；细胞焦亡由炎症体激活引发，经 caspase 家族及 gasdermin 家族蛋白介导，既可促进肿瘤细胞死亡，又通过释放 IL-1β、IL-18 等细胞因子影响肿瘤微环境，其作用具有双重性。针对炎癌转化和细胞焦亡的靶向策略展现出治疗潜力。本研究为理解结直肠癌发病机制提供了细胞分子层面的理论依据，为开发精准靶向治疗方案奠定基础，有助于推动结直肠癌治疗技术从外科为主向多机制联合干预发展，改善患者预后。

关键词: 结直肠癌, 细胞焦亡, 炎癌转化, 生长因子, 细胞因子