Suppr超能文献

探索分子复杂性的深度:STAT3作为结直肠癌发病机制中的关键构建者

Probing the Depths of Molecular Complexity: STAT3 as a Key Architect in Colorectal Cancer Pathogenesis.

作者信息

Suleman Muhammad, Khan Safir Ullah, Ali Shahid, Alghamdi Abdullah, Alissa Mohammed, Mushtaq Rayan Y, Crovella Sergio

机构信息

Laboratory of Animal Research Center (LARC), Qatar University, Doha, Qatar.

Center for Biotechnology and Microbiology, University of Swat, Swat, Pakistan.

出版信息

Curr Gene Ther. 2025;25(4):433-452. doi: 10.2174/0115665232336447241010094744.

Abstract

Colorectal cancer (CRC) has become a significant threat in recent decades, and its incidence is predicted to continue rising. Despite notable advancements in therapeutic strategies, managing CRC poses complex challenges, primarily due to the lack of clinically feasible therapeutic targets. Among the myriad molecules implicated in CRC, the signal transducer and activator of transcription 3 (STAT3) stands out as a promising target tightly regulated by various genes. This intracellular transcription factor, spanning 750-795 amino acids and weighing approximately 92 kDa, is crucial in key cellular activities such as growth, migration, invasion, inflammation, and angiogenesis. Aberrant activation of STAT3 signaling has been linked to various cancers, including CRC. Therefore, targeting this signaling pathway holds significance for potential CRC treatment strategies. STAT3, as a central intracellular transcription factor, is implicated in colorectal cancer development by activating aberrant signaling pathways. Numerous studies have demonstrated that the abnormal hyperactivation of STAT3 in CRC tissues enhances cell proliferation, suppresses apoptosis, promotes angiogenesis, and facilitates tumor invasion and metastasis. As a focal point in colorectal cancer research, STAT3 emerges as a promising candidate for detecting and treating CRC. This review aims to present recent data on STAT3, emphasizing the activation and functions of STAT3 inhibitors in CRC. Indeed, STAT3 inhibitors have been identified to have therapeutic potential in CRC, especially inhibitors targeting the DNA-binding domain (DBD). Indeed, STAT3 inhibitors have been identified to have a therapeutic potential in CRC, especially the inhibitors targeting the DNA binding domain (DBD). For example, imatinib acts by targeting cell surface receptors, and these inhibitors have shown potential for the control and treatment of tumor growth, angiogenesis, and metastasis. Imatinib, for example acts by targeting cell surface receptors, and these inhibitors have shown the future direction toward the control and treatment of tumor growth, angiogenesis, and metastasis.

摘要

近几十年来,结直肠癌(CRC)已成为一个重大威胁,预计其发病率将持续上升。尽管治疗策略取得了显著进展,但管理CRC仍面临复杂挑战,主要原因是缺乏临床可行的治疗靶点。在与CRC相关的众多分子中,信号转导和转录激活因子3(STAT3)作为一个受多种基因严格调控的有前景的靶点脱颖而出。这种细胞内转录因子由750 - 795个氨基酸组成,分子量约为92 kDa,在生长、迁移、侵袭、炎症和血管生成等关键细胞活动中起关键作用。STAT3信号通路的异常激活与包括CRC在内的多种癌症有关。因此,靶向该信号通路对潜在的CRC治疗策略具有重要意义。STAT3作为细胞内的核心转录因子,通过激活异常信号通路参与结直肠癌的发展。大量研究表明,CRC组织中STAT3的异常过度激活会增强细胞增殖、抑制细胞凋亡、促进血管生成,并促进肿瘤侵袭和转移。作为结直肠癌研究的一个焦点,STAT3成为检测和治疗CRC的一个有前景的候选者。本综述旨在介绍关于STAT3的最新数据,重点强调STAT3抑制剂在CRC中的激活和功能。事实上,已确定STAT3抑制剂在CRC中具有治疗潜力,尤其是靶向DNA结合域(DBD)的抑制剂。例如,伊马替尼通过靶向细胞表面受体发挥作用,这些抑制剂已显示出控制和治疗肿瘤生长、血管生成和转移的潜力。例如,伊马替尼通过靶向细胞表面受体发挥作用,这些抑制剂已显示出控制和治疗肿瘤生长、血管生成和转移的未来方向。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验