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已发表论文
SLC7A11 在结直肠癌铁死亡中的双重作用：从分子机制到治疗机会
Authors Hu S , Wang Y, Tian G, Qiu Z
Received 23 September 2025
Accepted for publication 23 December 2025
Published 9 January 2026 Volume 2026:19 569536
DOI https://doi.org/10.2147/OTT.S569536
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tohru Yamada
Siyu Hu,1 Yuting Wang,1 Guangyu Tian,2,* Zhiyuan Qiu1,*
1Department of Oncology, People’s Hospital Affiliated to Jiangsu University, Zhenjiang, Jiangsu, 212000, People’s Republic of China; 2Department of Oncology, Yangzhou University Jiangdu People’s Hospital, Yangzhou, Jiangsu, 225000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Guangyu Tian, Yangzhou Department of Oncology, Yangzhou University Jiangdu People’s Hospital, Yangzhou, Jiangsu, 225000, People’s Republic of China, Email 982987130@qq.com Zhiyuan Qiu, Department of Oncology, People’s Hospital Affiliated to Jiangsu University, Zhenjiang, Jiangsu, 212000, People’s Republic of China, Tel/Fax +86-0511-88915061, Email qzyjsu@sina.com
Abstract: Colorectal cancer (CRC) ranks as the third most prevalent malignancy globally based on recent epidemiological studies. In China, the rising incidence and mortality rates of CRC have underscored the importance of elucidating its pathogenic mechanisms, which remain major focus in current biomedical research. Ferroptosis, a regulated cell death process driven by iron-dependent lipid peroxidation, is closely associated with disruptions in iron homeostasis, lipid metabolism, and amino acid metabolism. This unique iron-catalysed death process plays a crucial role in both tumor initiation and malignant progression by disturbing cellular redox imbalance. The cystine/glutamate antiporter SLC7A11 (also known as xCT) has been identified as a central regulator of ferroptosis susceptibility. The tumor suppressor p53 and its associated microRNAs modulate ferroptotic responses through regulation of SLC7A11 expression, forming a critical axis in oncogenic transformation and metastasis. However, the precise role of SLC7A11 in CRC—particularly its context-dependent dual functions as both a tumor promoter and a therapeutic vulnerability—remains a critical unanswered question. This review aims to systematically summarize current advances in understanding the multiple roles of SLC7A11 in CRC-related ferroptosis pathways and to evaluate emerging therapeutic strategies targeting this axis. Importantly, we also underscore the existing knowledge gaps and outline future research directions essential for leveraging this unique molecular pathway to improve patient outcomes.
Keywords: SLC7A11, ferroptosis, colorectal cancer
1Department of Oncology, People’s Hospital Affiliated to Jiangsu University, Zhenjiang, Jiangsu, 212000, People’s Republic of China; 2Department of Oncology, Yangzhou University Jiangdu People’s Hospital, Yangzhou, Jiangsu, 225000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Guangyu Tian, Yangzhou Department of Oncology, Yangzhou University Jiangdu People’s Hospital, Yangzhou, Jiangsu, 225000, People’s Republic of China, Email 982987130@qq.com Zhiyuan Qiu, Department of Oncology, People’s Hospital Affiliated to Jiangsu University, Zhenjiang, Jiangsu, 212000, People’s Republic of China, Tel/Fax +86-0511-88915061, Email qzyjsu@sina.com
Abstract: Colorectal cancer (CRC) ranks as the third most prevalent malignancy globally based on recent epidemiological studies. In China, the rising incidence and mortality rates of CRC have underscored the importance of elucidating its pathogenic mechanisms, which remain major focus in current biomedical research. Ferroptosis, a regulated cell death process driven by iron-dependent lipid peroxidation, is closely associated with disruptions in iron homeostasis, lipid metabolism, and amino acid metabolism. This unique iron-catalysed death process plays a crucial role in both tumor initiation and malignant progression by disturbing cellular redox imbalance. The cystine/glutamate antiporter SLC7A11 (also known as xCT) has been identified as a central regulator of ferroptosis susceptibility. The tumor suppressor p53 and its associated microRNAs modulate ferroptotic responses through regulation of SLC7A11 expression, forming a critical axis in oncogenic transformation and metastasis. However, the precise role of SLC7A11 in CRC—particularly its context-dependent dual functions as both a tumor promoter and a therapeutic vulnerability—remains a critical unanswered question. This review aims to systematically summarize current advances in understanding the multiple roles of SLC7A11 in CRC-related ferroptosis pathways and to evaluate emerging therapeutic strategies targeting this axis. Importantly, we also underscore the existing knowledge gaps and outline future research directions essential for leveraging this unique molecular pathway to improve patient outcomes.
Keywords: SLC7A11, ferroptosis, colorectal cancer