Ask about this productRelated genes to: SLC7A11 antibody
- Gene:
- SLC7A11 NIH gene
- Name:
- solute carrier family 7 member 11
- Previous symbol:
- -
- Synonyms:
- xCT
- Chromosome:
- 4q28.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-02
- Date modifiied:
- 2016-02-17
Related products to: SLC7A11 antibody
Related articles to: SLC7A11 antibody
- Colorectal cancer (CRC) remains a leading cause of cancer-related mortality globally. Ferroptosis, a regulated form of cell death, has emerged as a promising frontier in CRC treatment. The transcriptional regulator ETV4 (ETS variant transcription factor 4) is implicated in CRC pathogenesis. However, its functional role has not been fully elucidated, and its potential to modulate ferroptosis in CRC is entirely unknown. This study aimed to investigate whether ETV4 modulates ferroptosis in CRC by regulating SLC7A11 and to explore the underlying mechanism involved. - Source: PubMed
Publication date: 2026/05/02
Chao ZhouzhouYin JinbaoHuang FengxiaXu JinlianLv YingyanChen JiayaoXu AijingZhu WeiWang Jinxing - In head and neck squamous cell carcinoma (HNSCC), solute carrier family 16 member 1 (SLC16A1) is associated with tumor advancement and reduced sensitivity to ferroptosis, yet the molecular basis of these effects remains unclear. This study seeks to uncover how SLC16A1 contributes to HNSCC tumorigenesis. - Source: PubMed
Publication date: 2026/04/22
Tian ChunhuiXie WeipinLi WenGu HuaiyuLiu XuebaoTong BushengLiu YehaiZong Huaiyuan - Kaempferol has been shown to be beneficial in the treatment of Alzheimer's disease (AD) in animal models. However, the action mechanism remains unclear. AKR1B1 has been identified as a target of kaempferol, initially suggested by the Therapeutic Target Database, DrugBank, and PubChem, and subsequently confirmed through experimental validation. Kaempferol treatment facilitated the expression of AKR1B1 in PC12 cells exposed to Aβ. Kaempferol treatment mitigated the Aβ-induced increases in Fe, MDA, and lipid ROS and Aβ-induced decreases in GSH synthesis and SOD activity. The reduction in ferroptosis-related proteins (GPX4, NQO1, SLC7A11, AKR1C1, and AKR1C3) and the inhibition of Nrf2 nuclear translocation and Nrf2/HO-1 signaling caused by Aβ were also reversed by kaempferol. Overexpressing AKR1B1 led to decreased levels of Fe, MDA, and lipid ROS, along with increased GSH synthesis and SOD activity in Aβ-treated cells, although these effects were negated by Nrf2 inhibition. The upregulation of GPX4 and AKR1C3 by AKR1B1 overexpression was also reversed when Nrf2 expression was inhibited. Notably, silencing AKR1B1 counteracted the protective effects of kaempferol against Aβ-induced neuronal ferroptosis. In vivo studies revealed that kaempferol improved cognitive impairments, reduced deposition of Aβ and p-Tau, and alleviated neuronal ferroptosis in the hippocampal tissues of an AD mouse model in a dose-dependent manner, effects that were diminished by inhibiting AKR1B1 expression. Following kaempferol treatment, the levels of GPX4 and AKR1C3 in the hippocampus of AD mice were found to be reduced. Overall, our findings indicate that kaempferol treatment enhances cognitive function and mitigates pathological alterations in AD mice by inhibiting neuronal ferroptosis through the activation of the Nrf2/HO-1/GPX4/AKR1C3 signaling via upregulation of AKR1B1. This research supports the need for further investigation and clinical exploration of kaempferol. - Source: PubMed
Li LeYang ManyingTao JialeZhao YonghongZhao NaSun Shiguo - Ferroptosis is an iron-dependent form of regulated cell death characterized by excessive lipid peroxidation. Molecules like GPX4, ACSL4, and SLC7A11 form the core regulatory network. GPX4 inhibits lipid peroxide accumulation, ACSL4 promotes ferroptosis through lipid metabolism remodeling, and SLC7A11 confers resistance to ferroptosis by maintaining redox homeostasis. Ferroptosis has a dual role in cancer: inducing it eliminates cancer cells, while its evasion enhances drug resistance and metastasis. Targeting ferroptosis represents an emerging investigational direction for anticancer therapeutic development, with single-target agents, combination regimens, and nanocarrier-based delivery systems exhibiting preliminary tumor-suppressive signals across diverse preclinical model systems. Despite extensive research, existing reviews lack systematic integration of ferroptosis-tumor microenvironment (TME) crosstalk, comparative analysis of cancer type-specific ferroptosis sensitivity, and critical evaluation of recent clinical progress. This review addresses these gaps by synthesizing molecular mechanisms, cancer-specific roles, TME interactions, and therapeutic applications, along with a critical assessment of clinical translation barriers, providing a framework for ferroptosis-targeted cancer therapy. - Source: PubMed
Publication date: 2026/04/30
Huang HonghuaNa JintongShao JijieYang QunSu JingyiXu YupeiZhao YongxiangZhong Liping - Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of global morbidity and mortality, driven by persistent inflammation, oxidative stress, and progressive tissue destruction. Current therapies alleviate symptoms but do not halt disease progression, highlighting the urgent need for novel pathogenic insights. The recent discovery of disulfidptosis, a regulated cell death driven by disulfide stress, offers a groundbreaking framework for understanding COPD. This review proposes that disulfidptosis constitutes a central pathogenic axis, creating a self-perpetuating cycle of metabolic stress, immunogenic cell death, and sterile inflammation that integrates core features of COPD. We synthesize evidence from bioinformatic analyses showing dysregulation of disulfidptosis-related genes (e.g., SLC7A11) in COPD. We detail the molecular cascade linking cigarette smoke-induced NADPH depletion to aberrant actin disulfide crosslinking and cell death. Furthermore, we explore its crosstalk with oxidative stress, DAMP-mediated inflammation, and impaired repair. Finally, we evaluate the translational potential of targeting this axis, proposing disulfidptosis signatures for patient stratification and discussing therapeutic strategies from SLC7A11 inhibition (with context-dependent or inhaled delivery) to NLRP3 inflammasome blockade and HS donors. By integrating disulfidptosis with COPD pathophysiology, this review aims to guide future research and establish this pathway as a pivotal target for developing disease-modifying therapies. - Source: PubMed
Publication date: 2026/04/28
Ni Feng-XianHu JieChen Pei-ShengHuang Dong-HuiJiang Ze-Bo