Ask about this productRelated genes to: TM9SF1 Blocking Peptide
- Gene:
- TM9SF1 NIH gene
- Name:
- transmembrane 9 superfamily member 1
- Previous symbol:
- -
- Synonyms:
- MP70, HMP70
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2016-10-05
Related products to: TM9SF1 Blocking Peptide
Related articles to: TM9SF1 Blocking Peptide
- Liver transplantation (LT) remains the only effective treatment for end-stage liver disease. Autophagy critically regulates liver ischemia–reperfusion (I/R) injury. Transmembrane 9 superfamily member 1 (TM9SF1) is a transmembrane protein associated with the elevation of autophagy. However, the role and mechanism of this protein in liver I/R injury have not been explored. We observed upregulated TM9SF1 expression in liver I/R mice models and AML12 cells subjected to hypoxia-reoxygenation (H/R). Using TM9SF1 adeno-associated virus (AAV) to generate overexpression and knockdown (KD) mice with liver I/R injury, we found that TM9SF1-overexpressing mice exhibited exacerbated liver damage, inflammation, and autophagy, whereas KD-TM9SF1 mice showed opposite results. Mechanistically, we found that TM9SF1 and Annexin A2 (ANXA2) interacted and jointly promoted the expression of autophagy levels during liver I/R injury. Virtual screening of FDA-approved compounds identified lomitapide as an inhibitor that selectively suppresses TM9SF1 expression, thereby attenuating I/R injury. In general, our findings indicated that TM9SF1 and ANXA2 interact with each other, promoting autophagy levels through activating the mitogen-activated protein kinase (MAPK) pathway, thereby aggravating liver I/R injury. Targeting TM9SF1-ANXA2 may be a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/02/05
Wu TongtongLi WendongZhu YingLiu XudongYu HaochengLi HaoZhang JiakaiTang HongweiDing MingjieGuo Wenzhi - Therapeutic resistance and recurrence in human epidermal growth factor receptor 2-positive breast cancer (HER2 + BC) remain critical challenges that portend poor patient outcomes. Dysregulated autophagy and lipid metabolism contribute to tumor progression, yet the crosstalk between these pathways is poorly understood. This study investigates the role of transmembrane 9 superfamily member 1 (TM9SF1) in lipophagy and lipid metabolic reprogramming in HER2 + BC under metabolic stress. Clinically, TM9SF1 was significantly upregulated in HER2 + BC tissues and correlated with poor prognosis. Functionally, its expression correlated with markers of enhanced autophagy and lysosomal lipid catabolism, and it promoted tumor cell proliferation in vitro and in vivo. Conversely, TM9SF1 knockdown suppressed lipophagy under both basal and starvation conditions, inhibiting lipid droplet (LD) hydrolysis and the conversion of triglycerides to free fatty acids. This suppression was phenotypically characterized by LD accumulation, reduced autophagosomes and lipophagosomes, and altered enzymatic and lipidomic profiles. Mechanistically, TM9SF1 sustained lipophagy by promoting the phosphorylation of AMP-activated protein kinase at Thr172 and UNC-51-like kinase 1 at Ser555. Consequently, TM9SF1 was pivotal for lipid metabolic reprogramming, maintaining energy homeostasis and enhancing adaptation to nutrient deprivation through lipophagy. Overall, our findings identify TM9SF1 as a key HER2 + BC-associated regulator that drives lipophagy via the AMP-activated protein kinase-UNC-51-like kinase 1 pathway, facilitating LD turnover and free fatty acids utilization to sustain energy homeostasis in HER2 + BC. This work establishes a critical link between malignant phenotypes and metabolic resilience. Targeting this regulatory network represents a promising strategy to dismantle the metabolic scaffolds underlying HER2 + BC aggressiveness and therapeutic resistance. - Source: PubMed
Publication date: 2025/10/24
Li XiaofenYu XiaoqinHuang KaiyanYu XinLuo ShipingHuang XieweiSong Chuangui - TNBC demonstrates poor prognosis compared to other breast cancer types due to the lack of targetable molecular markers. Protein expression of EBAG9 has been associated with unfavorable prognosis in patients with various malignancies. Recently, we identified TM9SF1 protein as a binding partner for EBAG9 protein. However, the clinical relevance of TM9SF1 and EBAG9 in TNBC remains unclear. - Source: PubMed
Publication date: 2025/09/17
Kinowaki KeiichiTakeiwa ToshihikoIkeda KazuhiroFujimoto AkihiroAzuma KotaroHorie KunikoKawabata HidetakaInoue Satoshi - Sepsis is a prevalent and detrimental condition in intensive care units (ICUs) and a leading cause of mortality. The present study evaluated the role and clinical importance of Transmembrane 9 superfamily member 1 (TM9SF1) as a potential indicator for the early detection of sepsis severity and prognosis. - Source: PubMed
Publication date: 2025/08/25
Wang KeZhang LuZhou FengqiaoZhao ZhenwangLiu MingmingHuang MinLiu YangQiu GuangyuShen XiaofangXiao HongCao FengshengChen HuaboXiao Juan - Selective autophagy is a finely regulated degradation pathway that can either promote or suppress cancer progression depending on its specific target cargoes. In this study, we report that transmembrane 9 superfamily member 1 (TM9SF1) suppresses colorectal cancer metastasis via selective autophagic degradation of Vimentin. Tm9sf1 knockout significantly increases tumor numbers and size, as well as enhances tumor invasion in colorectal cancer model. In vitro and in vivo phenotypical analyses reveal that TM9SF1 functions as a metastasis suppressor in colorectal cancer. Mechanistically, TM9SF1 facilitates the K63-linked ubiquitination of Vimentin by the E3 ligase TRIM21. The K63-linked ubiquitination of Vimentin serves as a recognition signal for autophagic degradation mediated by autophagic cargo receptor Tollip. Consequently, the downregulation of Vimentin results in a decreased number of F-actin-rich stress fibers and filopodium-like protrusions, ultimately inhibiting colorectal cancer metastasis. Moreover, TM9SF1 is downregulated in colorectal cancer patients with advanced stage compared to those with early stage and associated with favorable prognosis. Overall, our findings identify a novel TM9SF1-TRIM21-Vimentin-Tollip pathway involved in colorectal cancer metastasis, which may provide promising therapeutic targets for the treatment of metastatic colorectal cancer. - Source: PubMed
Publication date: 2025/04/02
Wang HuifenHu JiaWang DiCai YudieZhu WeiweiDeng RuiZhang YizeDong ZihuiYang ZheXiao JuanLi AngLiu Zhibo