VKORC1L1

Last update 23 Jan 2025

Basic Info

Synonyms

vitamin K epoxide reductase complex subunit 1 like 1, Vitamin K epoxide reductase complex subunit 1-like protein 1, VKORC1-like protein 1

+ [1]

Introduction

Involved in vitamin K metabolism. Can reduce inactive vitamin K 2,3-epoxide to active vitamin K, and may contribute to vitamin K-mediated protection against oxidative stress. Plays a role in vitamin K-dependent gamma-carboxylation of Glu residues in target proteins.

100 Clinical Results associated with VKORC1L1

100 Translational Medicine associated with VKORC1L1

0 Patents (Medical) associated with VKORC1L1

Literatures (Medical) associated with VKORC1L1

01 Nov 2024·Redox Biology

LncRNA-HMG incites colorectal cancer cells to chemoresistance via repressing p53-mediated ferroptosis

Article

Author: Wang, Kun ; Liu, Ming ; Xin, Zechang ; Zhang, Chunfeng ; Hu, Chenyu ; Hu, Yang ; Sun, Xiaoyan ; Liu, Xiaofeng ; Li, Juan

Upon chemotherapy, excessive reactive oxygen species (ROS) often lead to the production of massive lipid peroxides in cancer cells and induce cell death, namely ferroptosis. The elimination of ROS is pivotal for tumor cells to escape from ferroptosis and acquire drug resistance. Nevertheless, the precise functions of long non-coding RNAs (lncRNAs) in ROS metabolism and tumor drug-resistance remain elusive. In this study, we identify LncRNA-HMG as a chemoresistance-related lncRNA in colorectal cancer (CRC) by high-throughput screening. Abnormally high expression of LncRNA-HMG predicts poorer prognosis in CRC patients. Concurrently, we found that LncRNA-HMG protects CRC cells from ferroptosis upon chemotherapy, thus enhancing drug resistance of CRC cells. LncRNA-HMG binds to p53 and facilitates MDM2-mediated degradation of p53. Decreased p53 induces upregulation of SLC7A11 and VKORC1L1, which contribute to increase the supply of reducing agents and eliminate excessive ROS. Consequently, CRC cells escape from ferroptosis and acquire chemoresistance. Importantly, inhibition of LncRNA-HMG by anti-sense oligo (ASO) dramatically sensitizes CRC cells to chemotherapy in patient-derived xenograft (PDX) model. LncRNA-HMG is also a transcriptional target of β-catenin/TCF and activated Wnt signals trigger the marked upregulation of LncRNA-HMG. Collectively, these findings demonstrate that LncRNA-HMG promotes CRC chemoresistance and might be a prognostic or therapeutic target for CRC.

01 Aug 2024·Apoptosis

FSP1-mediated ferroptosis in cancer: from mechanisms to therapeutic applications

Review

Author: Liang, Desen ; Huang, Jingjing ; Guan, Jialu ; Meng, Qinghui ; Gao, Ran ; Liu, Wenlu ; Guo, Lingfeng ; Wang, Jinge ; Pan, Huayang ; Wang, Tong

Ferroptosis is a new discovered regulated cell death triggered by the ferrous ion (Fe²⁺)-dependent accumulation of lipid peroxides associated with cancer and many other diseases. The mechanism of ferroptosis includes oxidation systems (such as enzymatic oxidation and free radical oxidation) and antioxidant systems (such as GSH/GPX4, CoQ10/FSP1, BH4/GCH1 and VKORC1L1/VK). Among them, ferroptosis suppressor protein 1 (FSP1), as a crucial regulatory factor in the antioxidant system, has shown a crucial role in ferroptosis. FSP1 has been well validated to ferroptosis in three ways, and a variety of intracellular factors and drug molecules can alleviate ferroptosis via FSP1, which has been demonstrated to alter the sensitivity and effectiveness of cancer therapies, including chemotherapy, radiotherapy, targeted therapy and immunotherapy. This review aims to provide important frameworks that, bring the regulation of FSP1 mediated ferroptosis into cancer therapies on the basis of existing studies.

01 May 2024·Annals of Indian Academy of Neurology

Stability of Anticoagulation Following Acenocoumarin in Stroke Patients: Role of Pharmacogenomics and Acquired Factors

Article

Author: Nizami, Mohammad Firoz ; Dubey, Ashish Kant ; Kumar, Surendra ; Misra, Usha Kant ; Kalita, Jayantee

Objective:Pharmacogenomics plays an important role in drug metabolism. A stable anticoagulation is important for primary and secondary prevention of cardioembolic stroke and cerebral venous sinus thrombosis (CVST). We report the role of cytochrome P450 (CYP2C9*2/*3) and vitamin K epoxide reductase subunit 1 (VKORC1) genotypes and acquired causes in maintaining stability of anticoagulation following acenocoumarin in cardioembolic stroke and CVST.Methods:The study comprised 157 individuals with cardioembolic stroke and CVST who were on acenocoumarin. Their comorbidities, comedication, and dietary habits were noted. Prothrombin time and international normalized ratio (INR) were measured during follow-up, and the coagulation status was categorized as stable (>50% occasions in therapeutic range) and unstable (>50% below and above therapeutic range). Genotyping of VKORC1, CYP2C9*2, and CYP2C9*3 was done by polymerase chain reaction-restriction fragment length polymorphism. Bleeding and embolic complications were noted. The predictors of unstable INR were evaluated using multivariate analysis.Results:INR was stable in 47.8% and unstable in 52.2% of patients. Patients with mutant genotypes required low dose of acenocoumarin. The predictors of unstable INR were metallic valve (odds ratio [OR] 4.07, 95% confidence interval [CI] 1.23–13.49, P = 0.02), use of digoxin (OR 0.031, 95% CI 0.13–0.74, P = 0.09), proton pump inhibitor (OR 0.23, 95% CI 0.06–0.91, P = 0.037), sodium valproate (OR 0.22, 95% CI 0.05–0.85, P = 0.029), and CYP2C9*2 genotype (OR 5.57, 95% CI 1.19–26.06, P = 0.02).Conclusions:Variant genotypes of VKORC1, CYP2C9*2, and CYP2C9*3 required lower dose of acenocoumarin, and CYP2C9*2 was associated with unstable INR. Comedication is a modifiable risk factor that needs attention.

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VKORC1L1

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