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Tumor cells derived-extracellular vesicles transfer miR-3129 to promote hepatocellular carcinoma metastasis by targeting txnip

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DIGESTIVE AND LIVER DISEASE 2021年第4期53卷 474-485页

作者： Yang, Yang Mao, Feifei Guo, Lei Shi, Jie Wu, Mengchao Cheng, Shuqun Guo, Weixing Second Mil Med Univ Affiliated Hosp 3 Dept Hepat Surg 6 Shanghai 200438 Peoples R China Tongji Univ Sch Med Shanghai Peoples Hosp 10 Ctr Canc Shanghai 200072 Peoples R China

Background: Hepatocellular carcinoma (HCC) is the most predominant primary liver cancer. Extracellular vesicles (EV)-mediated microRNA (miRNA) delivery is critical in cancer metastasis. We aimed to identify the mechanism of HCC cell-derived EVs-mediated miR-3129 in HCC. Methods: After EVs isolation and identification, miR-3129 expression in plasma EVs was evaluated and its diagnostic efficiency was analyzed. miR-3129 inhibitor was transfected into HepG2 and SMMC7721 cells, and cell malignant episodes were assessed. HCC cells were incubated with EVs from MHCC-97H cells and transfected with miR-3129 inhibitor and/or txnip. The nude mice were injected with MHCC-97H cells-EV or MHCC-97H cells-EV/miR-3129 inhibitor, and HCC growth and metastasis were assessed. Results: miR-3129 was highly expressed in plasma EVs from HCC patients, which was the essential diagnostic biomarker for HCC. miR-3129 downregulation inhibited the malignant episodes of HCC cells. MHCC-97H cell-EVs were absorbed by HCC cells and transferred miR-3129 to HCC cells. EVs-carried miR3129 promoted malignant episodes of HCC cells, which were weakened by miR-3129 inhibition in EVs. miR-3129 targeted txnip. txnip overexpression averted the effect of EVs-carried miR-3129 in HCC. In vivo, MHCC-97H cell-EVs transferred miR-3129 to facilitate HCC growth and metastasis. Conclusion: MHCC-97H cell-EVs transferred miR-3129 to promote HCC metastasis by targeting txnip. (c) 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

关键词： Hepatocellular carcinoma Extracellular vesicles Metastasis microRNA-3129 txnip Epithelial-mesenchymal-transition

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UHRF1 Induces Methylation of the txnip Promoter and Down-Regulates Gene Expression in Cervical Cancer

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MOLECULES AND CELLS 2021年第3期44卷 146-159页

作者： Kim, Min Jun Lee, Han Ju Choi, Mee Young Kang, Sang Soo Kim, Yoon Sook Shin, Jeong Kyu Choi, Wan Sung Gyeongsang Natl Univ Coll Med Inst Hlth Sci Dept Anat & Convergence Med Sci Jinju 52727 South Korea Gyeongsang Natl Univ Coll Med Dept Obstet & Gynecol Jinju 52727 South Korea

DNA methylation, and consequent down-regulation, of tumour suppressor genes occurs in response to epigenetic stimuli during cancer development. Similarly, human oncoviruses, including human papillomavirus (HPV), up regulate and augment DNA methyltransferase (DNMT) and histone deacetylase (HDAC) activities, thereby decreasing tumour suppressor genes (TSGs) expression. Ubiquitin-like containing PHD and RING finger domain 1 (UHRF1), an epigenetic regulator of DNA methylation, is overexpressed in HPV-induced cervical cancers. Here, we investigated the role of UHRF1 in cervical cancer by knocking down its expression in HeLa cells using lentiviral-encoded short hairpin (sh)RNA and performing cDNA microarrays. We detected significantly elevated expression of thioredoxin-interacting protein (txnip), a known TSG, in UHRF1-knockdown cells, and this gene is hypermethylated in cervical cancer tissue and cell lines, as indicated by whole-genome methylation analysis. Up-regulation of UHRF1 and decreased txnip were further detected in cervical cancer by western blot and immunohistochemistry and confirmed by Oncomine database analysis. Using chromatin immunoprecipitation, we identified the inverted CCAAT domain-containing UHRF1binding site in the txnip promoter and demonstrated UHRF1 knockdown decreases UHRF1 promoter binding and enhances txnip expression through demethylation of this region. txnip promoter CpG methylation was further confirmed in cervical cancer tissue by pyrosequencing and methylation-specific polymerase chain reaction. Critically, down-regulation of UHRF1 by siRNA or UHRF1 antagonist (thymoquinone) induces cell cycle arrest and apoptosis, and ubiquitin-specific protease 7 (USP7), which stabilises and promotes UHRF1 function, is increased by HPV viral protein E6/E7 overexpression. These results indicate HPV might induce carcinogenesis through UHRF1-mediated txnip promoter methylation, thus suggesting a possible link between CpG methylation and cervical cancer.

关键词： cervical cancer DNA methylation epigenetic modulator txnip UHRF1

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Protective effect of dimethyl itaconate against fibroblast-myofibroblast differentiation during pulmonary fibrosis by inhibiting txnip

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JOURNAL OF CELLULAR PHYSIOLOGY 2021年第11期236卷 7734-7744页

作者： Han, Yong-Yue Gu, Xuan Yang, Chong-Yang Ji, Hui-Min Lan, Yue-Jiao Bi, Yu-Qian Si, Rong Qu, Jiao Cheng, Ming-Han Gao, Jian Dalian Med Univ Affiliated Hosp 2 467 Zhongshan Rd Dalian 116023 Liaoning Peoples R China

Fibroblast-myofibroblast differentiation (FMD) is a critical cellular phenotype during the occurrence and deterioration of pulmonary fibrosis (PF). FMD can increase with an elevated level of reactive oxygen species (ROS) on fibroblasts under oxidative stress. Thioredoxin-interacting protein (txnip) is an alpha-arrestin family protein that regulates the level of intracellular ROS. Nuclear factor erythroid 2-related factor 2 (Nrf2) can protect against FMD in PF. However, the relationship between Nrf2 and txnip in FMD remains elusive. Therefore, we established TGF-beta 1-induced FMD in vitro and bleomycin (BLM)-induced mouse PF model in vivo to explore whether the activation of Nrf2 can inhibit txnip-mediated FMD in PF. Dimethyl itaconate (DMI) was selected to activate Nrf2. Our results showed that txnip was elevated and FMD was aggravated in mice lung tissues after BLM administration compared with the saline group. Inversely, Nrf2 decreased txnip expression and alleviated FMD in PF. In vitro, txnip overexpression enhanced FMD and increased the level of ROS. In contrast, txnip deficiency by small interfering RNA (siRNA) attenuated TGF-beta 1-induced FMD and reduced ROS. An increase in ROS by H2O2 can upregulate txnip expression. Moreover, Nrf2 also inhibited TGF-beta 1-induced FMD and the increase of ROS, with reducing expression of txnip, and the inhibitory effect was better than txnip siRNA. These results suggest that activation of Nrf2 by DMI can protect against PF via inhibiting txnip expression. Our study may provide new therapeutic targets and treatment approaches for PF.

关键词： dimethyl itaconate fibroblast-myofibroblast differentiation Nrf2 pulmonary fibrosis txnip

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Synergistic effect of curcumin and resveratrol on the prevention of contrast-induced nephropathy by suppressing inflammation via regulating signaling pathways of microRNA-17/txnip/NRLP3 and microRNA-30c/FOXO3/NRLP3 (Withdrawal of Vol 2021, art no 2661025, 2021)

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BIOTECHNOLOGY AND APPLIED BIOCHEMISTRY 2023年第2期70卷 930-930页

作者： Chen, H. Yu, X. Ma, L. Department of Cardiology The First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Anhui Hefei 230001 China

In this study, we aimed to explore the molecular mechanism underlying the effect of resveratrol (RES) and curcumin (CUR) on the treatment of CIN. And we also investigated the potential additive interactions between RES and CUR. Rat models were established as a Sham group, a contrast induced nephropathy (CIN) group, a CIN+RES group, a CIN+CUR group and a CIN+RES+CUR group. ELISA was performed to observe the expression levels of serum creatinine, blood urea nitrogen (BUN) and neutrophil gelatinase-associated lipocalin (NGAL) in the rats. H&E staining was performed to measure renal dysfunction of each rat group. Real-time PCR, Western blot, computational analysis and luciferase assays were used to establish the signaling pathways responsible for the effect of RES and CUR on CIN. The levels of serum creatinine, BUN and serum NGAL were significantly increased in CIN rats, which were recovered by the administration of RES and/or CUR. The high injury score in the CIN group was preserved by the administration of RES and CUR. The expression of both miR-17 and miR-30c was markedly decreased while the expression of thioredoxin-interacting protein (txnip), forkhead box O3 (FOXO3), NLR family pyrin domain containing 3 (NRLP3), interleukin-1 beta (IL-1β) and cleaved caspase-3 was all markedly increased in the CIN group. RES or CUR treatment mitigated the above dysregulation in CIN rats, and the combined administration of RES+CUR exhibited a more impressive effect. txnip was a target gene of miR-17, while FOXO3 was a target gene of miR-30c. The combined administration of RES and CUR additively reduced the expression of NLRP3, and attenuated renal injury and inflammation in CIN treatment. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.

关键词： Contrast induced nephropathy Curcumin FOXO3 miRNA NRLP3 Resveratrol txnip

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Rutin attenuates ensartinib-induced hepatotoxicity by non-transcriptional regulation of txnip

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CELL BIOLOGY AND TOXICOLOGY 2024年第1期40卷 38-38页

作者： Wu, Wentong Li, Jinjin Yin, Yiming Zhou, Yourong Huang, Xiangliang Cao, Yashi Chen, Xueqin Zhou, Yunfang Du, Jiangxia Xu, Zhifei Yang, Bo He, Qiaojun Yang, Xiaochun Hu, Yuhuai Yan, Hao Luo, Peihua Zhejiang Univ Coll Pharmaceut Sci Ctr Drug Safety Evaluat & Res 866 Yuhangtang RdZijingang Campus Hangzhou 310058 Zhejiang Peoples R China Zhejiang Univ Affiliated Hangzhou Canc Hosp Key Lab Clin Canc Pharmacol & Toxicol Res Zhejiang Dept OncolSch Med Hangzhou 310002 Peoples R China Zhejiang Univ Canc Ctr Hangzhou 310058 Peoples R China Wenzhou Med Univ Affiliated Hosp 6 Peoples Hosp Lishui Lab Clin Pharm Lishui 323020 Peoples R China Zhejiang Univ Affiliated Hosp 2 Ctr Med Res & Innovat Digest Syst Tumors Sch MedMinist Educ Hangzhou 310017 Peoples R China Zhejiang Univ Inst Pharmacol & Toxicol Coll Pharmaceut Sci Hangzhou 310058 Peoples R China Hangzhou City Univ Sch Med Hangzhou 310015 Peoples R China Zhejiang Univ Innovat Inst Artificial Intelligence Med Hangzhou 310018 Peoples R China Innovat Inst Hangzhou Yuhong Pharmatech Co LTD Hangzhou 310018 Peoples R China Zhejiang Univ Hangzhou Inst Innovat Med Coll Pharmaceut Sci Dept Pharmacol & Toxicol Hangzhou 310018 Peoples R China Zhejiang Univ Affiliated Hangzhou Canc Hosp Key Lab Clin Canc Pharmacol & Toxicol Res Zhejiang Sch Med Hangzhou 310002 Peoples R China

Ensartinib, an approved ALK inhibitor, is used as a first-line therapy for advanced ALK-positive non-small cell lung cancer in China. However, the hepatotoxicity of ensartinib seriously limits its clinical application and the regulatory mechanism is still elusive. Here, through transcriptome analysis we found that transcriptional activation of txnip was the main cause of ensartinib-induced liver dysfunction. A high txnip level and abnormal txnip translocation severely impaired hepatic function via mitochondrial dysfunction and hepatocyte apoptosis, and txnip deficiency attenuated hepatocyte apoptosis under ensartinib treatment. The increase in txnip induced by ensartinib is related to AKT inhibition and is mediated by MondoA. Through screening potential txnip inhibitors, we found that the natural polyphenolic flavonoid rutin, unlike most reported txnip inhibitors can inhibit txnip by binding to txnip and partially promoting its proteasomal degradation. Further studies showed rutin can attenuate the hepatotoxicity of ensartinib without antagonizing its antitumor effects. Accordingly, we suggest that txnip is the key cause of ensartinib-induced hepatotoxicity and rutin is a potential clinically safe and feasible therapeutic strategy for txnip intervention.

关键词： Ensartinib Apoptosis txnip Hepatotoxicity Rutin

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Shexiang Tongxin dropping pills protect against ischemic stroke-induced cerebral microvascular dysfunction via suppressing txnip/NLRP3 signaling pathway

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JOURNAL OF ETHNOPHARMACOLOGY 2024年 322卷 117567页

作者： Zhu, Li Yang, Yi-Ming Huang, Yi Xie, Hong-Kai Luo, Yong Li, Chun Wang, Wei Chen, Yang Guangzhou Univ Chinese Med Sch Pharmaceut NMPA Key Lab Res Tradit Chinese Med Syndrome Guangzhou 51006 Guangdong Peoples R China Guangzhou Univ Chinese Med Inst Formula & Syndrome Guangzhou 51006 Guangdong Peoples R China Beijing Univ Chinese Med Modern Res Ctr Tradit Chinese Med Beijing 100029 Peoples R China Jinan Univ Sch Dent Med Affiliated Hosp 1 Dept Stomatol Guangzhou 510632 Peoples R China Guangzhou Univ Chinese Med Sch Pharmaceut Guangzhou 51006 Guangdong Peoples R China

Ethnopharmacological relevance: Patients with ischemic stroke (IS) often continue to exhibit cerebral microcirculatory dysfunction even after receiving thrombolytic therapy. Enhancing the function of cerebral microvascular endothelia represents a pivotal advancement in the therapeutic strategy for ischemic microcirculatory disturbances. A traditional Chinese medicinal formulation named Shexiang Tongxin Dropping Pills (STDP), has been clinically employed to ameliorate microcirculatory abnormalities. Existing literature attests to the beneficial role of STDP on endothelial cells (ECs). Nevertheless, specific impacts and underlying mechanisms of STDP in rectifying IS-induced cerebral microvascular dysfunction warrant further exploration. Aim of the study: This investigation seeks to delineate the effects of STDP on cerebral microvascular endothelial damage induced by ischemic stroke and to elucidate the underlying mechanism involved. Materials and methods: Middle cerebral artery occlusion and reperfusion (MCAO/R) technique was employed to established ischemic stroke model in mice. The therapeutic efficacy of STDP on cerebral microvascular function was assessed through laser speckle contrast imaging, behavioral assays, and histological evaluations. Biochemical markers in the brain tissue, including GSH, SOD, MDA, and ROS, were quantified using specific assay kits. In vitro study, oxygen-glucose deprivation and reperfusion (OGD/R) was performed in bEnd.3 cells. The cytoprotective potential of STDP was then evaluated by measuring cell viability, LDH activity, endothelial permeability, and oxidative stress parameters. Important targets in critical pathway were verified by immunoblotting and immunofluorescence both in mice brain slices and bEnd.3 cells. Results: STDP decrease brain infarct size, repaired microvascular cerebral blood flow and attenuated neurological deficiency in MCAO/R mice. Moreover, STDP abolished MCAO/R-induced oxidative stress which was reflected by res

关键词： Shexiang Tongxin dropping pill Ischemic stroke Cerebral microvascular dysfunction Endothelium Oxidative stress txnip NLRP3

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Epigallocatechin-3-gallate Inhibits LPS/AβO-induced Neuroinflammation in BV2 Cells through Regulating the ROS/txnip/NLRP3 Pathway

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JOURNAL OF NEUROIMMUNE PHARMACOLOGY 2024年第1期19卷 31-31页

作者： Xiao, Yanyan Yang, Chenglin Si, Nana Chu, Tao Yu, Jiahui Yuan, Xintong Chen, Xiang-Tao Anhui Med Univ Sch Pharm Hefei Peoples R China Anhui Inst Innovat Drugs Sch Pharm Anhui Key Lab Major Autoimmune Dis Hefei Peoples R China

Neuroinflammation is a key factor in cognitive dysfunction and neurodegenerative diseases such as Alzheimer's disease (AD), so inhibiting neuroinflammation is considered as a potential treatment for AD. Epigallocatechin-3-gallate (EGCG), a polyhydroxyphenol of green tea, has been found to exhibit anti-oxidative, anti-inflammatory and neuroprotective effects. The aim of this study was to investigate the inhibitory effect of EGCG on inflammation and its mechanism. In this study, BV2 cells were simultaneously exposed to lipopolysaccharides (LPS) and the amyloid-beta oligomer (A beta O) to induce inflammatory microenvironments. Inflammatory cytokines and NLRP3 inflammasome-related molecules were detected by RT-PCR and Western Blot. The results show that EGCG inhibits LPS/A beta O-induced inflammation in BV2 cells through regulating IL-1 beta, IL-6, and TNF-alpha. Meanwhile, EGCG reduces the activation of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome and levels of intracellular ROS in BV2 cells treated with LPS/A beta O by affecting the mitochondrial membrane potential (MMP). Further research found that EGCG inhibited MMP through regulating thioredoxin-interacting protein (txnip) in LPS/A beta O-induced neuroinflammation. In conclusion, EGCG may alleviate LPS/A beta O-induced microglial neuroinflammation by suppressing the ROS/ txnip/ NLRP3 pathway. It may provide a potential mechanism underlying the anti-inflammatory properties of EGCG for alleviating AD.

关键词： Alzheimer's Disease (AD) Amyloid beta (A beta) Epigallocatechin-3-gallate (EGCG) NLRP3 Inflammasome txnip

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Fecal microbiota transplantation derived from mild cognitive impairment individuals impairs cerebral glucose uptake and cognitive function in wild-type mice: Bacteroidetes and txnip-GLUT signaling pathway

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GUT MICROBES 2024年第1期16卷 2395907页

作者： Wang, Tao Hao, Ling Yang, Kexin Feng, Wenjing Guo, Zhiting Liu, Miao Xiao, Rong Capital Med Univ Sch Publ Hlth 10 Xitoutiao Beijing 100069 Peoples R China Beijing Ctr Dis Prevent & Control Inst Nutr & Food Hyg Beijing Peoples R China

Gut microbiome dysbiosis has been widely implicated in cognitive impairment, but the identity of the specific bacterial taxa and mechanisms are not fully elucidated. Brain glucose hypometabolism coincides with the cognitive decline. This study explored the link among cognition, gut microbiota and glucose uptake based on the fecal microbiota transplantation from mild cognitive impairment individuals (MCI-FMT) and investigated whether similar mechanisms were involved in 27-hydroxycholesterol (27-OHC)-induced cognitive decline. Our results showed that the MCI-FMT mice exhibited learning and memory decline and morphological lesions in the brain and colon tissues. There were reduced 18F-fluorodeoxyglucose uptake, downregulated expression of glucose transporters (GLUT1,3,4) and upregulated negative regulator of glucose uptake (txnip) in the brain. MCI-FMT altered the bacterial composition and diversity of the recipient mice, and the microbial signatures highlighted by the increased abundance of Bacteroides recapitulated the negative effects of MCI bacterial colonization. However, inhibiting Bacteroidetes or txnip increased the expression of GLUT1 and GLUT4, significantly improving brain glucose uptake and cognitive performance in 27-OHC-treated mice. Our study verified that cognitive decline and abnormal cerebral glucose uptake were associated with gut microbiota dysbiosis;we also revealed the involvement of Bacteroidetes and molecular mechanisms of txnip-related glucose uptake in cognitive deficits caused by 27-OHC.

关键词： Fecal microbiota transplantation Bacteroidetes cognitive decline 27-hydroxycholesterol cerebral glucose uptake txnip

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KLF4 interacts with txnip to modulate the pyroptosis in ulcerative colitis via regulating NLRP3 signaling

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IMMUNITY INFLAMMATION AND DISEASE 2024年第2期12卷 e1199页

作者： Chen, Yuan Sun, Lifeng Liu, Haiyan Li, Jiamei Guo, Lu Wang, Zhiyi Shandong First Med Univ Shandong Prov Hosp Dept Pediat Jinan Shandong Peoples R China Shandong First Med Univ Shandong Prov Hosp Shandong Prov Clin Res Ctr Childrens Hlth & Dis Off Jinan Shandong Peoples R China Shandong First Med Univ Shandong Prov Hosp Dept Pathol Jinan Shandong Peoples R China Shandong First Med Univ Shandong Prov Hosp Dept Hepatobiliary Surg 324 Jing Wu Rd Jinan 250021 Shandong Peoples R China

IntroductionUlcerative colitis (UC) is one of the most common diseases in the gastrointestinal tract related to abnormal inflammation. Pyroptosis, which is characterized by the formation of inflammasome, activation of caspase-1, and separation of N- and C-terminus of gasdermin D (GSDMD), and may be involved in the pathogenesis of IBD. Kruppel-like factor 4 (KLF4) is a zinc finger transcription factor expressed in differentiated epithelial cells. KLF4 mediates proinflammatory signaling in macrophages. Here, we tested whether KLF4 is functional in pyroptosis of *** human UC tissues and/or lipopolysaccharide (LPS)/adenosine 5-triphosphate (ATP) stimulation human colon epithelial cells, KLF4, txnip, Cleave-Caspase-1, and GSDMD expression were detected through quantitative reverse transcription polymerase chain reaction (PCR), immunohistochemical and western blot assay. Interleukin (IL)-1 beta and IL-18 levels were quantified by enzyme-linked immunosorbent assay. We successfully constructed a KLF4-silenced colon epithelial cell line using an adenovirus vector. We apply the UCSC and JASPAR to predict the KLF4 binding sites in the promoter region of *** human UC tissues and/or LPS/ATP stimulation human colon epithelial cells, KLF4, txnip, Caspase-1, and GSDMD expression level were significantly elevated via quantitative reverse transcription PCR, immunohistochemical and western blot assay. Moreover, We identified that there is an interaction between KLF4 and txnip through Yeast double hybrid assay and CO-IP assay. We successfully constructed a KLF4-silenced human intestinal epithelial cell line. In LPS/ATP stimulation KLF4-silenced human intestinal epithelial cells, KLF4, txnip, Cleave Caspase-1, ASC, and GSDMD expression level were significantly decreased via quantitative reverse transcription *** results confirm that KLF4 can positively regulate the expression of txnip and regulate the pyroptosis process of UC through the txnip/NLRP3 pa

关键词： ATP/LPS KLF4 NLRP3 txnip ulcerative colitis

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miR-30c-5p Alleviated Pyroptosis During Sepsis-Induced Acute Kidney InjuryviaTargeting txnip

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INFLAMMATION 2021年第1期44卷 217-228页

作者： Li, Xiang Yao, Linya Zeng, Xueming Hu, Bing Zhang, Xi Wang, Jun Zhu, Runyu Yu, Qiwei Kunshan Hosp Tradit Chinese Med Dept Urinary Surg Kunshan 215300 Jiangsu Peoples R China

Sepsis-induced acute kidney injury (SAKI) is a common complication of hospitalized patients, often leading to unacceptable mortality. Limited effective treatment or diagnosis biomarkers are available and the underlying mechanism remains unclear. The miR-30c-5p is considered as a critical mediator of kidney diseases and aberrantly decreased in patients with SAKI, while the mechanism is still unclear. For this purpose, the role of miR-30c-5p in SAKI has been investigated in this study. Here, we first confirmed that miR-30c-5p expression decreased in our septic models and was associated with the activation of NLRP3/caspase-1-mediated pyroptosis. Overexpression of miR-30c-5p alleviated the kidney injuryviasuppressing HK-2 cell pyroptosis. Furthermore, we identified that txnip was a direct target of miR-30c-5p. Upregulation of miR-30c-5p repressed the expression of txnip, which inhibited NLRP3, ASC, and caspase-1 expression, as well as secretion of inflammatory cytokines. In conclusion, our data suggested that miR-30c-5p negatively controlled the NLRP3 signal pathway-related pyroptosis and sepsis-induced injuryviatxnip, indicating that this axis might be a positive therapeutic target for the patient with SAKI.

关键词： sepsis-induced acute kidney injury pyroptosis miR-30c-5p txnip

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