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Silencing hnRNPD inhibits gastric cancer growth by increasing txnip-mediated oxidative stress

Discover Oncology 2025年第1期16卷 1-12页

作者： Zou, Xuan Li, Jin Zhou, Junshuo Ren, Qiulei Wang, Kelong Wang, Xiaoyan Reproductive Medicine Center Suizhou Hospital Hubei University of Medicine Hubei Suizhou 441300 China Gynaecology Ward 2 Suizhou Hospital Hubei University of Medicine Hubei Suizhou 441300 China Institute of Basic Medical Sciences Hubei University of Medicine Hubei Shiyan 442000 China Department of Clinical Oncology Taihe Hospital Hubei University of Medicine Hubei Shiyan 442000 China

Background: RNA-binding proteins (RBPs) are essential for controlling gene expression, and their dysregulation is a key factor in tumor development and progression. Heterogeneous nuclear ribonucleoprotein D (hnRNPD), a member of the hnRNP family of RBPs, is aberrantly expressed in various tumors. However, its role and underlying mechanisms in gastric cancer have not been determined. Methods: The expression patterns of hnRNPD in gastric cancer were analyzed using publicly available datasets and clinical specimens. The effects of hnRNPD on gastric cancer cell growth were assessed using the Cell Counting Kit-8 (CCK-8) and colony formation assays. Target genes regulated by hnRNPD were identified through RNA sequencing (RNA-seq) and RNA immunoprecipitation sequencing (RIP-seq). Results: Elevated expression of hnRNPD was observed in gastric cancer, and this overexpression was associated with an unfavorable prognosis. Knocking down hnRNPD could suppress the growth of gastric cancer cells and enhance endogenous oxidative stress. Thioredoxin-interacting protein (txnip) was identified as a downstream target of hnRNPD. Further analysis confirmed that hnRNPD diminished txnip expression by binding to and destabilizing its mRNA. Moreover, silencing txnip reversed the decrease in cell growth and the increase in oxidative stress caused by hnRNPD knockdown. Conclusion: Our study highlights hnRNPD as a major contributor to gastric carcinogenesis. The knockdown of hnRNPD hinders gastric cancer growth by directly interacting with txnip, promoting its expression, and inducing oxidative stress. These findings suggest that hnRNPD may serve as a valuable target for the treatment of gastric cancer. © The Author(s) 2025.

关键词： Gastric cancer hnRNPD Oxidative stress Tumor growth txnip

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Mechanistic insights into the protective potential of ambrisentan against L-arginine induced acute pancreatitis and multiorgan damage (role of NRF2/HO-1 and txnip/NLRP3 pathways)

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Biomedicine and Pharmacotherapy 2025年 187卷 118119-118119页

作者： Almutary, Khaled H. Zaghloul, Marwa S. Nader, Manar A. Elsheakh, Ahmed R. Department of Pharmacology and Toxicology Faculty of Pharmacy Mansoura University Mansoura 35516 Egypt Majmaah University P.O.Box 66 Majmaah 11952 Saudi Arabia Department of Pharmacology and Toxicology Faculty of Pharmacy Mansoura National University Gamasa 7731168 Egypt Future Studies and Risks Management & National Committee of Drugs Academy of Scientific Research Ministry of Higher Education Elsayeda Zeinab Egypt

Acute pancreatitis (AP) is an abrupt inflammation of the pancreatic tissue. The severity of AP varies from mild and self-limiting to severe, potentially fatal, and can affect several organ systems. The most severe type of AP causes multiple organ damage (MOD) due to systemic inflammation. In this study, ambrisentan (AMB), an endothelin A receptor antagonist (ETA), was investigated for its potential to ameliorate L-arginine (L-Arg) induced AP and MOD in rats. AP was induced using L-Arg (100 mg/100 g). Two doses of AMB were tested and compared to N-acetylcystiene (NAC) effect. AMB restored the normal structure of the pancreatic, hepatic, pulmonary, and renal tissues. In addition, it normalized the levels of pancreatic enzymes, lactate dehydrogenase (LDH), serum liver enzymes, and kidney biomarkers. Furthermore, AMB corrected the imbalance in the levels of oxidants/antioxidants caused by L-Arg. In contrast, AMB (5 mg/kg) significantly upregulated the protein levels of adenosine monophosphate protein kinase (AMPK), nuclear factor erythroid 2-related factor 2 (NRF2), heme oxidase-1(HO-1) and thioredoxin reductase 1 (TXNRD1) by approximately 69.59 %, 85.14 %, 688 % and 96 % respectively, compared with those in rats treated with L-Arg. Furthermore, AMB (5 mg/kg) significantly lowered the thioredoxin-interacting protein (txnip), nod-like Receptor Protein 3 (NLRP3), glycogen synthase kinase-3β (GSK-3β), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), CD68, autophagic markers (P62 and LC3) and apoptotic marker caspase 3 by around 62.43 %, 73.56 %, 62.5 %,70 %, 80.3 %, 93 %, 96.7 %, 95 %, 39.6 % respectively, compared to the group treated with L-Arg. AMB effectively improved the AP and MOD produced by L-Arg through its anti-inflammatory and antioxidant properties. NRF2/HO-1 and txnip/NLRP3 pathways play major roles in these protective effects. © 2025 The Authors

关键词： Acute pancreatitis Ambrisentan, NRF2 HO-1 NLRP3 txnip

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Emodin delays rheumatoid arthritis progression by inhibiting the ROS/txnip/NLRP3 signaling pathway

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International Immunopharmacology 2025年 158卷 114861页

作者： Zhou, Linlan Liu, Jun Yang, Kang Cai, Chunlei Cheng, LianYing Du, Dehao He, Haohua Hua, Xinyu Rong, Xiaofeng Department of Combination of Chinese and Western Medicine The First Affiliated Hospital of Chongqing Medical University Chongqing 400016 China Chongqing Key Laboratory of Traditional Chinese Medicine for Prevention and Cure of Metabolic Diseases Chongqing 400016 China Department of Rehabilitation Medicine of Jiangbei Campus The First Affiliated Hospital of Army Medical University Chongqing 401315 China Jiangbei District Hospital of Traditional Chinese Medicine No. 35 Village 1 Jianxin East Road Jiangbei District Chongqing 400020 China College of Traditional Chinese Medicine Chongqing Medical University Chongqing 400016 China

Rheumatoid arthritis (RA) is a chronic autoimmune disorder affecting small joints of the hands, feet, and ankles, causing synovitis, pannus formation, and vasculitis. RA can lead to joint destruction and multi-system complications. Emodin (EMO), the primary active component of rhubarb, has significant anti-inflammatory properties and therapeutic potential in alleviating RA symptoms. This study focused on this therapeutic efficacy and underlying mechanisms. Collagen-induced arthritis (CIA) mouse models and lipopolysaccharide (LPS)-stimulated RAW264.7 cells were used to investigate the effects of EMO on pathological markers, inflammatory factors, and oxidative stress through histopathological analysis, western blotting, micro-computed tomography (CT), and immunohistochemistry (IHC). Proteomics, molecular docking, and molecular dynamics (MD) simulations were used to identify key targets and to elucidate the mechanisms of action underlying the therapeutic efficacy of EMO. EMO alleviated joint swelling, reduced arthritis scores, and mitigated bone damage in mice with CIA. EMO significantly decreased inflammatory factor levels and attenuated oxidative stress, as shown through reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) activity. EMO inhibited inflammasome activation, as indicated by reduced NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), caspase-1, apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1β, and IL-18 expression. The analyses showed that the anti-inflammatory effects of EMO are mediated through ROS/txnip/NLRP3 signaling pathway inhibition. Collectively, EMO downregulated inflammatory responses and oxidative stress, inhibited inflammasome activation, and alleviated RA symptoms through ROS/txnip/NLRP3 signaling pathway suppression. These findings highlight its potential for RA treatment and provide insights into its mechanisms and clinical applications. ©

关键词： Emodin NLRP3 Oxidative stress Rheumatoid arthritis txnip

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Ginsenoside Rg1 attenuates T2DM-induced renal damage and fibrosis by inhibiting TRPC6-ChREBP-txnip signaling

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Journal of Ethnopharmacology 2025年 348卷 119863页

作者： Zhang, Hui Liang, Haoyu Fan, Lei Zhu, Xing Ji, Pengmin Su, Yong Li, Weiping Li, Weizu Department of Pharmacology School of Basic Medical Sciences Key Laboratory of Anti-inflammatory and Immunopharmacology Ministry of Education Anhui Medical University Hefei 230032 China Department of Pharmacy The First Affiliated Hospital of Anhui Medical University Hefei 230032 China

Ethnopharmacological relevance: As a traditional Chinese medicine, ginseng has many benefits, including regulating blood sugar, blood pressure and so on. Ginsenoside Rg1 is the main active component of ginseng and has been found to significantly improve renal pathological injury in type 2 diabetes mellitus (T2DM) mice. However, the effects and mechanisms of Rg1 in attenuating T2DM are not fully understood. Aim of the study: This study aims to investigate the role of Rg1 in the treatment of renal damage and fibrosis induced by T2DM and its molecular mechanism. Materials and methods: T2DM models were constructed on mice and cells respectively and were administered with corresponding drugs. SA-β-Gal and Oil Red O were used to observe cell senescence and lipid droplet deposition;H&E and PAS were used to observe pathological changes in the kidney;masson and sirius red were used to evaluate the level of renal fibrosis. Immunohistochemistry, immunofluorescence and Western blotting were performed to analyze the relevant indexes which resulted in the detection of ROS levels in vitro and in vivo. Calcium imaging was used to test the level of [Ca²⁺]_i. Results: Rg1 and Trpc6 knockout could significantly improve kidney dysfunction, attenuate renal injury and fibrosis and also decrease the expression levels of TRPC6, CaN, txnip, ChREBP, p-ASK1 and NLRP3 inflammasome. Meanwhile, Rg1 and Trpc6 knockout significantly inhibited mitochondrial damage and apoptosis protein release. Additionally, Rg1 treatment has been shown to markedly reduce lipid deposition and ROS accumulation in T2DM, while Trpc6 knockout exhibited no effect on these parameters. Conclusion: Rg1 treatment can inhibit the TRPC6-ChREBP-txnip pathway, thereby improving chronic T2DM-induced renal injury and fibrosis. © 2025 Elsevier B.V.

关键词： Diabetic kidney disease Ginsenoside Rg1 NLRP3 inflammasome TRPC6 txnip

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M2 macrophage derived exosomal miR-20a-5p ameliorates trophoblast pyroptosis and placental injuries in obstetric antiphospholipid syndrome via the txnip/NLRP3 axis

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Life Sciences 2025年 370卷 123561页

作者： Zhang, Hongyuan Jiang, Ning Xu, Mingyang Jing, Die Dong, Tingting Liu, Qian Lv, Qingfeng Huo, Ruiheng Chen, Pengzheng Li, Lei Wang, Xietong Department of Obstetrics and Gynecology Shandong Provincial Hospital Shandong University Shandong Jinan 250021 China Department of Obstetrics and Gynecology Shandong Provincial Hospital Affiliated to Shandong First Medical University Shandong Jinan 250021 China The Laboratory of Medical Science and Technology Innovation Center (Institute of Translational Medicine) Shandong First Medical University (Shandong Academy of Medical Sciences) of China Shandong Jinan 250117 China Department of Obstetrics and Gynecology Feixian County People's Hospital Shandong Linyi 273400 China The Affiliated Taian City Central Hospital of Qingdao University Shandong Taian 271000 China

Aim: Obstetric antiphospholipid syndrome (OAPS) is a pregnancy-related complication characterized by trophoblast pyroptosis and placental injury induced by antiphospholipid antibodies (aPLs). M2-polarized macrophage-derived exosomes (M2-exos) exert anti-inflammatory, immunomodulatory, and growth-promoting effects in various autoimmune diseases and tumors. However, their role in OAPS is not yet clear. Therefore, in this study, we isolated M2-exos from M2 macrophages and investigated their effects on trophoblast proliferation, death, migration, invasion, and pyroptosis following stimulation using aPLs. Main methods: First, we established an animal model of OAPS and thereafter treated the OAPS mice with exogenous M2-exos via injection through the tail vein. Then to clarify the roles of miR-20a-5p and thioredoxin-interacting protein (txnip) in OAPS, we performed gain- or loss-of-function assays, and used GraphPad Prism software to analyze the collected data with statistical significance set at P < 0.05. Key findings: MicroRNAs (miRNAs) sequencing revealed the enrichment of miR-20a-5p in M2-exos, and these M2-exos significantly alleviated aPLs-induced trophoblast dysfunction. Our results also indicated that M2-exos delivered miR-20a-5p to trophoblast cells directly targeted thioredoxin-interacting protein (txnip), and thus suppressed the txnip/NLRP3 pathway, reduced pyroptosis and inflammation in trophoblast cells, and improved placental function and fetal development. Significance: M2-exos improve pregnancy outcomes in OAPS via the miR-20a-5p/txnip/NLRP3 axis, and thus represent as a novel therapeutic approach for aPLs-induced OAPS. © 2025

关键词： Exosome M2-polarized macrophage miR-20a-5p Obstetric antiphospholipid syndrome Pyroptosis txnip

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Palmitic acid enhances the sensitivity of ferroptosis via endoplasmic reticulum stress mediated the ATF4/txnip Axis in polycystic ovary syndrome

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Phytomedicine 2025年 142卷 156777页

作者： Zhang, Xumin Liu, Jianrong Bai, Chunmei Fan, Yanxin Song, Haixia Huang, Ziwei Li, Yang Luo, Ting The Fifth Clinical Medical College of Shanxi Medical University 29 Shuangtaisi street Shanxi Taiyuan 030012 China Department of reproductive Shanxi Provincial People's Hospital Affiliated to Shanxi Medical University 29 Shuangtaisi street Shanxi Taiyuan 030012 China Department of Orthopedics Shanxi Provincial People's Hospital Affiliated to Shanxi Medical University 29 Shuangtasi Street Shanxi Taiyuan 030012 China

Background: Palmitic acid (PA), the most prevalent saturated fatty acid in humans, is closely associated with ovarian dysfunction. Elevated PA levels in the follicular fluid of patients with polycystic ovary syndrome (PCOS) are correlated with the outcomes of assisted reproductive technology (ART), though the underlying mechanism remains unclear. Methods: Multi-omics analysis identified PA and txnip as potential pathogenic factors in PCOS. CCK-8 and apoptosis assay were conducted to detect the cytotoxicity of PA. To further investigate the molecular mechanisms underlying PA-induced ferroptosis, we established COV434 cell models with both txnip overexpression and knockdown. Transmission electron microscopy (TEM), western blot (WB), ELISA assays, and flow cytometry were employed to assess ferroptosis-related markers. A PCOS mouse model was also developed, and histopathological staining, TEM, ELISA, and WB were performed to evaluate clinical parameters related to PCOS ovarian ferroptosis levels. To clarify the targeting relationship between ATF4 and txnip, we utilized luciferase reporter gene assays, chromatin immunoprecipitation (ChIP), and RT-qPCR for a comprehensive analysis. Results: In vivo and in vitro, PA enhanced the sensitivity of PCOS ovarian ferroptosis. The protein levels of txnip and ACSL4 were upregulated in both PCOS patients and mouse models after PA treatment. PA also induces the expression of the ferroptosis inhibitor SLC7A11 as part of an adaptive response. Elevated intracellular ROS levels, increased MDA content, decreased GSH/GSSG ratios, elevated ferrous iron levels, and TEM findings collectively indicated that PA induces ferroptosis in KGN/COV434 cells. The ER stress inhibitor 4-PBA reduces PA-induced ferroptosis in PCOS ovaries by suppressing ER stress, thereby improving PA-induced PCOS-like traits. Moreover, the UPR gene ATF4 regulates cellular ferroptosis by activating the transcriptional expression of txnip. Conclusion: PA stimulated ovarian

关键词： Endoplasmic reticulum stress Ferroptosis Palmitic acid Polycystic ovary syndrome txnip

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Thioredoxin-1 inhibits NLRP3-mediated pyroptosis by regulating txnip in models of Alzheimer’s disease

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Scientific Reports 2025年第1期15卷 1-14页

作者： Jia, Jinjing Sheng, Zixuan Zhang, Yuqian Guo, Lunxi Chen, Zhuo’er Zhu, Dongsheng Zeng, Xiansi Liu, Hongjun Research Center of Neuroscience Jiaxing University Medical College Jiaxing 314001 China Department of Physiology Jiaxing University Medical College Jiaxing 314001 China Department of Neurology The Affiliated Hospital of Jiaxing University Jiaxing 314000 China Department of Biochemistry and Molecular Biology Jiaxing University Medical College Jiaxing 314001 China Judicial Expertise Center Jiaxing University Jiaxing 314001 China Department of Neurology Zhejiang Xin’an International Hospital affiliated to Jiaxing University Jiaxing 314000 China Research Center of Neuroscience Department of Biochemistry Jiaxing University Medical College Jiaxing 314001 China

Alzheimer’s disease (AD) is the most common neurodegenerative disease characterized by memory loss. Our recent study has demonstrated that thioredoxin-1 (Trx-1) could protect neurons via repressing NLRP1‑mediated neuronal pyroptosis in AD models. However, whether Trx-1 could inhibit NLRP3 activation is largely unknown. Here, we found that AAV-mediated Trx-1 overexpression significantly inhibited NLRP3-mediated pyroptosis in the hippocampus of APP/PS1 mice. A mouse hippocampal neuron HT22 cell line overexpressing Trx-1 was successfully obtained through lentivirus transfection. Further study showed that Trx-1 overexpression protected HT22 cells against the neurocytotoxicity of Aβ₂₅₋₃₅. Consistently with the results of in vivo experiments, overexpression of Trx-1 remarkedly inhibited the activation of NLRP3. In the contrary, knockdown of Trx-1 by siRNA transfection further aggravated the activation of NLRP3. Mechanistically, Trx-1 overexpression significantly inhibited the increase of thioredoxin-interacting protein (txnip) in in vivo and in vitro and weakened the interaction between txnip and NLRP3. Taken together, Trx-1 inhibits NLRP3-mediated pyroptosis by regulating txnip expression and its interaction with NLRP3 in AD models. © The Author(s) 2025.

关键词： Alzheimer’s disease Aβ25−35 NLRP3 Pyroptosis Trx-1 txnip

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txnip-mediated nuclear factor-κB signaling pathway and intracellular shifting of txnip in uric acid-induced NLRP3 inflammasome

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2019年第4期511卷 725-731页

作者： Kim, Seong-Kyu Choe, Jung-Yoon Park, Ki-Yeon Catholic Univ Daegu Dept Internal Med Div Rheumatol Sch Med Daegu South Africa Catholic Univ Daegu Arthrit & Autoimmun Res Ctr Daegu South Africa

Objective: The aim of this study was to assess the role of thioredoxin-interacting protein (txnip) in nuclear factor-kappa B (NF-kappa B) signaling and the interaction between txnip and NOD-like receptor protein 3 (NLRP3) in activation of the NLRP3 inflammasome in monosodium urate (MSU)-induced inflammation. Methods: Interleukin-1 beta (IL-1 beta), IL-18, caspase-1, phospho-I kappa B alpha (pI kappa B alpha), phospho-NF-kappa B, (pNF-kappa B), and txnip in U937 macrophage-like cells treated with MSU crystals were analyzed using western blotting and real-time polymerase chain reaction (RT-PCR). Expression of these molecules was also assessed in U937 macrophages transfected with txnip siRNA and treated with antioxidants. Results: U937 macrophages treated with MSU crystals showed increased expression of IL-1 beta, IL-18, caspase-1, and txnip and activation of NF-kappa B signaling, which were strongly inhibited by addition of antioxidants or transfection with txnip siRNA. Intracellular translocation of txnip from the nucleus to mitochondria was observed in cells treated with MSU crystals. And quercetin and ascorbic acid suppressed translocation of txnip. Binding between txnip and NLRP3 under oxidative stress caused by MSU crystals was observed and was blocked by quercetin or ascorbic acid. Conclusion: This study showed that activation of MSU-induced NLRP3 inflammasome requires txnip-mediated NF-kappa B signaling pathway and intracellular txnip shifting. (C) 2019 Published by Elsevier Inc.

关键词： txnip NLRP3 Monosodium urate NF-kappa B Reactive oxygen species

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txnip regulates germinal center generation by suppressing BCL-6 expression

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IMMUNOLOGY LETTERS 2010年第2期129卷 78-84页

作者： Shao, Yan Kim, Sang Yong Shin, Daesung Kim, Mi Sun Suh, Hyun-Woo Piao, Zheng-Hao Jeong, Mira Lee, Suk Hyung Yoon, Suk Ran Lim, Byung Ho Kim, Woo-Ho Ahn, Jeong Keun Choi, Inpyo Korea Res Inst Biosci & Biotechnol Cell Therapy Res Ctr Taejon 305333 South Korea BHK Inc Res Inst Cell Therapy Seoul 135832 South Korea Korea Adv Inst Sci & Technol Dept Biol Sci Taejon 305701 South Korea Seoul Natl Univ Coll Med Dept Pathol Seoul 110406 South Korea Chungnam Natl Univ Dept Microbiol Sch Biosci & Biotechnol Taejon 305764 South Korea

The detailed mechanism driving the germinal center (GC) reaction to B cell lymphomagenesis has not been clarified. Thioredoxin interacting protein (txnip), also known as vitamin D3 up-regulated protein 1 which is an important tumor repressor, is involved in stress responses, redox regulation, and cellular proliferation. Here, we report that txnip has a potential role in the formation of GC in peripheral lymphoid organs where B lymphocytes divide rapidly. First, we compared changes in GC from wild type mice and txnip(-/-) mice. After immunization, txnip(-/-) mice exhibited higher expression level of BCL-6 and larger percentage of GC B cells with the reduction in antibody production and plasma cell numbers. In addition, txnip(-/-) spleens had a much larger population which expressed Ki-67, a marker of cell proliferation, in the red pulp border than WT spleens. Furthermore, the expression of BCL-6 was decreased in txnip overexpressing cells and elevated in txnip deficient cells. Taken together, we conclude that txnip may contribute to the formation of GCs after immunization. During this process, txnip suppresses BCL-6 expression. (C) 2010 Elsevier B.V. All rights reserved.

关键词： Germinal center B cells txnip BCL-6

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txnip potentiates Redd1-induced mTOR suppression through stabilization of Redd1

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ONCOGENE 2011年第35期30卷 3792-3801页

作者： Jin, H-O Seo, S-K Kim, Y-S Woo, S-H Lee, K-H Yi, J-Y Lee, S-J Choe, T-B Lee, J-H An, S. Hong, S-I Park, I-C Korea Inst Radiol & Med Sci Div Radiat Canc Res Seoul 139706 South Korea Korea Inst Radiol & Med Sci Lab Modulat Radiobiol Responses Seoul 139706 South Korea Hanyang Univ Dept Chem Lab Mol Biochem Seoul 133791 South Korea Konkuk Univ Dept Microbiol Engn Seoul South Korea

The mammalian target of rapamycin (mTOR) is a highly conserved serine-threonine kinase activated in response to growth factors and nutrients. Because of frequent dysregulation of the mTOR signaling pathway in diverse human cancers, this kinase is a key therapeutic target. Redd1 is a negative regulator of mTOR, mediating dissociation of 14-3-3 from tuberous sclerosis complex (TSC)2, which allows formation of a TSC-TSC2 complex. In the present study, we identify txnip that inhibits mTOR activity by binding to and stabilizing Redd1 protein. Redd1 and txnip expression was induced by a synthetic glucose analog, 2-deoxyglucose (2-DG). Moreover, Redd1 expression in response to 2-DG was regulated by activating transcription factor 4 (ATF4). Overexpression of txnip was associated with reduced mTOR activity mediated by an increase in Redd1 level, whereas knockdown of txnip using small interfering RNA resulted in recovery of mTOR activity via downregulation of Redd1 during treatment with 2-DG. Interestingly, Redd1 was additionally stabilized via interactions with N-terminal-truncated txnip, leading to suppression of mTOR activity. Our results collectively demonstrate that txnip stabilizes Redd1 protein induced by ATF4 in response to 2-DG, resulting in potentiation of mTOR suppression. To the best of our knowledge, this is the first study to identify txnip as a novel member of the mTOR upstream that acts as a negative regulator in response to stress signals. Oncogene (2011) 30, 3792-3801;doi:10.1038/onc.2011.102;published online 4 April 2011

关键词： ATF4 mTOR Redd1 txnip 2-deoxyglucose

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