General physiology and biophysics最新文献

Upregulation of SLC25A1 by MAZ reprograms fatty acid synthesis and fuels LUAD malignancy. MAZ对SLC25A1的上调重编程脂肪酸合成，并促进LUAD恶性肿瘤。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-29 DOI: 10.4149/gpb_2025036

Xiaomeng Li, Jing Li

{"title":"Upregulation of SLC25A1 by MAZ reprograms fatty acid synthesis and fuels LUAD malignancy.","authors":"Xiaomeng Li, Jing Li","doi":"10.4149/gpb_2025036","DOIUrl":"https://doi.org/10.4149/gpb_2025036","url":null,"abstract":"Lung adenocarcinoma (LUAD) is a type of lung cancer with high incidence and mortality rates. Zinc finger protein 801 (MAZ) regulates cellular growth, proliferation, and differentiation, and its abnormal expression is associated with the occurrence of various tumors. In this study, the objective is to investigate the impact and underlying mechanism of MAZ on the malignant progression of LUAD. The expression of solute carrier family 25 member 1 (SLC25A1) was found to be elevated in LUAD, which indicated a relationship with a negative prognosis. Within LUAD cells, SLC25A1 was observed to not only boost proliferation but also hinder apoptosis and further augment fatty acid synthesis. MAZ, which was identified as the upstream regulator of SLC25A1, was also overexpressed in LUAD, thereby positively regulating the expression of SLC25A1. In addition, MAZ was found to accelerate the malignant behaviors of LUAD cells, specifically through its regulation of SLC25A1. Furthermore, in vivo studies confirmed that MAZ stimulated the malignant progression of LUAD via its influence on SLC25A1. In conclusions, MAZ mediates the upregulation of SLC25A1, which modifies the fatty acid synthesis pathway and fuels the malignant progression of LUAD. These findings suggest a new strategy for the targeting therapy in LUAD patients.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tripterygium glycosides alleviate CSE-induced lung injury by inhibiting IL-33 in bronchial epithelial cells. 雷公藤多苷通过抑制支气管上皮细胞IL-33减轻cse所致肺损伤。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025026

Nan Zhang, Jian Fan, Zhiping Deng

{"title":"Tripterygium glycosides alleviate CSE-induced lung injury by inhibiting IL-33 in bronchial epithelial cells.","authors":"Nan Zhang, Jian Fan, Zhiping Deng","doi":"10.4149/gpb_2025026","DOIUrl":"https://doi.org/10.4149/gpb_2025026","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is characterized by airway remodeling and inflammation. Cigarette smoke extract (CSE) induces apoptosis, inflammation, and oxidative stress in COPD. Tripterygium glycosides (TG) are an active compound found in the root extracts of Tripterygium wilfordii Hook F (TWHF) that possesses anti-inflammatory and immunosuppressive effects. However, its role in COPD remains elusive. Herein, 2.5% CSE was used to treat human bronchial epithelial cells (BEAS-2B) to construct a cell injury model. Cell viability, apoptosis, and proliferation were assessed using MTT, flow cytometry, and EdU. Gene expression was analyzed using ELISA, Western blot, and RT-qPCR. TG treatment abolished 2.5% CSE-induced BEAS-2B cell viability and proliferation inhibition, apoptosis and inflammatory response promotion, and IL-33 level increase. Moreover, the repression of TG treatment on 2.5% CSE-triggered BEAS-2B cell damage was abrogated by IL-33 overexpression. Phosphorylation of JNK, ERK1/2, and p38 in 2.5% CSE-treated BEAS-2B cells was enhanced, manifesting that MAPK signaling pathways were activated. TG administration attenuated 2.5% of CSE-activated MAPK pathways through IL-33 upregulation. TG treatment repressed CSE-induced BEAS-2B cell damage partly by regulating the IL-33-mediated MAPK signaling pathway, providing a better understanding of the role of TG in the anti-inflammatory therapeutics for COPD treatment.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"429-438"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Calycosin attenuates neuronal ferroptosis in Alzheimer's disease mice by activating the Nrf2/HO-1 pathway. 毛囊异黄酮通过激活Nrf2/HO-1通路减轻阿尔茨海默病小鼠的神经元铁下垂。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025021

Qin Li, Bihua He, Ying Xiong

{"title":"Calycosin attenuates neuronal ferroptosis in Alzheimer's disease mice by activating the Nrf2/HO-1 pathway.","authors":"Qin Li, Bihua He, Ying Xiong","doi":"10.4149/gpb_2025021","DOIUrl":"https://doi.org/10.4149/gpb_2025021","url":null,"abstract":"In this study, we investigated the therapeutic potential of calycosin (from Astragalus) in Alzheimer's disease (AD), focusing on ferroptosis modulation. APP/PS1 mice received 40 mg/kg calycosin for 3 months. Cognitive function was assessed via Morris water maze test. Tau hyperphosphorylation and amyloid-β (Aβ) aggregation were analyzed using immunofluorescence and Western blotting. In vitro, Aβ1-42-treated HT22 neuronal cells were exposed to calycosin. Ferroptosis-related phenotypes were assessed in vivo and in vitro using Prussian blue staining, commercial kits, and Western blotting. The nuclear factor-erythroid factor 2-related factor 2 (Nrf2) signaling was examined by Western blotting. Calycosin treatment significantly improved cognitive deficits in APP/PS1 mice and inhibited Tau hyperphosphorylation and Aβ aggregation. Calycosin attenuated neurotoxicity and Tau hyperphosphorylation in Aβ1-42-treated HT22 cells. Moreover, calycosin inhibited ferroptosis in vivo and in vitro by decreasing iron aggregation and lipid peroxidation, downregulating transferrin receptor expression, and upregulating ferroportin, cystine/glutamate antiporter, and glutathione peroxidase 4 expression. Mechanistically, the anti-ferroptosis effects of calycosin were linked to the activation of the Nrf2-mediated pathway. These findings suggest that calycosin may exhibit neuroprotective effects against neuronal ferroptosis in AD, indicating its potential as a therapeutic candidate for further investigation in AD.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"363-375"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

circ_0049271 downregulation ameliorates lipopolysaccharide-induced human renal tubular endothelial cell apoptosis, inflammation and oxidative stress. Circ_0049271下调可改善脂多糖诱导的人肾小管内皮细胞凋亡、炎症和氧化应激。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025024

Xiaozhen Ji, Jinjuan Zhang, Lefeng Zhang

{"title":"circ_0049271 downregulation ameliorates lipopolysaccharide-induced human renal tubular endothelial cell apoptosis, inflammation and oxidative stress.","authors":"Xiaozhen Ji, Jinjuan Zhang, Lefeng Zhang","doi":"10.4149/gpb_2025024","DOIUrl":"https://doi.org/10.4149/gpb_2025024","url":null,"abstract":"Circular RNA (circRNA) has been confirmed to be a regulator for septic acute kidney injury (AKI). It is reported that circ_0049271 has abnormal expression in AKI patients, but its role and mechanism in septic AKI remain unclear. Lipopolysaccharide (LPS)-stimulated HK-2 cells were served as the cellular model of sepsis-associated AKI (SAKI). qRT-PCR was conducted for examining the expression of circ_0049271, KEAP1 and miR-331-3p. Cell proliferation and apoptosis were detected by EdU assay and flow cytometry. The protein levels of apoptosis-related markers, RUNX family transcription factor 1 (RUNX1), and PI3K/AKT/mTOR pathway-related markers were tested using Western blot. RNA interaction was confirmed by dual-luciferase reporter assay, RIP assay, and RNA pull-down assay. Our data showed that circ_0049271 was enhanced in LPS-induced HK-2 cells. Silencing of circ_0049271 attenuated LPS-induced HK-2 cell oxidative stress, apoptosis, and inflammation. In terms of mechanism, circ_0049271 targeted miR-331-3p to promote LPS-induced HK-2 cell injury. RUNX1 was a target of miR-331-3p, and RUNX1 overexpression reversed miR-331-3p-mediated inhibitory effects on LPS-induced HK-2 cell injury. Moreover, circ_0049271 sponged miR-331-3p to positively regulate RUNX1 expression, thus activating the PI3K/AKT/mTOR pathway. In conclusion, our data indicated that circ_0049271 contributed to LPS-induced HK-2 cell injury by regulating miR-331-3p/RUNX1 pathway, providing potential molecular targets for the treatment of SAKI.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"391-403"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

WTAP regulates DDX3Y mRNA via m6A modification to promote high glucose-induced podocytes injury and diabetic nephropathy progression. WTAP通过m6A修饰调节DDX3Y mRNA，促进高糖诱导的足细胞损伤和糖尿病肾病进展。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025020

Guanxi Li, Huijuan Zeng, Guojia Ru, Fang Yin, Siyi Liu, Jie He

{"title":"WTAP regulates DDX3Y mRNA via m6A modification to promote high glucose-induced podocytes injury and diabetic nephropathy progression.","authors":"Guanxi Li, Huijuan Zeng, Guojia Ru, Fang Yin, Siyi Liu, Jie He","doi":"10.4149/gpb_2025020","DOIUrl":"https://doi.org/10.4149/gpb_2025020","url":null,"abstract":"Diabetic nephropathy (DN) is a major complication of diabetes, imposing substantial socioeconomic and public health challenges. N6-methyladenosine (m6A) modification, a prevalent epigenetic mechanism, influences cellular processes and disease progression. Wilms' tumor 1-associating protein (WTAP), an m6A methyltransferase subunit, was investigated for its role in DN. Bioinformatics identified differentially expressed genes in DN, and a high glucose (HG)-induced podocyte model was established to mimic DN in vitro. Techniques like Western blot, CCK-8, ELISA, flow cytometry, and TUNEL evaluated protein expression, cell viability, inflammation, oxidative stress, and apoptosis. SRAMP predicted m6A sites in DDX3Y mRNA, validated by MeRIP, while xenograft models confirmed in vivo effects. DDX3Y expression was elevated in DN and HG-induced podocytes, and sh-DDX3Y attenuated HG-induced injury. WTAP promoted DDX3Y mRNA stability via m6A methylation, exacerbating podocyte dysfunction. In diabetic mice, WTAP modulated DDX3Y to induce renal insufficiency and histopathological damage. Collectively, WTAP regulates DDX3Y via m6A methylation to promote HG-induced podocyte injury and DN progression.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"405-417"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biophysical study of calcium-containing DPPC liposomes prepared in water and a glycerol aqueous solution. 在水和甘油水溶液中制备含钙DPPC脂质体的生物物理研究。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025018

Tamaz J Mdzinarashvili, Mariam M Khvedelidze, Salome V Chinchaladze, Eka R Shekiladze, Mariam T Mdzinarashvili

{"title":"Biophysical study of calcium-containing DPPC liposomes prepared in water and a glycerol aqueous solution.","authors":"Tamaz J Mdzinarashvili, Mariam M Khvedelidze, Salome V Chinchaladze, Eka R Shekiladze, Mariam T Mdzinarashvili","doi":"10.4149/gpb_2025018","DOIUrl":"https://doi.org/10.4149/gpb_2025018","url":null,"abstract":"In this study, both pure and calcium-containing complex liposomes made from DPPC phospholipids were investigated using calorimetric and spectrophotometric methods. Liposomes were prepared using a new technology in both water and a 20% glycerol aqueous solution. Glycerol allows drug-containing DPPC liposomes to penetrate the dermis of the skin through the epidermis. Calorimetric and spectrophotometric experiments show that calcium ions are incorporated into the structure of DPPC liposomes. Consequently, these nanoparticles can be used to treat diseases that require a significant amount of calcium, ensuring that the calcium within the liposomes will not cause side effects when it enters the bloodstream. Through the conducted experiments, we examined the structure and thermal stability of calcium DPPC liposomes prepared in water and glycerol, which is essential for their effective practical use. We found that the structure of all complex liposomes is multilamellar, which enables them to incorporate a larger amount of calcium ions than unilamellar liposomes. Based on the calorimetric experiments conducted, we identified a new approach to determine the maximum amount of drug, including calcium, that can be incorporated into nanoparticles, which is a crucial factor.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"419-427"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hypoxia-conditioned cardiomyocyte-derived exosomes attenuate myocardial injury via ANP-mediated M2 macrophage polarization. 缺氧条件心肌细胞来源的外泌体通过anp介导的M2巨噬细胞极化减轻心肌损伤。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025022

Mingye Wang, Chi Zhao, Tongtong Li, Tao Song, Yuanyuan Hao, Wenwen Cui, Min Guan, Yunlong Hou, Yang Li

{"title":"Hypoxia-conditioned cardiomyocyte-derived exosomes attenuate myocardial injury via ANP-mediated M2 macrophage polarization.","authors":"Mingye Wang, Chi Zhao, Tongtong Li, Tao Song, Yuanyuan Hao, Wenwen Cui, Min Guan, Yunlong Hou, Yang Li","doi":"10.4149/gpb_2025022","DOIUrl":"https://doi.org/10.4149/gpb_2025022","url":null,"abstract":"Exosomes derived from various cells have been demonstrated to contribute to cardiac repair by regulating macrophage polarization in myocardial infarction. However, how exosomes secreted from cardiomyocytes under hypoxia-ischemia (Hypo-Exo) regulate macrophage polarization in the local tissues is elusive. This study aimed to determine the underlying mechanisms by which Hypo-Exo polarized M2 macrophages. Hypo-Exo was harvested from the supernatant of oxygen glucose deprivation (OGD)-conditioned H9c2, identified using transmission electron microscopy, nanoparticle tracking analysis, and western blot, and then applied to RAW264.7 and C57BL/6N mice. Echocardiography, TTC, H&E, Masson, and immunofluorescence staining were used to evaluate the therapeutic effects of Hypo-Exo in the MI mouse model. The effects of Hypo-Exo on RAW264.7 were examined by RT-qPCR. Hypo-Exo labeled with PKH26 could be engulfed by RAW264.7 cells and promote M2 macrophage polarization. Hypo-Exo inhibited atrial natriuretic peptide (ANP) mRNA expression in RAW264.7 cells, and three cargo miRNAs of Hypo-Exo were upregulated to degrade the ANP expression. Instead of downregulating ANP, OGD supernatant upregulated ANP expression to activate M1 macrophages. Our study demonstrated a novel mechanism that Hypo-Exo carried with miRNAs as a communicator to degrade the expression level of ANP mRNA in macrophages by which Hypo-Exo polarized M2 macrophages to improve recovery from MI in mice.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"377-389"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HuR enhances the stability of FGF19 mRNA to suppress Kupffer cell activation and mitigate inflammation and fibrosis in non-alcoholic fatty liver disease. HuR增强FGF19 mRNA的稳定性，抑制Kupffer细胞活化，减轻非酒精性脂肪性肝病的炎症和纤维化。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-09-01 DOI: 10.4149/gpb_2025023

XiaoQing Mo, SiJun Zhou, XiaoGe Zhou, Chun Huang

{"title":"HuR enhances the stability of FGF19 mRNA to suppress Kupffer cell activation and mitigate inflammation and fibrosis in non-alcoholic fatty liver disease.","authors":"XiaoQing Mo, SiJun Zhou, XiaoGe Zhou, Chun Huang","doi":"10.4149/gpb_2025023","DOIUrl":"https://doi.org/10.4149/gpb_2025023","url":null,"abstract":"This study explores how human antigen R (HuR) stabilizes fibroblast growth factor 19 (FGF19) mRNA, inhibiting Kupffer cell (KC) activation to reduce inflammation and fibrosis in non-alcoholic fatty liver disease (NAFLD). An animal model of NAFLD was established in mice by administering a high-fat diet (HFD). In vitro study utilized a lipopolysaccharide-induced immortalized mouse KC model. HuR expression markedly decreased in HFD-induced NAFLD liver tissue. Overexpression of HuR via adeno-associated virus (AAV) vectors mitigated key pathological features of NAFLD, including hepatic inflammation and fibrosis. Moreover, HuR overexpression suppressed KC activation in both in vitro and in vivo models. Mechanistically, HuR bound AU-rich elements in FGF19 mRNA, enhancing its stability. FGF19 overexpression similarly mitigated HFD-induced liver pathology. Conversely, FGF19 silencing reversed HuR's inhibition of KC activation and abrogated HuR's protection against liver inflammation and fibrosis. This research elucidates a novel mechanism underlying the interaction between HuR and FGF19 in mitigating the pathological progression of NAFLD, providing potential therapeutic targets for this prevalent liver disease.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 5","pages":"349-361"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hydroxysafflor yellow A ameliorates transforming growth factor-β1-triggered fibroblast activation via inactivation of the NF-κB/STAT3 pathway by suppressing ADAM17 expression. 羟基红花黄A通过抑制ADAM17表达，通过抑制NF-κB/STAT3通路的失活，改善转化生长因子-β1触发的成纤维细胞活化。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-05-01 DOI: 10.4149/gpb_2025008

Yan Wang, Wenjing Zhang, Suhuan Wu, Xiaofang Sun, Yanmei Han, Xiaoxu Wang, Yu Wang

{"title":"Hydroxysafflor yellow A ameliorates transforming growth factor-β1-triggered fibroblast activation via inactivation of the NF-κB/STAT3 pathway by suppressing ADAM17 expression.","authors":"Yan Wang, Wenjing Zhang, Suhuan Wu, Xiaofang Sun, Yanmei Han, Xiaoxu Wang, Yu Wang","doi":"10.4149/gpb_2025008","DOIUrl":"https://doi.org/10.4149/gpb_2025008","url":null,"abstract":"The abnormal proliferation and activation of fibroblasts have been implicated in idiopathic pulmonary fibrosis. Herein, the present research explored the impacts of the relationship between hydroxysafflor yellow A (HSYA) and a disintegrin and metalloproteinase 17 (ADAM17) on fibroblast activation, which can provide novel insight into the treatment and management of idiopathic pulmonary fibrosis. MRC-5 fibroblasts were firstly activated with TGF-β1, followed by measurement of ADAM17 expression through qRT-PCR and Western blot. Fibrosis-related gene and protein expression levels, cell viability, proliferation, migration, and fibroblast-to-myofibroblast transdifferentiation were determined by qRT-PCR and Western blot, MTS, EdU, Transwell, and immunofluorescence assays, respectively. Moreover, the regulatory relationships among HSYA, ADAM17, and the NF-κB/STAT3 pathway in MRC-5 cells were analyzed by bioinformatics analysis, qRT-PCR, and Western blot. The results show that HSYA treatment could diminish the fibrosis-related gene and protein expression patterns, proliferation, migration, and fibroblast-to-myofibroblast transdifferentiation in TGF-β1-stimulated MRC-5 cells. Moreover, HSYA could repress the TGF-β1-triggered ADAM17 up-regulation, thereby suppressing the NF-κB/STAT3 pathway. Furthermore, over-expression of ADAM17 negated the inhibitory effect of HSYA on fibroblast activation induced by TGF-β1. The findings revealed that HSYA blocked the NF-κB/STAT3 pathway activation by down-regulating ADAM17, thereby inhibiting TGF-β1-induced fibroblast activation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 3","pages":"187-200"},"PeriodicalIF":1.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ZNF471 inhibits nasopharyngeal carcinoma cell growth and stemness. ZNF471抑制鼻咽癌细胞生长和干性。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2025-05-01 DOI: 10.4149/gpb_2025010

Xiaodan Wang, Minqiang Chang, Zhuyin Wen, Qin Wang, Chenglan Liu

{"title":"ZNF471 inhibits nasopharyngeal carcinoma cell growth and stemness.","authors":"Xiaodan Wang, Minqiang Chang, Zhuyin Wen, Qin Wang, Chenglan Liu","doi":"10.4149/gpb_2025010","DOIUrl":"https://doi.org/10.4149/gpb_2025010","url":null,"abstract":"We investigated how zinc finger protein 471 (ZNF471) affects nasopharyngeal carcinoma (NPC) cell growth, migration, invasion and stemness and offer possible treatment targets for NPC research. The GEO2R online dataset was used to query the expression of ZNF471 in NPC tissues. ZNF471 overexpression plasmid was transfected into NPC cell lines. Cell Counting Kit-8 (CCK8) was used to detect cell viability, 5-Ethynyl-2'-deoxyuridine (Edu) to detect cell proliferation, Wound Healing Assay to detect cell migration, Transwell Assay to detect cell invasion, and Spheroid Formation Assay to detect the stemness characteristics of NPC cells. Western blot assay was used to determine the downstream genes matrix metalloproteinase 7 (MMP-7) and Myelocytomatosis viral oncogene homolog (c-Myc), as well as the protein expression of β-catenin, a protein linked to the Wnt/β-catenin pathway. Overexpression of ZNF471 significantly inhibited NPC cell viability, reduced the number of Edu-positive cells, migration rate, cell invasion number, and tumor cell spheroid formation number. Besides, overexpression of ZNF471 reduced the protein expression of β-catenin and the downstream genes c-Myc and MMP-7. In conclusion, ZNF471 inhibits the growth, migration, invasion and stemness of NPC cells, which may be related to its inhibition of Wnt/β-catenin pathway activation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"44 3","pages":"235-244"},"PeriodicalIF":1.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0