Journal of Toxicological Sciences最新文献_第4页

Toxicological effects of Sb(III), Sb(V), and NMG-Sb(V) in human lung, kidney, and liver cells: cytotoxicity and fibrotic factor induction. Sb（III）、Sb(V)和NMG-Sb(V)在人肺、肾和肝细胞中的毒理学效应：细胞毒性和纤维化因子诱导。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.283

Nicole Roldán, Marcelo Verdugo, Noriyuki Suzuki, Natali Zamora, Waldo Quiroz, Alexis Gonzalez, Javier Tognarelli, Yasumitsu Ogra

{"title":"Toxicological effects of Sb(III), Sb(V), and NMG-Sb(V) in human lung, kidney, and liver cells: cytotoxicity and fibrotic factor induction.","authors":"Nicole Roldán, Marcelo Verdugo, Noriyuki Suzuki, Natali Zamora, Waldo Quiroz, Alexis Gonzalez, Javier Tognarelli, Yasumitsu Ogra","doi":"10.2131/jts.50.283","DOIUrl":"https://doi.org/10.2131/jts.50.283","url":null,"abstract":"Antimony ecotoxicity studies are often hindered by the incorrect selection of Sb(III) standards and the application of concentrations that do not reflect real environmental exposure. In this study, we used environmentally relevant concentrations of inorganic Sb in its pentavalent [Sb(V)] and trivalent [Sb(III)] oxidation states, as well as the organic species NMG-Sb(V), which is present in Meglumine Antimoniate, to evaluate the effects of Sb on cell viability in human lung (A549), kidney (HEK293), and liver (HepG2) cell lines. Cell viability was assessed in these cells following treatment with 0.001 to 1 µg/L of Sb(V), 1 to 500 µg/L of Sb(III), and 0 to 1000 mg/L of MA. We also measured ROS production and the expression of the profibrotic markers CTGF, α-SMA, and PAI-1, which are associated with fibrosis activation. No significant changes in cell viability were observed in HepG2 and A549 cells. However, in HEK293 cells, viability decreased by 20-40% at Sb(III) concentrations between 1 µg/L and 1 mg/L. CTGF expression was significantly increased at 17 µg/L of Sb(III), while α-SMA and PAI-1 expression increased at 21 µg/L of Sb(V). These findings suggest that different species of Sb can induce increased expression of mRNA for fibrotic genes in human liver and kidney cell lines at concentrations found in the environment.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 6","pages":"283-292"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Determination of putrefactive amine and ammonia concentrations around decomposed corpses. 腐尸周围腐胺和氨浓度的测定。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.75

Hiroaki Sato, Takahiro Umehara, Satoshi Kimura, Toshiko Tanaka, Sang-Eun Kim

{"title":"Determination of putrefactive amine and ammonia concentrations around decomposed corpses.","authors":"Hiroaki Sato, Takahiro Umehara, Satoshi Kimura, Toshiko Tanaka, Sang-Eun Kim","doi":"10.2131/jts.50.75","DOIUrl":"10.2131/jts.50.75","url":null,"abstract":"The surface of a rotting corpse is covered with liquid decomposition products that have flowed out of the body that include putrefactive amines produced via putrefaction and decarboxylation reactions of proteins. Ammonia generated by deamination is also present around the corpse as a liquid or gas. As these putrefactive substances are toxic to humans, we attempted to measure the concentration of putrefactive substances in decomposed corpses in this study. Liquid putrefaction products were collected from the surface of a corpse, and the concentrations of putrefactive amines such as histamine, tyramine, phenethylamine, and tryptamine were analyzed by LC-MS/MS. Ammonia in the liquid and air around the corpse was also measured. Putrefactive amines and ammonia were present on all corpse surfaces. The highest concentrations and postmortem days in parentheses were as follows: histamine 2.26 mg/g (15 days), tyramine 1.77 mg/g (16 days), phenethylamine 4.90 mg/g (24 days), tryptamine 1.58 mg/g (17 days) and ammonia 25.6 mg/g (24 days postmortem). The highest concentration of ammonia in the air was 1310 ppm at 24 days postmortem. The ammonia level in the air around a corpse is toxic to humans. Inhalation of putrefactive amines and ammonia can cause chemical irritation to the respiratory tract and the skin and damage the mucous membrane of the eye. Oral ingestion can also cause poisoning symptoms such as blood pressure changes and headaches. Adequate protection against putrefactive substances is required when in contact with decaying corpses.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 2","pages":"75-81"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Induction of systemic inflammation by welding fume exposure in office workers as well as welders in welding factories. 办公室工作人员和焊接工厂的焊工接触焊接烟雾引起全身炎症。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.215

Mayumi Tsuji, Chihaya Koriyama, Tatsuto Nakane, Susumu Ueno, Yasuhiro Ishihara

{"title":"Induction of systemic inflammation by welding fume exposure in office workers as well as welders in welding factories.","authors":"Mayumi Tsuji, Chihaya Koriyama, Tatsuto Nakane, Susumu Ueno, Yasuhiro Ishihara","doi":"10.2131/jts.50.215","DOIUrl":"https://doi.org/10.2131/jts.50.215","url":null,"abstract":"Welding fumes are metal particles of 1 µm or less generated during welding. Welding fumes generated in welding factories spread throughout the workplace. However, the effects of exposure have been measured primarily in welding workers, and no research has been conducted on the effects of fumes on workplace office workers. In this study, we recruited welding and office workers who worked in the same factories at ten workplaces in Japan, mainly in the Kyushu and Kanto regions, and separated their serum after blood sampling. We also obtained serum from the general subjects of Minami-Kagoshima City, which is located far from the welding factory. Cytokines and chemokines were quantified in the serum samples, and the concentration of interleukin (IL)-1β was significantly increased in office workers and welders compared with general subjects. Importantly, the serum concentrations of IL-12p70, IL-17A, IL-33, tumor necrosis factor α, and C-C motif chemokine ligand 3 in office workers were significantly higher than those in the general subjects, and there was no significant difference in the levels of these inflammatory molecules between welders and general subjects. This study suggests that office workers exposed to high fume concentrations exhibit increased systemic inflammation. Exposure assessments should be conducted not only for welders but also for office workers to reduce exposure risks.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 5","pages":"215-221"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of postmortem product of amlodipine decomposition by hemoglobin with LC-Q-Orbitrap-MS. 用LC-Q-Orbitrap-MS鉴别氨氯地平尸体分解产物。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.325

Yoshikazu Yamagishi, Hiroyuki Inoue, Sayaka Nagasawa, Hirotaro Iwase, Yasumitsu Ogra

{"title":"Identification of postmortem product of amlodipine decomposition by hemoglobin with LC-Q-Orbitrap-MS.","authors":"Yoshikazu Yamagishi, Hiroyuki Inoue, Sayaka Nagasawa, Hirotaro Iwase, Yasumitsu Ogra","doi":"10.2131/jts.50.325","DOIUrl":"https://doi.org/10.2131/jts.50.325","url":null,"abstract":"Amlodipine (AM), a dihydropyridine calcium channel blocker, is frequently prescribed for hypertension in the clinical setting. Because AM has been detected in various lethal poisoning and suicide cases, it is important to determine its precise concentration in postmortem blood to serve as definitive evidence of death by intoxication. However, blood AM concentration at autopsy frequently differs from that at the time of death. In this study, we found that AM undergoes dehydrogenation by H2O2 at temperatures ranging from 4 to 45ºC. Mass spectra measured by quadrupole-Orbitrap mass spectrometry hyphenated with liquid chromatography showed the generation of 3-ethyl 5-methyl 2-((2-aminoethoxy)methyl)-4-(2-chlorophenyl)-6-methylpyridine-3,5-dicarboxylate (AM-PDP-1) in H2O2 and Hb/H2O2 reaction solutions incubated with AM and in postmortem blood of persons who died of drowning, fire, disease, drug poisoning, CO poisoning, traumatic shock, falling, or choking, after intentional ingestion of AM. AM-PDP-1 is the novel postmortem degradation compound of AM in blood. This compound in the Hb/H2O2 reaction solution was more stable than AM at 4-45ºC. These results show that AM-PDP-1, formed by H2O2-mediated postmortem AM decomposition, is a potential biomarker to correct for AM concentration in postmortem blood.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 7","pages":"325-332"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oral exposure to polystyrene nanoplastics induces anxiety-like behavior and cognitive deficit accompanied with alteration of neuroimmune markers in rats. 口服聚苯乙烯纳米塑料可诱导大鼠焦虑样行为和认知缺陷，并伴有神经免疫标记物的改变。

IF 1.5 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.507

Tin-Tin Win-Shwe, Chaw Kyi-Tha-Thu

{"title":"Oral exposure to polystyrene nanoplastics induces anxiety-like behavior and cognitive deficit accompanied with alteration of neuroimmune markers in rats.","authors":"Tin-Tin Win-Shwe, Chaw Kyi-Tha-Thu","doi":"10.2131/jts.50.507","DOIUrl":"https://doi.org/10.2131/jts.50.507","url":null,"abstract":"Microplastic (MP) pollution has become a global environmental issue, but its potential health effect remains unknown. We aimed to investigate the effect of oral administration of polystyrene nanoplastics (PSNPs) on brain functions and behaviors. Five-week-old Sprague Dawley male rats were given 50 nm PSNPs orally at doses of 10 or 50 mg/kg thrice per week for four weeks. At 9-week-old after completion of oral exposure, novel object recognition test and open field test were performed. The hippocampus from each rat was collected to detect neurological, immunological, and antioxidative stress markers using ELISA, real-time RT-PCR and immunohistochemical analyses. High-dose PSNP-treated rats showed decreased exploration time with a novel object, and reduced entry time and time spent in the center. Increased glutamate concentration, decreased glutamate receptor NMDA subunits (NR1, NR2B) and transcription factors CREB1 and CaMKIV mRNAs and increased cFos and early growth response 1, reduced postsynaptic density protein-95, synaptophysin mRNAs, were observed in high-dose PSNP-treated rats. Moreover, antioxidative stress markers such as superoxide dismutase and catalase were significantly decreased whereas inflammatory cytokines (interleukin 1β, tumor necrosis factor-α) and microglial marker (ionized calcium-binding adapter molecule 1) were significantly higher in high-dose PSNP-treated rats. Our results indicate oral exposure to PSNPs induced anxiety-like behavior and learning, memory impairment by altering neuron-glia-immune cells interaction at synaptic regions in the rat hippocampus. This study would be helpful to understand the association between MP pollution and increasing neurological disorders like dementia, anxiety, and Alzheimer's disease in humans.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 9","pages":"507-521"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

1,2-Naphthoquinone promotes cell migration through EGFR-ERK signaling pathway in human A549 cells. 1,2-萘醌通过EGFR-ERK信号通路促进人A549细胞迁移。

IF 1.5 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.459

Yuexuan Pan, Sho Kubota, Yuzhu Zhang, Shuang Fang, Nobumasa Takasugi, Yoshito Kumagai, Takashi Uehara

{"title":"1,2-Naphthoquinone promotes cell migration through EGFR-ERK signaling pathway in human A549 cells.","authors":"Yuexuan Pan, Sho Kubota, Yuzhu Zhang, Shuang Fang, Nobumasa Takasugi, Yoshito Kumagai, Takashi Uehara","doi":"10.2131/jts.50.459","DOIUrl":"https://doi.org/10.2131/jts.50.459","url":null,"abstract":"Hazardous environmental factors contribute to various irreversible threats to human health worldwide. Accumulating evidence suggests that exposure to particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) plays a critical role in lung carcinogenesis. Previously, we reported that 1,2-naphthoquinone (1,2-NQ), a component of atmospheric PM2.5 and diesel exhaust particles, forms a covalent bond with the epidermal growth factor receptor (EGFR) via protein N-arylation, thereby activating the downstream protein kinase B (Akt) signaling pathway. Here, we elucidate a regulatory mechanism by which 1,2-NQ modulates the migratory activity of human lung adenocarcinoma A549 cells. Specifically, exposure of A549 cells to 1,2-NQ induces phosphorylation of EGFR, leading to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). This activation is significantly suppressed by anti-EGFR antibodies (cetuximab and panitumumab) and inhibitors targeting rapidly accelerated fibrosarcoma (Raf; LY3009120) and mitogen-activated protein kinase kinase (MEK; U0126). These findings suggest that 1,2-NQ induces ERK1/2 phosphorylation by activating the Raf-MEK pathway. Notably, suppression of EGFR-ERK1/2 signaling resulted in a decrease in migratory activity. Our findings provide new insights into lung cancer carcinogenesis and may contribute to the development of novel therapeutic strategies.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 9","pages":"459-469"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential of connexin 32 as a predictive marker for drug-induced cholestatic liver injury in a collagen vitrigel-culture model of HepG2-NIAS cells, a new subline of HepG2 cells, with bile canaliculus-like structures. 连接蛋白32在HepG2- nias细胞（一种具有胆管样结构的HepG2细胞亚系）胶原培养模型中作为药物性胆汁淤积性肝损伤预测标志物的潜力

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.135

Miaki Uzu, Toshiaki Takezawa

{"title":"Potential of connexin 32 as a predictive marker for drug-induced cholestatic liver injury in a collagen vitrigel-culture model of HepG2-NIAS cells, a new subline of HepG2 cells, with bile canaliculus-like structures.","authors":"Miaki Uzu, Toshiaki Takezawa","doi":"10.2131/jts.50.135","DOIUrl":"10.2131/jts.50.135","url":null,"abstract":"Cholestatic drug-induced liver injury (DILI) is caused by the aberrant excretion of bile acids (BAs) from hepatocytes via bile canaliculus-like structures (BCLSs) into the bile ducts. The precise in vitro evaluation method for cholestatic DILI has not been established due to a lack of specific markers and cell resources. We previously reported that HepG2-NIAS cells cultured on a collagen vitrigel (CV) membrane formed BCLSs with high protein expression of transporters involved in the excretion of BAs, including bile salt export pump (BSEP). In this study, the potential of connexin (Cx) 32, a component of gap junction, as a predictive marker for cholestatic DILI was investigated using a CV-culture model of HepG2-NIAS cells. The cells were treated with 7 drugs with different DILI-risk levels, and cell toxicity and Cx32 expression were evaluated. Cell toxicity was significantly increased not only by high DILI-risk drugs (troglitazone and cyclosporine A) but also by chlorpromazine with low DILI-risk. Furthermore, cell toxicity of troglitazone was not enhanced by a co-treatment with taurocholate, suggesting the low involvement of inhibition of BA excretion via BSEP in cholestatic DILI. In contrast, the total protein expression of Cx32 and co-localization of Cx32 and F-actin, which is composed of BCLSs, were significantly increased only by high DILI-risk drugs. Treatment with high DILI-risk drugs also induced the increased protein expression of zonula occludens (ZO)-1, which supports BCLSs concerted with Cx32. These results suggest that Cx32 expression in the CV-culture model of HepG2-NIAS cells may be a prominent predictive marker for cholestatic DILI.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 3","pages":"135-145"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Perfluorooctane sulfonate induces hepatotoxicity through promoting inflammation, cell death and autophagy in a rat model. 在大鼠模型中，全氟辛烷磺酸通过促进炎症、细胞死亡和自噬诱导肝毒性。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.45

Leilei Tang, Jianjun Zhu, Sheng Zhuge, Jiawen Yu, Guojun Jiang

{"title":"Perfluorooctane sulfonate induces hepatotoxicity through promoting inflammation, cell death and autophagy in a rat model.","authors":"Leilei Tang, Jianjun Zhu, Sheng Zhuge, Jiawen Yu, Guojun Jiang","doi":"10.2131/jts.50.45","DOIUrl":"10.2131/jts.50.45","url":null,"abstract":"Perfluorooctane sulfonate (PFOS) is reported to cause hepatotoxicity in animals and humans. However, the underlying mechanism by which it affects organelle toxicity in the liver are not well elucidated yet. This study aimed to investigate the mechanisms underlying PFOS-induced hepatic toxicity, focusing on inflammation, cell death, and autophagy. We established a PFOS-exposed Sprague-Dawley (SD) rat liver injury model by intraperitoneal injection of PFOS (1 mg/kg and 10 mg/kg body weight) every alternate day for 15 days. Our findings indicated that PFOS increased liver weight, caused lipid disorder and hepatic steatosis in rats. Meanwhile, PFOS disrupted the structure of mitochondria, increased accumulation of reactive oxygen species (ROS), repressed superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels, and elevated malondialdehyde (MDA) and nitric oxide synthase (NOS) amounts. We found PFOS induced inflammation as evidenced by activation of NOD-like receptor protein 3 (NLRP3), Cleaved cysteine-aspartic acid protease (caspase)1, tumor necrosis factor (TNF)α and interleukin (IL)-1β levels. Moreover, PFOS exposure significantly decreased B-cell lymphoma2 (Bcl2)/Bcl2 associated X (Bax) ratio and increased the protein expression of Cleaved caspase-3. Compared with the control group, PFOS upregulated the protein expression of necroptotic markers and autophagy-related proteins. In conclusion, PFOS induced inflammation, cell death, and autophagy through oxidative stress by ROS overload, thereby providing a mechanistic explanation for PFOS-induced hepatotoxicity.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 2","pages":"45-55"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Journal of Toxicological Sciences and Fundamental Toxicological Sciences to become open access journals. 《毒理学科学杂志》和《基础毒理学科学》成为开放获取期刊。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.R1

Toshiyuki Kaji, Akira Naganuma

{"title":"The Journal of Toxicological Sciences and Fundamental Toxicological Sciences to become open access journals.","authors":"Toshiyuki Kaji, Akira Naganuma","doi":"10.2131/jts.50.R1","DOIUrl":"https://doi.org/10.2131/jts.50.R1","url":null,"abstract":"We would like to express our gratitude for your contributions to our official scientific journals, The Journal of Toxicological Sciences and Fundamental Toxicological Sciences.We have decided to make both journals open access in order to internationalize them and expand their reach to a broader audience. Articles will be published under the Creative Commons license with the highest degree of freedom, CC BY (4.0). As a result of this change, article copyright will belong to the authors, and secondary use, including copying, distribution, display, storage, modification, and commercial use, can be carried out without the relevant society's permission.The new Instructions for Authors will be published on the journal websites in advance. These new submission guidelines \u2028will apply to papers submitted on or after June 1, 2025 (Japan time). Please note that the previous Instructions for Authors will apply to papers submitted until May 31, 2025 (Japan time).We hope that this change will encourage you to submit more of your excellent papers to The Journal of Toxicological Sciences and Fundamental Toxicological Sciences.Toshiyuki Kaji, Ph.D.Editor-in-ChiefThe Journal of Toxicological SciencesAkira Naganuma, Ph.D.Editor-in-ChiefFundamental Toxicological Sciences.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 5","pages":"R1"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miRNA-214-3p targets BNIP3 to affect autophagy and thus drive gastric cancer progression. miRNA-214-3p通过靶向BNIP3影响自噬从而驱动胃癌进展。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.235

Changjiang Chen, Shen Guan, Yong Zhuang, Mingming Xie, Qingxia Huang, Xiaoling Li, Chunkang Yang, Jinliang Jian

{"title":"miRNA-214-3p targets BNIP3 to affect autophagy and thus drive gastric cancer progression.","authors":"Changjiang Chen, Shen Guan, Yong Zhuang, Mingming Xie, Qingxia Huang, Xiaoling Li, Chunkang Yang, Jinliang Jian","doi":"10.2131/jts.50.235","DOIUrl":"https://doi.org/10.2131/jts.50.235","url":null,"abstract":"With a fourth-place death rate among all malignancies, gastric cancer (GC) is one of the most prevalent tumors globally. As a primary malignant characteristic of GC, metastasis contributes substantially to a high death rate and unfavorable prognosis. miRNA-214-3p can influence cell apoptosis since it is an autophagy-regulating molecule. Its significance in GC malignant development has not, however, been investigated in terms of mechanism. qRT-PCR was utilized to confirm expression of miRNA-214-3p in GC tissues and cells. Bioinformatics analysis was then implemented to examine BNIP3 expression in GC as well as binding interaction between BNIP3 and miRNA-214-3p. The targeting capability of miRNA-214-3p on BNIP3 was confirmed using the dual-luciferase assay. Capacities of cells to proliferate, migrate, and invade were assayed using Transwell assays and colony formation. In order to determine if GC cells were capable of autophagy, immunofluorescence and western blot were employed. In GC, miRNA-214-3p was substantially expressed in GC tissues and cells, but BNIP3 was downregulated, as shown by bioinformatics analysis and verified by cell tests. MiRNA-214-3p targeted BNIP3, as shown by further bioinformatics analysis, and dual-luciferase experiment verified this binding connection. MicroRNA-214-3p facilitated cell invasion, migration, and proliferation, as shown by Transwell tests and colony formation. MiRNA-214-3p accelerated malignant development of GC by targeting BNIP3 to impact autophagy, as demonstrated by immunofluorescence and western blot analyses. By targeting BNIP3 to affect autophagy, miRNA-214-3p aided in the malignant growth of GC. This suggested that miRNA-214-3p may function as a likely therapeutic target or biomarker for the disease, with significant implications for early diagnosis and treatment of patients.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 5","pages":"235-244"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0