Cytotechnology最新文献

{"title":"Research on the mechanism of GRIM-19 affecting lung adenocarcinoma through regulating MDM2 and EMT pathways.","authors":"Pengfei Guo, Song Zhao, Xiaoli Han, Jingtao Huang, Zongying Liang","doi":"10.1007/s10616-025-00797-5","DOIUrl":"10.1007/s10616-025-00797-5","url":null,"abstract":"<p><p>Previously, there have been reports of decreased expression of GRIM-19 and increased expression of MDM2 in lung adenocarcinoma. However, the relationship between GRIM-19 and MDM2 in lung adenocarcinoma has not been reported yet. In this study, we demonstrated that GRIM-19mRNA expression was reduced in lung adenocarcinoma tissue while MDM2mRNA expression was increased. Pearson correlation coefficient analysis showed a significant correlation between GRIM-19mRNA and MDM2mRNA (r = -0.970, <i>p</i> < 0.001). In this study, we further detected by experiments that the overexpression of GRIM-19 lowered the expression level of MDM2 protein, suggesting that GRIM-19 may affect the occurrence and development of lung adenocarcinoma by inhibiting the expression of MDM2. Cellular functional and subcutaneous tumour formation experiments in nude mice have shown that GRIM-19 inhibits the proliferation, invasion, and migration ability of lung adenocarcinoma cells, promotes cell apoptosis, and ultimately inhibits lung adenocarcinoma development. In addition, overexpression of GRIM-19 in A549 cells resulted in significant changes in the expression of EMT-related proteins Snail, N-Cadherin, E-Cadherin, and Vimentin, indicating that GRIM-19 may inhibit the metastasis of lung adenocarcinoma cells by regulating the EMT pathway.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00797-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"130"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12206682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A web-based pharmacological approach to the mechanism of action of Radix Bupleuri in the treatment of chronic atrophic gastritis.","authors":"Peiqing Yang, Yong Tan, Shunmin Hu, Zhongzhen Xu, Gan Ji, Shaoli Tai, Xia Zhang, Weizhou Yu","doi":"10.1007/s10616-025-00802-x","DOIUrl":"https://doi.org/10.1007/s10616-025-00802-x","url":null,"abstract":"<p><p>Radix Bupleuri (RB) is used as a traditional Chinese medicine for treating gastric disorders. However, the active components and pharmacological targets of RB are unknown. In this study, we aimed to reveal the pharmacological effects of RB on gastritis by combining a rat model and a network pharmacology approach. The results showed that quercetin was the most activate ingredient in the treatment of chronic atrophic gastritis (CAG). The molecular docking results showed that RB had a strong affinity with TNF. In vivo and in vitro experiments showed that RB alleviated MNNG-induced gastritis by inhibiting the TNF-α/NF-κB signaling pathway. Through network pharmacology, molecular docking, and in vitro and in vivo experiments, the mechanisms and potential effects of RB on CAG were demonstrated, and a theoretical basis for RB in the treatment of CAG was provided.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"136"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Protective effects of lidocaine on polycystic ovary syndrome through modulating ovarian granulosa cell physiology via PI3K/AKT/mTOR pathway.","authors":"Haixia Xiong, Qiong Hu, Qun Jiang","doi":"10.1007/s10616-025-00771-1","DOIUrl":"https://doi.org/10.1007/s10616-025-00771-1","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-022-00528-0.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"127"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12181593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragalus polysaccharide regulates the cervical cancer cell cycle and inhibits cisplatin resistance by blocking the Wnt/β-catenin pathway through the PPARD/CDC20 axis.","authors":"Wenzhi Liu, Yuanyuan Fu, Xiaohong Jiang, Jinting Tan, Ying Zhang, Lu Zhang","doi":"10.1007/s10616-025-00785-9","DOIUrl":"10.1007/s10616-025-00785-9","url":null,"abstract":"<p><p>Astragalus polysaccharide (APS) can prevent tumor progression and cisplatin resistance. This paper investigates the downstream mechanism of APS in regulating cervical cancer (CC) cisplatin resistance. Cisplatin-resistant CC cell lines were constructed. APS inhibited the proliferation of Hela/DDP and SiHa/DDP cells and increased apoptosis. The downstream transcription factors of APS and the downstream targets of the transcription factor PPARD were predicted using bioinformatics tools. PPARD and CDC20 levels were detected in parental and drug-resistant cell lines. CC cells were treated with APS or a combined knockdown of PPARD and CDC20, or a Wnt/β-catenin pathway agonist, and the proliferation, cell cycle distribution, and apoptosis were examined. A xenograft tumor model was constructed to monitor tumor growth under cisplatin treatment. APS promoted PPARD expression, and PPARD knockdown reduced apoptosis. PPARD transcriptionally repressed CDC20 by binding to its promoter and CDC20 downregulation hindered the proliferation of cisplatin-resistant CC cells and increased the apoptotic rate. Wnt/β-catenin pathway agonist annulled the ameliorative effect of CDC20 knockdown on CC cell growth. CDC20 overexpression reversed the hindered tumor growth by APS treatment. Overall, APS inhibits CC progression and cisplatin resistance by promoting PPARD and suppressing CDC20 transcription to inhibit the Wnt/β-catenin pathway.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00785-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"126"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12174005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycyrrhizin mediates autophagy through the STAT3/survivin pathway to inhibit proliferation and angiogenesis in hepatoma cells.","authors":"Xiao-Fen Bu, Jun Li, Hong Zhu","doi":"10.1007/s10616-025-00819-2","DOIUrl":"10.1007/s10616-025-00819-2","url":null,"abstract":"<p><p>Liver cancer exhibits a covert onset, high propensity for recurrence and metastasis, ultimately leading to unfavourable prognosis and increased mortality. Glycyrrhizin (GL) exhibits diverse pharmacological activities and can serve as an autophagy inducer, thereby demonstrating its potential anticancer efficacy against various cancer cell types. The impact of GL on apoptosis, migration, the STAT3/Survivin pathway, and autophagy was analysed by administering GL to human hepatocellular carcinoma cell lines. Human liver cancer cell lines were treated with 3-MA (an autophagy inhibitor) and colivelin (STAT3 agonist) to analyze glycyrrhetin's effects on autophagy, angiogenesis, and the STAT3/Survivin pathway. The GL group showed significant decreases in cell proliferation, migration, and levels of p-STAT3, Survivin, LC3-I, P62, and VEGF-A compared to controls. Conversely, apoptosis rates and expressions of LC3-II and Beclin1 increased. In the 3-MA group, proliferation, migration, p-STAT3, Survivin, LC3-I, P62, and VEGF-A were higher than in controls, but apoptosis rates and LC3-II and Beclin1 levels were lower. Colivelin inhibited GL's effects, while GL countered 3-MA's actions. Supernatants from various cell groups also yielded similar results in Human umbilical vein endothelial cells (HUVECs). Thus, GL has ability to hinder the STAT3/Survivin signalling pathway, consequently fostering autophagy and delaying the onset and progression of liver cancer cell.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"149"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12267807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144674097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Falcarindiol promotes beige adipocyte-related gene expression and mitochondrial respiration in human preadipocyte-derived adipocytes.","authors":"Shingo Takahashi, Haruka Okaze, Seiji Kawamoto","doi":"10.1007/s10616-025-00790-y","DOIUrl":"10.1007/s10616-025-00790-y","url":null,"abstract":"<p><p>Falcarindiol, a typical polyacetylene compound found in Apiaceae vegetables, activates peroxisome proliferator-activated receptor γ (PPARγ). However, whether it induces the browning of adipocytes through PPARγ activation is unclear. In this study, we aimed to clarify the effects of falcarindiol on adipocyte browning and mitochondrial respiration in human preadipocyte-derived adipocytes. Human primary cultured cells were differentiated for 8 days in the presence of falcarindiol. The expression of PPARγ target and beige adipocyte-related genes was measured using quantitative real-time PCR, and the accumulation of lipid droplets and uncoupling protein 1 (UCP1) protein expression were evaluated using immunohistochemistry. The oxygen consumption rate was measured using a Seahorse flux analyzer. Falcarindiol increased the expression of PPARγ target genes, including <i>PPARγ</i>, <i>FABP4</i>, <i>SLC2A4</i>, and <i>ADIPOQ</i>. It also increased the expression of beige adipocyte-related genes, such as <i>PPARGC1A</i>, <i>PPARA</i>, <i>CITED1</i>, and <i>TBX1</i>, and increased the expression of UCP1 protein. Falcarindiol also significantly increased basal respiration, ATP-linked respiration, maximal respiration, spare capacity, and proton-leak respiration, and significantly decreased the coupling efficiency in a concentration-dependent manner. These results indicate that falcarindiol promotes a beige adipocyte-like phenotype and oxygen consumption of adipocytes in vitro, suggesting that dietary intake of falcarindiol and falcarindiol-containing Apiaceae vegetables may be effective in obesity prevention.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"125"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLC35F2 promotes the progression of NSCLC via regulating CREB1 expression.","authors":"Du Wei, Ge Wenyu, Yu Ling, Chen Hongzhe, Wang Dongmei, Xu Xinglu","doi":"10.1007/s10616-025-00814-7","DOIUrl":"10.1007/s10616-025-00814-7","url":null,"abstract":"<p><p>SLC35F2 has emerged as a potential oncogenic driver in non-small cell lung cancer (NSCLC), yet its mechanistic role in tumor progression remains poorly understood. This study aimed to explore the mechanism of SLC35F2 in mediating non-small cell lung cancer (NSCLC) progression through the cAMP signaling pathway. By analyzing TCGA and GEPIA databases, the present research found that SLC35F2 expression was significantly elevated in NSCLC tissues compared to normal lung tissues, with high SLC35F2 levels correlating with poor patient prognosis (P < 0.05). Functional enrichment analysis using R language revealed significant alterations in multiple pathways, including cAMP signaling, in SLC35F2-high NSCLC. Experimental validation through RT-qPCR and Western blot confirmed upregulated SLC35F2 expression in NSCLC cell lines. Knockdown of SLC35F2 inhibited cell proliferation, migration, and invasion while promoting apoptosis (P < 0.05), as demonstrated by CCK-8, EdU, colony formation, flow cytometry, TUNEL, scratch, and Transwell assays. Mechanistically, SLC35F2 suppression activated the cAMP signaling pathway, particularly through upregulation of the transcription factor CREB1. These findings suggest that SLC35F2 drives NSCLC progression by modulating the cAMP/CREB1 axis, highlighting its potential as a therapeutic target.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"146"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The reducing effect of TNF-α on carbonic anhydrase III gene expression in colon carcinoma and osteosarcoma cells.","authors":"Sümeyye Aydoğan Türkoğlu, Derya Okuyan, Feray Köçkar","doi":"10.1007/s10616-025-00815-6","DOIUrl":"https://doi.org/10.1007/s10616-025-00815-6","url":null,"abstract":"<p><p>The appropriate acid-base balance in organisms is maintained by Carbonic Anhydrase proteins (CAs), which have hydratase activity and regulate intracellular pH. CAs are required for both physiological and pathophysiological processes such as cancer development, and there are differences in their expression profiles in different cancer types. Some members of the CA family like CAIX and CAXII have been suggested as potential cancer biomarkers in various studies. CAIX has been proposed as a possible biomarker for hypoxic colorectal carcinoma. Expression of CAIII, another member of the CA family, was also found to be reduced by TGF-β via the MAPK and PI3K signaling pathways in human colon cancer cells. Additionally, not much is known regarding the interaction between TNF-α, inflammation-related cytokine, and CAIII in colorectal carcinoma (CRC). This study investigates the effect of TNF-α on CAIII expression in different cancer cells, namely HT-29 and Saos-2. CAIII mRNA expression was analyzed by qRT-PCR at both late (24, 48, and 72 h) and early time points (1, 3, and 6 h). Western blot analysis was also used to confirm the reducing effect of TNF-α at the CAIII protein level. To analyze the transcriptional regulation of CAIII by TNF-α, CAIII promoter constructs were transiently transfected to HT-29 and Saos-2 cells, and transcriptional activities of truncated promoter constructs were analyzed with luciferase/SEAP activities. 500U/mL TNF-α led to a drastic decrease at 24 and 48 h time points at CAIII mRNA level. Western blot analysis showed that this decreasing effect of 500 U/mL TNF-α at 24 h, 48 h, and 72 h resulted in a reduction of the CAIII protein level by 0.5 times. P1 (- 939/+ 86), P2 (- 699/+ 86), P3 (- 236/+ 86), and P4 (- 108/+ 86) CAIII promoter constructs were transiently transfected to HT-29 cells, P4 (- 108/+ 86) promoter basal activity is greater than the other promoter constructs. Transcriptional activity of all CAIII promoter constructs was reduced by TNF-α. As a result of pathway inhibition analysis, we deduce that TNF- α decreases CAIII mRNA expression in a colon cancer cell via the PI3K pathway. In addition, the similar reducing effect of TNF-α on CAIII in Saos-2 cells, which is a model of osteosarcoma, was also obtained at mRNA and transcriptional levels.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00815-6.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"148"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12263498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual effects of erastin on aggressive osteosarcoma cells: ferroptosis sensitization and anti-ferroptotic gene activation.","authors":"Gordon Daniel Burns, Kevin Schneider, Shari Atilano, Marilyn Chwa, Steven Chang, M Cristina Kenney, Mithalesh Kumar Singh","doi":"10.1007/s10616-025-00795-7","DOIUrl":"10.1007/s10616-025-00795-7","url":null,"abstract":"<p><p>Osteosarcoma (OS) is a rare cancer, yet the most prevalent primary bone cancer in adolescents and young adults OS can be fatal and detrimental due to its high aggressiveness, early metastases, and chemo-resistance. Recent research suggests that drugs that induce ferroptosis could treat osteosarcoma. It is unknown how erastin-induced ferroptosis influences differential gene expression of System Xc, iron absorption, heme synthesis, and mono- (MUFA) and polyunsaturated (PUFA) fatty acid levels in aggressive OS cells. In this study, we show that erastin-induced ferroptosis decreases OS cell growth and survival by raising total ROS, mitochondrial membrane potential, and downregulating <i>VDAC2</i>. Furthermore, erastin induces elevated levels of <i>SLC7A11</i> and <i>SLC3A2</i>, but downregulation of <i>TFRC</i> and <i>HMOX1</i> in OS cells. Notably, the addition of Ferrostatin-1 protects against Erastin-induced cytotoxicity, implying that these agents induce ferroptosis. We also showed that Ferrostatin-1 provides partial protection against Erastin-induced ferroptosis by stimulating the unique transcriptional gene profile of System Xc-, MUFA, and PUFA while inhibiting iron uptake and heme production in OS cells. These findings show that Erastin inhibits the survival of aggressive OS cells, but it also increases the expression of genes linked with anti-ferroptosis activity, which could lead to preventing ferroptosis in the aggressive OS phenotype. Targeting this anti-ferroptotic differential gene expression mediated by erastin-induced ferroptosis in OS cells may help to improve erastin's efficacy.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00795-7.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"128"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12185812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic insights into Aloin-mediated regulation of STAT3/SLC7A11 signaling in head and neck squamous cell carcinoma.","authors":"Li-Jian Wang, Jun Wang","doi":"10.1007/s10616-025-00798-4","DOIUrl":"10.1007/s10616-025-00798-4","url":null,"abstract":"<p><p>This study aims to investigate the mechanisms by which Aloin (AloAB) mediates the signal transducer and activator of transcription 3 (STAT3)/solute carrier family 7 member 11 (SLC7A11) signaling pathway in head and neck squamous cell carcinoma (HNSCC). HNSCC cells were treated with 50-1000 μM AloAB to assess dose-dependent cytotoxicity and its effects on the STAT3/SLC7A11 pathway. CRISPR activation plasmids were used to overexpress STAT3 or SLC7A11 in FaDu cells. Subsequent analyses included migration and invasion assays, lipid peroxidation (LPO) assay, intracellular iron assay, as well as the measurement of oxidative stress markers and ferroptosis-related factors. Epithelial-mesenchymal transition (EMT) markers and matrix metalloproteinase (MMP) expression levels were also assessed. AloAB treatment significantly reduced cell viability in HNSCC cells at higher concentrations. It inhibited FaDu cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while downregulating STAT3/SLC7A11 expression. Additionally, AloAB induced oxidative stress and ferroptosis, as indicated by elevated malondialdehyde (MDA), Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4), lipid peroxidation (LPO), and iron levels, alongside decreased levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase 4 (GPX4), reduced glutathione (GSH), and glutathione peroxidase (GPx). Overexpression of STAT3 or SLC7A11 reversed these effects, restoring oxidative stress markers and ferroptosis-related factors to control levels. Moreover, the suppression of EMT was alleviated by the upregulation of E-cadherin and the downregulation of N-cadherin, Vimentin, MMP2, and MMP9. AloAB exerts anti-tumor effects on HNSCC cells by inhibiting the STAT3/SLC7A11 signaling pathway, inducing oxidative stress, ferroptosis, and suppression of migration, invasion, and EMT.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00798-4.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"137"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}