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Genes and proteins expression profile of 2D vs 3D cancer models: a comparative analysis for better tumor insights.
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-25 DOI: 10.1007/s10616-025-00714-w
Sunaina Bhuker, Abhinav Kumar Sinha, Anuksha Arora, Hardeep Singh Tuli, Sonal Datta, Adesh K Saini, Reena V Saini, Seema Ramniwas
{"title":"Genes and proteins expression profile of 2D vs 3D cancer models: a comparative analysis for better tumor insights.","authors":"Sunaina Bhuker, Abhinav Kumar Sinha, Anuksha Arora, Hardeep Singh Tuli, Sonal Datta, Adesh K Saini, Reena V Saini, Seema Ramniwas","doi":"10.1007/s10616-025-00714-w","DOIUrl":"10.1007/s10616-025-00714-w","url":null,"abstract":"<p><p>When juxtaposed with 2D cell culture models, multicellular tumor spheroids demonstrate a capacity to faithfully replicate certain features inherent to solid tumors. These include spatial architecture, physiological responses, the release of soluble mediators, patterns of gene expression, and mechanisms of drug resistance. The morphological and behavioural similarities between 3D-cultured cells and cells within tumor masses highlight the potential of these models in studying cancer biology and drug responses. The liquid overlay method, hanging drop technique, and ultra-low adhesion plates are among the various methods for generating tumor spheroids, each with its advantages and applications. Gene expression studies, employing advanced methods such as microarrays, suppression subtractive hybridization, qRT-PCR, and mass-spectrometry-based proteomics revealed distinct expression patterns in 3D spheroids compared to 2D cultures, uncovering upregulation and downregulation of genes associated with tumor development, metastasis, and drug resistance. Protein expression studies identified alterations in key signaling pathways, metabolic characteristics, and phosphorylation levels, highlighting the impact of 3D culture on cellular responses. This study explores genes and proteins expression variations in various cancer cell lines cultivated in 3D spheroids, shedding light on the complexity of interactions in a more tumor-mimicking environment. The fusion of these analytical approaches not only advances scientific understanding but also holds promise for the development of more effective cancer treatments.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"51"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045508","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}
引用次数: 0
Suppressive effect of curcumin on apoptosis of articular chondrocytes via regulation on NF-κB pathway and NLRP3 inflammasome.
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-01-31 DOI: 10.1007/s10616-024-00695-2
Haobo Li, Shuai Yuan, Zhipeng Yue, Lei Zhang, Shu Chen, Qirong Qian, Qiwei Fu, Yi Chen
{"title":"Suppressive effect of curcumin on apoptosis of articular chondrocytes via regulation on NF-κB pathway and NLRP3 inflammasome.","authors":"Haobo Li, Shuai Yuan, Zhipeng Yue, Lei Zhang, Shu Chen, Qirong Qian, Qiwei Fu, Yi Chen","doi":"10.1007/s10616-024-00695-2","DOIUrl":"10.1007/s10616-024-00695-2","url":null,"abstract":"<p><p>Our study probed into how curcumin modulates NF-κB pathway to regulate articular chondrocytes. ATDC5 cells were exposed to varying concentrations of curcumin (0, 10, 20, 50, or 100 μM) for 48 h, followed by an assessment of curcumin's cytotoxicity. Cells were also treated with 10 ng/ml IL-1β, curcumin, 5 μg/L NF-κB inhibitor (PDTC), and 5 μM NLRP3 inflammasome inducer (nigericin) for 48 h, before cell viability, apoptosis, NF-κB pathway-related proteins, NLRP3 inflammasome-related proteins and inflammatory cytokines were detected. IL-1β treatment notably diminished chondrocyte viability and increased apoptosis, evidenced by elevated level of Bax and cleaved caspase-3, and reduced level of Bcl2, while such expression patterns were reversed by curcumin treatment in a concentration-dependent fashion. Additionally, NF-κB pathway and NLRP3 inflammasome in chondrocytes were activated by IL-1β treatment, but can also be suppressed following curcumin intervention. Furthermore, inhibition of NF-κB pathway curtailed the NLRP3 inflammasome activation and chondrocyte apoptosis, while activation of the NLRP3 inflammasome partially reversed the protective impacts of curcumin against chondrocyte apoptosis. Curcumin inhibits NF-κB pathway, thereby preventing the NLRP3 inflammasome activation and ameliorating IL-1β-induced apoptosis in articular chondrocytes.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"52"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078838","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}
引用次数: 0
Dihydroartemisinin suppresses COX-2-mediated apoptosis resistance in hepatocellular carcinoma under endoplasmic reticulum stress.
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-13 DOI: 10.1007/s10616-025-00717-7
Lulu Cao, Jun Lin, Yun Fang, Junhua Yu, Shengwei Du, Jianxin Chen, Shufeng Xu, Bolun Xu, Jian Zhao
{"title":"Dihydroartemisinin suppresses COX-2-mediated apoptosis resistance in hepatocellular carcinoma under endoplasmic reticulum stress.","authors":"Lulu Cao, Jun Lin, Yun Fang, Junhua Yu, Shengwei Du, Jianxin Chen, Shufeng Xu, Bolun Xu, Jian Zhao","doi":"10.1007/s10616-025-00717-7","DOIUrl":"10.1007/s10616-025-00717-7","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, and its treatment still faces numerous challenges. Dihydroartemisinin (DHA), a derivative of artemisinin, has shown significant antitumor activity in preclinical research. Our study seeks to uncover the molecular mechanisms of DHA in HCC, potentially providing scientific evidence for its use as a supportive therapy in clinical settings. This study was conducted using various experimental approaches to systematically analyze the effects of DHA in HCC. Cell viability was evaluated by CCK-8 to determine the IC<sub>50</sub> of DHA in HCC cells. Flow cytometry was used to measure the rates of apoptosis and reactive oxygen species (ROS) levels. Colony formation assays were performed to examine the inhibitory effects of DHA on HCC cell proliferation. The toxicity of DHA on HCC cells was evaluated through the lactate dehydrogenase release assay. Western blot was conducted to examine expression levels of proteins related to endoplasmic reticulum (ER) and apoptosis. Fluo-3 AM was utilized to label calcium ions (Ca<sup>2+</sup>), allowing for the detection of intracellular Ca<sup>2+</sup> level changes. Additionally, ER tracker was employed to label the ER, with its morphological changes observed via immunofluorescence. DHA notably inhibited the vitality and proliferation of HCC cells and promoted cell apoptosis. Following DHA exposure, there were notable increases in ER stress markers, ROS, and Ca<sup>2+</sup> levels. The morphology of the ER exhibited a loose and expanded state. The use of ER stress inhibitors attenuated these effects. Additionally, ER stress inducers facilitated the upregulation of COX-2, mediating apoptosis in HCC cells. Upon COX-2 knockdown, the apoptotic effect of DHA was markedly amplified. In HCC, DHA induces apoptosis in tumor cells by curbing the COX-2-mediated apoptotic resistance that arises during ER stress. This breakthrough reveals the molecular pathways through which DHA can aid in HCC treatment, offering valuable experimental data to support its clinical use as an adjuvant drug.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"59"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11825429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432683","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}
引用次数: 0
The role of serun lipid, cytokine production in sudden sensorineural hearing loss.
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-02-24 DOI: 10.1007/s10616-025-00722-w
Xiaoqing Zhang, Zhihua Xu, Yehai Liu
{"title":"The role of serun lipid, cytokine production in sudden sensorineural hearing loss.","authors":"Xiaoqing Zhang, Zhihua Xu, Yehai Liu","doi":"10.1007/s10616-025-00722-w","DOIUrl":"10.1007/s10616-025-00722-w","url":null,"abstract":"<p><p>Sudden sensorineural hearing loss (SSNHL) has serious harm to human hearing health, where blood lipid and inflammatory levels may play a key role in it. Thus, the purpose of this investigation was to assess the connection between inflammatory and lipid variables and SSNHL. Patients diagnosed with SSNHL had an analysis of serum lipid parameters, such as total cholesterol (TC), triglycerides, HDL-C, LDL-C, apolipoprotein A (apo A), apolipoprotein B (apo B), and lipoprotein A (Lp(a)), as well as inflammatory factors like TNF-α and IL-10. After that, risk factor analysis was carried out utilizing univariate, multivariate regression, and LASSO retrospective modeling. In all, 72 SSNHL patients and 67 healthy control individuals were involved. The LDL/HDL, total cholesterol, ApoB, LP(a), IL-10, TNF-α, and IFN-γ considerably higher in the SSNHL group than in the healthy control group, however, nervonic acid and coenzyme Q were decreased significantly in SSNHL than Control group. The multivariate logistic regression model's analysis using multifactorial retrospective modeling revealed significant changes in LDL, LDL/HDL, IL-10, and TNF-α. In addition, in the LASSO regression model, the model demonstrated high discrimination, as evidenced by the C-index for the cohort's prediction nomogram, which was 0.998 (95% CI, 0.154-1.115) and confirmed to be 0.925 following bootstrapping validation. Finally, IL-10 and LDL/HDL were the main risk factors in SSNHL. LDL/HDL and IL-10 may be closely related to SSNHL's progress and should be evaluated promptly before treating patients with SSNHL.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"67"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514979","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}
引用次数: 0
Taraxasterol mediated autophagy inhibition in pancreatic encephalopathy involves its regulation on L1 cell adhesion molecule.
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-04-01 Epub Date: 2025-03-04 DOI: 10.1007/s10616-025-00721-x
Peng Cao, Shuangxi Chen, Huiqing Wang, Yanfang Chen
{"title":"Taraxasterol mediated autophagy inhibition in pancreatic encephalopathy involves its regulation on L1 cell adhesion molecule.","authors":"Peng Cao, Shuangxi Chen, Huiqing Wang, Yanfang Chen","doi":"10.1007/s10616-025-00721-x","DOIUrl":"10.1007/s10616-025-00721-x","url":null,"abstract":"<p><p>Pancreatic encephalopathy (PE) is a frequent complication of acute pancreatitis. This study explored the mechanism of taraxasterol (TAS) in PE treatment by inhibiting pyroptosis via L1 cell adhesion molecule (L1CAM) up-regulation. PE rat models were established and treated with TAS, NLRP3 activator, and sh-L1CAM lentivirus. Serum amylase and lipase activities and Serum, hippocampus, and amygdala IL-18 and IL-1β levels were determined by ELISA, followed by TUNEL and HE staining. Rat nerve injury was evaluated by modified Neurological Severity Score (mNSS). Spontaneous behaviors, learning, memory, and emotions in rats were separately assessed by open field, new object recognition, tail suspension, and forced swimming tests. Microstructures of hippocampal CA1 region and amygdala were observed. NLRP3 + GSDMD + cells, pyroptosis markers, L1CAM, and myelin basic protein (MBP) were detected. PE rat model displayed elevated serum amylase and lipase activities and IL-18 and IL-1β levels, increased mNSS, shortened moving distance, reduced discrimination rate, prolonged immobility time, pathological damage in hippocampal CA1 region and amygdala, increased TUNEL-positive and NLRP3 + GSDMD + cells, raised NLRP3, cleaved caspase-1, GSDMD-N, IL-1β and IL-18 levels, and reduced L1CAM and MBP levels. TAS mitigated behavioral deficits and brain injury and curbed NLRP3-mediated pyroptosis in hippocampal CA1 region and amygdala in PE rats. NLRP3 activation partly averted the beneficial impacts of TAS on PE rats. TAS suppressed nerve cell pyroptosis and facilitated myelin regeneration by up-regulating L1CAM. L1CAM silencing partially abrogated TAS's effect on behavioral deficits and brain injury in PE rats. TAS treated PE by inhibiting pyroptosis via L1CAM up-regulation.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00721-x.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"72"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572425","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}
引用次数: 0
Functional improvements in β-conglycinin by preparing bioconjugates with carboxymethyl cellulose. 通过与羧甲基纤维素制备生物共轭物改善β-红霉素的功能。
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-02-01 Epub Date: 2024-11-21 DOI: 10.1007/s10616-024-00664-9
Yui Hataishi, Aya Tanaka, Misaki Ishizuka, Hibine Mizobuchi, Tadashi Yoshida, Makoto Hattori
{"title":"Functional improvements in β-conglycinin by preparing bioconjugates with carboxymethyl cellulose.","authors":"Yui Hataishi, Aya Tanaka, Misaki Ishizuka, Hibine Mizobuchi, Tadashi Yoshida, Makoto Hattori","doi":"10.1007/s10616-024-00664-9","DOIUrl":"10.1007/s10616-024-00664-9","url":null,"abstract":"<p><p>β-Conglycinin was conjugated with carboxymethyl cellulose (CMC) by using water-soluble carbodiimide to improve its function. Two kinds of CMC differing in average molecular weight (about 1 kDa and 90 kDa) were used to investigate the relationship between molecular weight of conjugated saccharide and saccharide content in the conjugates and degree of functional changes in β-conglycinin. The β-conglycinin-CMC conjugates were purified by dialysis using a dialysis membrane whose molecular weight cutoff is 100 kDa. Composition of the β-conglycinin-low molecular weight (LMW) CMC and β-conglycinin-high molecular weight (HMW) CMC was β-conglycinin: CMC = 1:3.3 and 1:2.1 (weight ratio) respectively which was confirmed by BCA method and phenol sulfuric acid method. Conjugation was confirmed by SDS-PAGE with CBB. Solubility of β-conglycinin in the range of pH4.0-7.0 was much improved by conjugation with both LMW and HMW CMC. Emulsifying property of β-conglycinin at pH5.0 and pH7.0 was much improved by conjugation with HMW CMC and greater improvement was achieved by conjugation with LMW CMC. Immunogenicity of β-conglycinin was decreased by conjugation with LMW CMC.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"6"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11582224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709406","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}
引用次数: 0
Anti-angiogenic and anti-oxidant effects of 2-NTI indole derivative vs. suramin in ex vivo, in vivo, and in vitro studies. 2-NTI吲哚衍生物与苏拉明在体内、体内和体外的抗血管生成和抗氧化作用研究。
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-02-01 Epub Date: 2025-01-07 DOI: 10.1007/s10616-024-00701-7
Bayan Jamal Khaleel, Hayder Ridha-Salman, Haitham Mahmood Kadhim, Omeed M Hassan, Ammar Kubba, Hayder B Sahib
{"title":"Anti-angiogenic and anti-oxidant effects of 2-NTI indole derivative vs. suramin in ex vivo, in vivo, and in vitro studies.","authors":"Bayan Jamal Khaleel, Hayder Ridha-Salman, Haitham Mahmood Kadhim, Omeed M Hassan, Ammar Kubba, Hayder B Sahib","doi":"10.1007/s10616-024-00701-7","DOIUrl":"10.1007/s10616-024-00701-7","url":null,"abstract":"<p><p>Angiogenesis is an intricate pathway that involves the formation of new blood capillaries from old, functioning ones. Improper angiogenesis is a feature of numerous maladies, including malignancy and autoimmune disorders. Indole-related derivatives are believed to interfere with the mitotic spindle, inhibiting the multiplication, and invasion of cancerous human cells. 5-bromo-2-(5-(4-nitrophenyl)-4H-1,2,4-triazol-3-yl)-1H-indole (2-NTI) is one of such compounds with outstanding anti-angiogenic, and anti-proliferative properties. To evaluate 2-NTI's antiangiogenic and anti-oxidant activities and potential mechanisms of action in comparison with the standard agent, suramin. The rat aortic ring (RAR) and Chick chorioallantois membrane (CAM) assays were employed to determine antiangiogenic efficacy and dose response, while the DPPH assay estimated free radical scavenging activity. Besides, an MTT test was performed to evaluate antiproliferative activity in HUVECs; however, RT-PCR assessed the gene expression level of VEGF in HCT116 cells. 2-NTI displayed a significant and dose-dependent suppression of angiogenesis (83.04%) at 100 μg/mL concentration versus the negative controls in the RAR assay. 2-NTI also showed no toxicity in the HUVEC cell line, with an IC50 of 876.6 μg/mL, but it significantly reduced the formation of free radicals (IC50 of 135.2 µg/mL) and VEGF gene expression (at doses of 200 and 400 µg/mL) versus the negative controls and suramin. In CAM model, 2-NTI generated considerable blood vessel regression as compared to the negative control. 2-NTI possesses potent anti-angiogenic actions, which might be explained by its profound anti-proliferative and free radical detoxifying activities.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"38"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11706827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946103","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}
引用次数: 0
High mobility group protein N2 inhibits the progression of hepatocellular carcinoma and the related molecular mechanisms. 高迁移率基团蛋白N2抑制肝癌进展及其分子机制研究
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-02-01 Epub Date: 2024-12-12 DOI: 10.1007/s10616-024-00678-3
Gang Li, Guanbo Zhang, Jinsong Li, Jie Zhang, Zhi Yang, Lin Yang, Jiaxing Wang
{"title":"High mobility group protein N2 inhibits the progression of hepatocellular carcinoma and the related molecular mechanisms.","authors":"Gang Li, Guanbo Zhang, Jinsong Li, Jie Zhang, Zhi Yang, Lin Yang, Jiaxing Wang","doi":"10.1007/s10616-024-00678-3","DOIUrl":"10.1007/s10616-024-00678-3","url":null,"abstract":"<p><p>High mobility group protein N2 (HMGN2) related pathways are involved in chromatin regulation/acetylation. It has been reported to be involved in several types of cancers. A recent sequencing study suggested that HMGN2 might be involved in the progression of hepatocellular carcinoma (HCC). This study aimed to explore the role of HMGN2 in HCC, which has been proven to be involved in the development of HCC. In this study, we collected clinical samples and cultured normal hepatocytes and hepatocellular carcinoma cell lines to detect HMGN2 expression levels using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and western blot assay. Subsequently, to determine the role of HMGN2 in HCC, HMGN2 was overexpressed in HCC cell lines. MTT (3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide) assay was used to detect the cell proliferative capacity, and proliferation-related proteins were detected by RT-qPCR and western blot assay. To observe the effect of HMGN2 on cell migration and invasion capacity, Transwell assay was performed. Then, cell apoptosis was detected by flow cytometry, and caspase3 and cleaved-caspase3 were detected using western blot assay. Finally, EMT (epithelial to mesenchymal transition)-related proteins, and matrix metalloproteinase-2 (MMP-2) and MMP-9 expression were detected by RT-qPCR and western blot assay. HMGN2 expression was decreased in HCC tissues as well as in HCC cell lines. After overexpression of HMGN2, MTT results suggested that cell proliferation was decreased, and flow cytometry results showed that the apoptosis level was increased and ki-67 and proliferating cell nuclear antigen (PCNA) expression levels were decreased. On the contrary, cleaved-caspase 3 expression level was increased. HCC cells overexpressing HMGN2 showed a drastic reduction in the number of migrating and invading cells, and the expression levels of MMP-2 and MMP-9 were significantly decreased. Finally, E-cadherin expression was elevated in HCC cells transfected with the HMGN2-plasmid, while N-cadherin showed the opposite result. HMGN2 expression was significantly decreased in patients with HCC. HMGN2 inhibits the malignant behavior of HCC cells and is a potential therapeutic target for HCC.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"20"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11638430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827676","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}
引用次数: 0
Triptolide attenuates LPS-induced chondrocyte inflammation by inhibiting inflammasome activation via the Wnt/β-catenin and NF-κB signaling pathways. 雷公藤甲素通过Wnt/β-catenin和NF-κB信号通路抑制炎性体激活,从而减轻lps诱导的软骨细胞炎症。
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-02-01 Epub Date: 2024-12-09 DOI: 10.1007/s10616-024-00680-9
Hangchu Shi, Qiming Liu, Wang He, Xuming Ma, Xiaoqiang Shen, Yang Zou
{"title":"Triptolide attenuates LPS-induced chondrocyte inflammation by inhibiting inflammasome activation via the Wnt/β-catenin and NF-κB signaling pathways.","authors":"Hangchu Shi, Qiming Liu, Wang He, Xuming Ma, Xiaoqiang Shen, Yang Zou","doi":"10.1007/s10616-024-00680-9","DOIUrl":"10.1007/s10616-024-00680-9","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a common form of arthritis characterized by subchondral bone proliferation and articular cartilage degeneration. Recently, the Nod-like receptor pyrin domain 3 (NLRP3) inflammasome has gained attention due to its association with synovial inflammation in OA. Triptolide (TP), known for its immunosuppressive and anti-inflammatory effects, has been studied in various diseases. However, the specific impact of TP on OA and its underlying mechanism remains largely unexplored. In this study, chondrocytes were treated with a specific concentration of TP, and subsequent analysis through Western blotting and immunofluorescence staining revealed decreased expression levels of MMP-13, NLRP3, Caspase-1, ASC, β-catenin, p-p65, and IκB compared to the model group. ELISA results demonstrated significantly lower levels of IL-1β, IL-18, and TNF-α in the TP treatment group compared to the model group. In addition, triptolide ameliorates the degradation of the extracellular matrix (ECM) by enhancing the expression of collagen-II. In conclusion, our findings suggest that TP exhibits anti-inflammatory effects on chondrocytes in the presence of LPS-induced inflammation by inhibiting the activation of the NLRP3 inflammasome via the Wnt/β-catenin and NF-κB pathway. These results contribute to a better understanding of TP's potential therapeutic benefits in managing OA.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"13"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812661","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}
引用次数: 0
Yinjia pills inhibits the malignant biological behavior of HeLa cells through PKM2-medicated inhibition of JAK/STAT3 pathway. 银翘丸通过 PKM2 抑制 JAK/STAT3 通路,抑制 HeLa 细胞的恶性生物学行为。
IF 2 4区 生物学
Cytotechnology Pub Date : 2025-02-01 Epub Date: 2024-11-20 DOI: 10.1007/s10616-024-00668-5
Ying Shi, Xiaoli Min, Yi Li, Lihua Guo, Zheng Cai, Dongge Li, Xueying Jiang, Ni Feng, Xiaolin Li, Xiaoxia Yang
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