Biocell最新文献

{"title":"Ganoderic acid A ameliorates renal fibrosis by suppressing the expression of <i>NPC1L1</i>","authors":"T. Han, Zhong Li, LUONING ZHANG, Linshen Xie","doi":"10.32604/biocell.2024.055029","DOIUrl":"https://doi.org/10.32604/biocell.2024.055029","url":null,"abstract":"Objective: The study aimed to explore the protective mechanism of Ganoderic acid A (GAA) in renal fibrosis and to verify that GAA can ameliorate renal fibrosis by regulating the Niemann-pick C1-like 1 (NPC1L1) gene. Methods:... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 11","pages":"1625-1638"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://cdn.techscience.press/files/biocell/2024/TSP_BIOCELL-48-11/Biocell-48-11-55029/Biocell-48-55029.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147912716","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":"<i>Bhlhe40</i> protects cochlear hair cell-like HEI-OC1 cells against HO‑triggered oxidative injury","authors":"Liting Wen, XIAOXIA ZENG, P. Chen, DAPENG ZHAO, Y Li, XIANHAI ZENG","doi":"10.32604/biocell.2024.050219","DOIUrl":"https://doi.org/10.32604/biocell.2024.050219","url":null,"abstract":"Background: Cochlear hair cell injury is a common pathological feature of hearing loss. The basic helix-loop-helix family, member e40 (Bhlhe40), a gene belonging to the basic helix-loop-helix (bHLH) family, exhibits strong transcriptional repression activity. Methods: Oxidative damage, in House Ear Institute-Organ of Corti 1 (HEI‑OC1) cells, was caused using hydrogen peroxide (HO). The Ad-Bhlhe40 particles were constructed to overexpress Bhlhe40 in HEI-OC1 cells. Various assays including cell counting kit-8 (CCK-8), terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay (TUNEL), flow cytometry, immunofluorescence, and corresponding commercial kits were employed to investigate the impacts of Bhlhe40 on cell viability, apoptosis, oxidative stress levels, mitochondrial membrane potential and cellular senescence. Additionally, a dual-luciferase reporter assay was performed to confirm the targeting of the histone deacetylases 2 (Hdac2) by Bhlhe40. Results: The results revealed that Bhlhe40 was downregulated in HO‑treated HEI‑OC1 cells, but its overexpression improved cell viability and mitigated HO‑induced oxidative injury in HEI‑OC1 cells with increase of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities and decrease of reactive oxygen species (ROS) levels. Besides, overexpression of Bhlhe40 suppressed HO‑triggered cell senescence, as evidenced by the fact that the upregulation of P53, P21, and P16 in HEI-OC1 cells treated with HO were all alleviated by Bhlhe40 overexpression. And we further verified that overexpression of Bhlhe40 could inhibit the expression of Hdac2, which may be related to the repression of Hdac2 transcription. Conclusion: This study suggests that Bhlhe40 plays a protective role against senescence and oxidative damage in cochlear hair cells exposed to HO.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 6","pages":"991-999"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20497/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892711","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":"Knockdown of circular RNA (CircRNA)_001896 inhibits cervical cancer proliferation and stemness <i>in vivo</i> and <i>in vitro</i>","authors":"Jia Shao, CAN ZHANG, YAONAN TANG, AIQIN HE, WEIPEI ZHU","doi":"10.32604/biocell.2024.049092","DOIUrl":"https://doi.org/10.32604/biocell.2024.049092","url":null,"abstract":"Objective:: Previous studies indicated that aberrant circular RNA (circRNA) expression affects gene expression regulatory networks, leading to the aberrant activation of tumor pathways and promoting tumor cell growth. However, the expression, clinical significance, and effects on cell propagation, invasion, and dissemination of circRNA_001896 in cervical cancer (CC) tissues remain unclear. Methods:: The Gene Expression Omnibus (GEO) datasets (GSE113696 and GSE102686) were used to examine differential circRNA expression in CC and adjacent tissues. The expression of circRNA_001896 was detected in 72 CC patients using fluorescence quantitative PCR. Correlation analysis with clinical pathological features was performed through COX multivariate and univariate analysis. The effect of circRNA_001896 downregulation on CC cell propagation was examined using the cell counting kit-8 (CCK-8) test, clonogenic, 3D sphere formation, and in vivo tumorigenesis assays. Results:: Intersection of the GSE113696 and GSE102686 datasets revealed an increased expression of four circRNAs, including circRNA_001896, in CC tissues. Fluorescence quantitative PCR confirmed circRNA_001896 as a circular RNA. High expression of circRNA_001896 was considerably associated with lymph node metastasis, International Federation of Gynecologists and Obstetricians (FIGO) stage, tumor diameter, and survival period in CC patients. Proportional hazards model (COX) univariate and multivariate analyses revealed that circRNA_001896 expressions are a distinct risk factor affecting CC patients’ prognosis. Cellular functional experiments showed that downregulating circRNA_001896 substantially suppressed CC cell growth, colony formation, and 3D sphere-forming ability. In vivo, tumorigenesis analysis in nude mice demonstrated that downregulating circRNA_001896 remarkably reduced the in vivo proliferation capacity of CC cells. Conclusion:: CircRNA_001896 is highly expressed in CC tissues and is substantially related to lymph node metastasis, FIGO stage, tumor size, and survival period in patients. Moreover, downregulating circRNA_001896 significantly inhibits both in vivo and in vitro propagation of CC cells. Therefore, circRNA_001896 might be used as a biomarker for targeted therapy in cervical cancer.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 4","pages":"571-580"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20241/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147896841","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":"Quercetin regulates depression-like behavior in CUMS rat models via TLR4/NF-κB signaling","authors":"Yuanyuan Li, BITAO ZHANG, ZILONG CUI, PEIJIAN FAN, SHAOXIAN WANG","doi":"10.32604/biocell.2024.048820","DOIUrl":"https://doi.org/10.32604/biocell.2024.048820","url":null,"abstract":"Background: Depression is becoming increasingly prevalent around the world, imposing a substantial burden on individuals, families, as well as society. Quercetin is known to be highly effective in treating depression. However, additional research is needed to dissect the mechanisms of its anti-depressive effects. Methods: For this study, Sprague-Dawley (SD) rats were randomized into the control, model, quercetin, or fluoxetine group. The latter three groups were exposed to chronic unpredictable mild stress (CUMS) for 42 d. The first two groups received saline solution daily via oral gavage. Meanwhile, the quercetin group was orally administered a quercetin suspension (52.08 mg/kg) every day, while the fluoxetine group was orally administered a fluoxetine solution (2.08 mg/kg). Here, fluoxetine served as the positive control drug to compare the therapeutic effects of quercetin. The experimental period was 6 weeks. Depressive behaviors in rats were assessed through various physiological and behavioral measures. Additionally, pathological changes in hippocampal tissues were examined using Nissl staining. Serum cytokines were detected using an enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry was employed to quantify the levels and integral optical density (IOD) values of ionized calcium binding adaptor molecule-1 (Iba-1) expression in the brain. Real-time fluorescence quantitative PCR (RT-qPCR) was utilized to evaluate the mRNA levels of inflammatory indicators as well as toll-like receptor 4 (TLR4), and nuclear factor-κappa B P65 (NF-κB P65) in hippocampus. Western blot (WB) technique was employed to observe the protein levels of TLR4, NF-κB P65, and phospho-NF-κB P65 (p-NF-κB P65). Results: After 42 d of exposure to CUMS, rats exhibited a slow increase in body weight, a reduction in food intake, an abnormal preference for sugar water, and aberrant open-field behaviors. Pathological analysis revealed the disintegration, rupture, interruption, and disorganization of hippocampal neuronal cells after CUMS exposure, along with a decrease in Nissl bodies in the CA1 region. This was accompanied by the elevated expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in the serum and the upregulation of IL-1β, IL-6, and TNF-α mRNA expression in the hippocampus. Increases in Iba-1-positive cells and the IOD values of Iba-1 were detected in hippocampal microglia. Furthermore, TLR4 and NF-κB P65 mRNA and protein levels were upregulated in hippocampal tissues. Quercetin, an antidepressant, could alleviate depression-like symptoms in rats and downregulate inflammatory factors associated with the TLR4/NF-κB signaling pathway in hippocampal microglia, and its therapeutic effect was comparable to fluoxetine. Conclusion: In rat models of CUMS, quercetin may act as an antidepressant by inhibiting inflammation in hippocampal microglia via TLR4/NF-κB signaling pathway. These results offer experimental and theor","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 5","pages":"731-744"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20435/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905894","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":"Inhibition of SLC26A4 regulated by electroacupuncture suppresses the progression of myocardial ischemia-reperfusion injury","authors":"Fei Kong, QIYUAN TIAN, Bin Kuang, LILI SHANG, XIAOXIAO ZHANG, Dongyang Li, YING KONG","doi":"10.32604/biocell.2024.046342","DOIUrl":"https://doi.org/10.32604/biocell.2024.046342","url":null,"abstract":"Introduction: Myocardial ischemia-reperfusion (IR) injury has received widespread attention due to its damaging effects. Electroacupuncture (EA) pretreatment has preventive effects on myocardial IR injury. SLC26A4 is a Na+ independent anion reverse transporter and has not been reported in myocardial IR injury. Objectives: To find potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury. Methods: RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment. Myocardial infarction size was detected by TTC staining. Serum CK, creatinine kinase-myocardial band, Cardiac troponin I, and lactate dehydrogenase levels were determined by ELISA. The effect of SLC26A4 on cardiomyocyte apoptosis was explored by TUNEL staining and western blotting. The effects of SLC26A4 on inflammation were determined by HE staining, ELISA, and real-time PCR. The effect of SLC26A4 on the NF-κB pathway was determined by western blotting. Results: SLC26A4 was up-regulated in IR rats but downregulated in IR rats with EA pretreatment. Compared with IR rats, those with SLC26A4 knockdown exhibited improved cardiac function according to decreased myocardial infarction size, reduced serum LDH/CK/CK-MB/cTnI levels, and elevated left ventricular ejection fraction and fractional shortening. SLC26A4 silencing inhibited myocardial inflammation, cell apoptosis, phosphorylation, and nuclear translocation of NF-κB p65. Conclusion: SLC26A4 exhibited promoting effects on myocardial IR injury, while the SLC26A4 knockdown had an inhibitory effect on the NF-κB pathway. These results further unveil the role of SLC26A4 in IR injury.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 4","pages":"665-675"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20120/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910251","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":"<i>In vitro</i> engineered models of neurodegenerative diseases","authors":"Zehra Gül Morçimen, Şeyma Taşdemir, Aylin Şendemir","doi":"10.32604/biocell.2023.045361","DOIUrl":"https://doi.org/10.32604/biocell.2023.045361","url":null,"abstract":"Neurodegeneration is a catastrophic process that develops progressive damage leading to functional and structural loss of the cells of the nervous system and is among the biggest unavoidable problems of our age. Animal models do not reflect the pathophysiology observed in humans due to distinct differences between the neural pathways, gene expression patterns, neuronal plasticity, and other disease-related mechanisms in animals and humans. Classical in vitro cell culture models are also not sufficient for pre-clinical drug testing in reflecting the complex pathophysiology of neurodegenerative diseases. Today, modern, engineered techniques are applied to develop multicellular, intricate in vitro models and to create the closest microenvironment simulating biological, biochemical, and mechanical characteristics of the in vivo degenerating tissue. In THIS review, the capabilities and shortcomings of scaffold-based and scaffold-free techniques, organoids, and microfluidic models that best reflect neurodegeneration in vitro in the biomimetic framework are discussed.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 1","pages":"79-96"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19707/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910560","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":"Mesenchymal stromal cells modulate unfolded protein response and preserve β-cell mass in type 1 diabetes","authors":"SIYUAN LIU, YUAN ZHAO, yu yu, Dou Ye, QIAN WANG, ZHAOYAN WANG, ZUO LUAN","doi":"10.32604/biocell.2024.050493","DOIUrl":"https://doi.org/10.32604/biocell.2024.050493","url":null,"abstract":"Introduction: Transplantation of mesenchymal stromal cells (MSCs) is a promising therapy for type 1 diabetes (T1D). However, whether the infused MSCs affect the endoplasmic reticulum stress or subsequent unfolded protein response in β cells remains unclear. Methods: To investigate this, we induced early-onset T1D in non-obese diabetic mice using streptozotocin. Subsequently, T1D mice were randomly assigned to receive either MSCs or phosphate-buffered saline. We observed the in vivo homing of MSCs and assessed their effectiveness by analyzing blood glucose levels, body weight, histopathology, pancreatic protein expression, and serum levels of cytokines, proinsulin, and C-peptide. Results: Infused MSCs were found in the lungs, liver, spleen, and pancreas of T1D mice. They exhibited various effects, including reducing blood glucose levels, regulating immunity, inhibiting inflammation, increasing β-cell areas, and reducing the expression of key proteins in the unfolded protein response pathway. Fasting serum proinsulin and C-peptide levels were significantly higher in the MSCs treatment group than in the T1D model group. However, there was no significant difference in the biomarker of β-cell endoplasmic reticulum stress, the ratio of fasting serum proinsulin to C-peptide, between the two groups. Conclusion: Our findings reveal that MSCs infusion does not alleviate endoplasmic reticulum stress in β cells directly but modulates the unfolded protein response pathway to preserve β-cell mass and function in T1D mice.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 7","pages":"1115-1126"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20718/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911638","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":"CMTM6 deletion affects chemoresistance and macrophage M2 polarization in colorectal cancer cells","authors":"Xu Yang, HONGYUN LI, GE YOU","doi":"10.32604/biocell.2023.045030","DOIUrl":"https://doi.org/10.32604/biocell.2023.045030","url":null,"abstract":"Background: Colorectal cancer (CRC) constitutes the leading cause of death worldwide. Chemoresistance and tumor immune evasion are critical contributors to therapeutic failure in cancer patients. CKLF-like MARVEL transmembrane domain-containing 6 (CMTM6) is aberrantly expressed in various cancers and can regulate tumor immunity. However, its role in chemoresistance and tumor immunity of CRC is not well understood. Methods: Online bioinformatics tools were used to analyze expression and prognosis of CMTM6 in CRC patients. CRC cells were transfected with si-CMTM6. Subsequently, the effects on CRC cell viability and chemoresistance were investigated by CCK-8 assay and flow cytometer. Furthermore, CRC cell-induced macrophage recruitments and polarization were also explored. Results: High expression of CMTM6 was detected in CRC tissues and cells, and its expression was associated with the prognosis of patients with CRC. Notably, CMTM6 knockdown suppressed cancer cell viability. Moreover, CMTM6 loss enhanced cancer cell sensitivity to 5-FU by reducing cell viability and enhancing apoptosis and activity of caspase-3. Importantly, CMTM6 loss inhibited CRC cells-evoked macrophage recruitments and polarization towards M2 phenotype by increasing the ratio of CD206+ cells and expression of M2 macrophage markers (arginase1, IL-10, CD206 and TGF-β). Intriguingly, targeting CMTM6 activated the AMPK singling and suppressed the subsequent activation of the NF-κB pathway. Blockage of the AMPK signaling reversed the suppressive efficacy of CMTM6 loss in 5-FU resistance and cancer cells-evoked macrophage M2-like polarization. Conclusion: CMTM6 may affect the progression of CRC by regulating chemoresistance and macrophage-related immune evasion, implying a promising target to overcome chemoresistance and immune escape in the treatment of CRC.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 2","pages":"229-237"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19894/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914515","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":"E3 ubiquitin ligase CBL-B suppresses vascular endothelial cell pyroptosis and injury in intracranial aneurysm by facilitating NLRP3 degradation","authors":"Wei Zheng, Cheng Liu","doi":"10.32604/biocell.2023.044211","DOIUrl":"https://doi.org/10.32604/biocell.2023.044211","url":null,"abstract":"Objective: Intracranial aneurysm (IA) represents a devastating disease with high rates of disability and mortality, which is initiated by dysfunction of endothelial cells (ECs). Evidence suggests the dysregulation of the E3 ubiquitin ligase family during EC injury. In this work, the role of an E3 ubiquitin ligase, casitas B lymphoma-B (CBL-B), was explored in human brain microvascular EC (HBMEC) function through the NLRP3 pathway. Methods: In vitro IA model was induced by treating HBMECs with oxidized low-density lipoprotein (ox-LDL). The levels of CBL-B and pyroptosis-related proteins NLRP3, ASC, cleaved caspase-1, and GSDME-N were determined by real-time-quantitative polymerase chain reaction and western blotting. HBMEC apoptosis, proliferation, and migration were evaluated by flow cytometry, MTT, and scratch tests. An enzyme-linked immunosorbent assay was conducted to measure interleukin (IL)-1β and IL-18 levels in cell culture supernatant. The ubiquitination of NLRP3 was detected by co-immunoprecipitation. Results: NLRP3 was highly expressed while CBL-B was weakly expressed in ox-LDL-treated HBMECs. Cell apoptosis was enhanced, proliferation and migration were weakened, NLRP3 inflammasome was activated, and levels of gasdermin E-N, IL-1β, and IL-18 were increased in ox-LDL-induced HBMECs. The above tendencies were counteracted by NLRP3 knockdown or CBL-B overexpression. Additionally, CBL-B overexpression increased NLRP3 ubiquitination, suggesting that CBL-B hampered the activation of NLRP3 inflammasome by ubiquitinating NLRP3. Conclusion: E3 ubiquitin ligase CBL-B accelerates NLRP3 degradation to impede HBMEC pyroptosis, thus palliating vascular EC injury in IA.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 2","pages":"293-301"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19893/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147919624","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":"Valtrate exerts anticancer effects on gastric cancer AGS cells by regulating reactive oxygen species-mediated signaling pathways","authors":"JINGLONG CAO, Shumei Li, TONG ZHANG, Jian Liu, WENSHUANG HOU, ANQI WANG, CHANG WANG, Cheng‐Hao Jin","doi":"10.32604/biocell.2023.043474","DOIUrl":"https://doi.org/10.32604/biocell.2023.043474","url":null,"abstract":"Background: Valtrate (Val) was extracted from the Valeriana jatamansi Jones plant, had good antitumor activity. However, its precise molecular mechanism in cancer cells was still unclear. This study investigated the effect of Val on gastric cancer (GC) cells and its potential molecular mechanism. Methods: Cell viability was examined by CCK-8 assay. Cell cycle, apoptosis, and Reactive oxygen species (ROS) level were analyzed by flow cytometry. The migration effect of Val on AGS cells was analyzed by transwell and wound-healing assay. The expression levels of proteins were analyzed by western blot. Results: The cell viability assay results demonstrated that Val significantly decreased GC cell viability. Apoptosis assay results revealed that Val induced mitochondria-dependent apoptosis through the Bad/Bcl-2/cyto-c/cle-casp-3/cle-PARP pathways. Further exploration found that Val induced apoptosis through increasing the expression of phosphorylated p38 mitogen-activated protein kinase (p-p38), phosphorylated c-Jun N-terminal kinase (p-JNK), and Inhibitor kappa B alpha (IκB-α) proteins and decreasing the expression of phosphorylated extracellular signal-regulated kinase (p-ERK), phosphorylated signal transducer and activator of transcription 3 (p-STAT3), and nuclear factor kappa-B (NF-κB) proteins; these expression levels of proteins were reversed by mitogen-activated protein kinase (MAPK) inhibitor. Furthermore, Val induced G2/M phase arrest in AGS cells through downregulating the expression of phosphorylated protein kinase B (p-AKT). Moreover, Val induced inhibition of AGS cell migration through downregulating the expression of p-GSK-3β and β-catenin. In addition, Val promoted the ROS accumulation of AGS cells. Further investigation found that Val-induced apoptosis, arrested the cell cycle, and inhibited cell migration, and that its signaling pathways related to protein expressions were reversed by the ROS scavenger, N-acetyl-L-cysteine. Conclusion: Val induced apoptosis, arrested the cell cycle, and inhibited migration by ROS-mediated MAPK/STAT3/NF-κB, AKT/Cyclin B/CDK1/2, and GSK-3β/β-catenin signaling pathways in AGS cells.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 2","pages":"313-325"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19913/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147881766","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}