Biocell最新文献

{"title":"Inhibition of proliferation, migration, and invasiveness of bladder cancer cells through SAPCD2 knockdown","authors":"Chong Shen, Jiajun Yan, Yu Ren, ZHIRONG ZHU, Xiaolong Zhang, SHUIXIANG TAO","doi":"10.32604/biocell.2023.045303","DOIUrl":"https://doi.org/10.32604/biocell.2023.045303","url":null,"abstract":"Introduction: Bladder cancer (BC) has a high incidence and mortality rate worldwide. Suppressor anaphase-promoting complex domain containing 2 (SAPCDC2) is over-expressed in a variety of tumors. Objectives: This study investigated the effects of SAPCD2 knockdown on BC cells. Methods: T24 and UMUC3 cell models and the xenografted BC tumor model with SAPCD2 knockdown were established to observe the malignant phenotype of BC cells by cell counting kit-8 assay, colony formation test, wound healing, and Transwell assay, mRNA and proteins expressions were measured with quantitative real-time polymerase chain reaction, western blotting, and tissue immunohistochemistry. Lithium chloride agonist on the Wnt/β-catenin pathway was used to clarify the molecular mechanism of SAPCD2 knockdown. Results: SAPCD2 expression was significantly higher in BC cell lines than in SV-HUC-1 cells. SAPCD2 knockdown inhibited viability and cloning, hindered the G0/G1 phase of the cell cycle in UMUC3 and T24 cells, and decreased the migration and invasiveness of BC cells. SAPCD2 knockdown inhibited expression levels of cyclin D1, cyclin B1, N-cadherin, vimentin, Snail, β-catenin, c-Myc, and cyclin-dependent kinase 4, while the P21 and E-cadherin were raised by SAPCD2 knockdown. Furthermore, lithium chloride reversed the effects of SAPCD2 knockdown on the expression levels of the above proteins in UMUC3 and T24 cells. In vivo, SAPCD2 knockdown inhibited the volume, weight, and expression of Ki-67 and β-catenin in tumors and increased the E-cadherin expression. Conclusion: SAPCD2 knockdown inhibits the malignant phenotype of BC via a pathway involving β-catenin.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 1","pages":"97-109"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19705/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910295","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>DAPK2</i> promotes autophagy to accelerate the progression of ossification of the posterior longitudinal ligament through the <i>mTORC1</i> complex","authors":"Lei Shi, JIANSHI YIN, Yú Chen, Jiangang Shi, Jinhao Miao","doi":"10.32604/biocell.2024.049562","DOIUrl":"https://doi.org/10.32604/biocell.2024.049562","url":null,"abstract":"Background: Ossification of the posterior longitudinal ligament (OPLL) is a prevalent condition in orthopedics. While death-associated protein kinase 2 (DAPK2) is known to play roles in cellular apoptosis and autophagy, its ... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 9","pages":"1389-1400"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911249","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":"Silvestrol alleviates glioblastoma progression through ERK pathway modulation and MANBA and NRG-1 expression","authors":"Lan Zhou, Qi Zhang, Bo Tian, Feng Yang","doi":"10.32604/biocell.2024.049878","DOIUrl":"https://doi.org/10.32604/biocell.2024.049878","url":null,"abstract":"Background: Glioblastoma, a notably malignant tumor within the central nervous system, is distinguished by its aggressive behavior. Silvestrol, a robust inhibitor of the RNA helicase eukaryotic initiation factor 4A (eIF4A), has shown significant potential as an anticancer compound. Yet, the impact of silvestrol on glioblastoma, especially its molecular mechanisms, has not been fully elucidated. Methods: This investigation employed a variety of in vitro assays, such as cell counting kit-8 (CCK-8), clonogenic, 5-ethynyl-2′-deoxyuridine (EDU), wound healing, and flow cytometry, to evaluate cell cycle progression, apoptosis, cell viability, and migration. Western blot analysis was also performed to study the apoptosis and extracellular regulated kinase (ERK) pathways. After the ERK pathway was inhibited, differentially expressed genes (DEGs) in U87 cells were identified, followed by an analysis of target genes using the gene expression profiling interactive analysis (GEPIA) database. Results: Silvestrol significantly suppressed the proliferation, migration, and colony formation of glioma cells. It caused cell cycle arrest and enhanced apoptosis in these cells. Additionally, silvestrol stimulated the ERK pathway, with these effects being reversible by an ERK phosphorylation inhibitor. Transcriptome combined with GEPIA, GSCA, UALCAN, TIMER database screened 4 potential drug targets of silvestrol: chromosome 1 open reading frame 226 (C1ORF226), mannosidase beta A (MANBA), IQ motif and Sec7 domain 2 (IQSEC2), neuregulin 1 (NRG-1). Among them, C1ORF226 was lower risk gene while MANBA, IQSEC2, and NRG-1 were high-risk genes. Furthermore, silvestrol notably reduced MANBA mRNA levels, which could be reversed by inhibiting ERK phosphorylation. Furthermore, silvestrol markedly decreased NRG-1 protein levels, with an additional reduction observed when the ERK pathway was blocked. Conclusion: Silvestrol’s anti-glioma effects are primarily due to the suppression of MANBA expression via the ERK pathway and possibly by hindering the translation of NRG-1 protein, thus reducing its expression. The downregulation of MANBA and NRG-1 proteins may be crucial in hindering glioma development and progression. These results highlight the intricate relationship between the ERK pathway and gene expression regulation in silvestrol’s therapeutic effectiveness against glioma.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 7","pages":"1081-1093"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20735/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916654","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":"Chemokine-like factor 1 (CKLF1) is expressed in myocardial ischemia injury <i>in vivo</i> and <i>in vitro</i>","authors":"JULING FENG, H. Chen, YANGBO LIU, Qidi Ai, YANTAO YANG, Lei Zhao, Shifeng Chu, NAIHONG CHEN","doi":"10.32604/biocell.2024.050011","DOIUrl":"https://doi.org/10.32604/biocell.2024.050011","url":null,"abstract":"Introduction: Chemokine-like factor 1 (CKLF1) is a chemokine that is overexpressed in several diseases. Our previous findings revealed a significant increase in CKLF1 expression in the ischemic brain, suggesting its potential as a therapeutic target for ischemic stroke. Methods: In this study, we examined the expression dynamics of CKLF1 in both in vivo and in vitro models of ischemic cardiac injury. Myocardial infarction (MI) was induced in vivo by ligation of the left anterior descending artery (LAD) of the rat heart. The levels of CKLF1, Creatine Kinase MB Isoenzyme (CK-MB), and Lactate dehydrogenase (LDH) in the serum were detected using Enzyme-linked immunosorbent assay (ELISA). The expression of CKLF1 in the infarcted area was detected by immunohistochemistry, immunofluorescence, quantitative PCR (qPCR), and Western blotting (WB). H9C2 and AC16 cardiomyocytes cultured in vitro were subjected to oxygen and glucose deprivation (OGD). LDH was used to detect cell damage, and CKLF1 expression was detected by qPCR and WB. Results: CKLF1 mRNA and protein expression were significantly increased in h9c2 cells at 1.5 h and in AC16 cells at 4 h after OGD. The serum CK-MB in rats increased significantly on the first day after infarction, while the LDH concentration increased significantly on the third day after infarction. CKLF1 blood levels significantly increased on the first day following MI in rats. CKLF1 expression notably increased in the infarct area on days 1, 3, and 7 post-MI. In MI tissue, CKLF1 colocalizes with cardiomyocytes, macrophages, and neutrophils. Conclusion: CKLF1 was substantially expressed during myocardial ischemia injury both in vivo and in vitro and was colocalized with macrophages and neutrophils, indicating that CKLF1 is expected to be a biomarker and a drug target for the treatment of myocardial infarction.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 6","pages":"981-990"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20690/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147918501","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>SENEX</i>-mediated CDK4/6 inhibition promotes senescence and confers apoptosis resistance in B-cell non-Hodgkin lymphoma","authors":"JIYU WANG, Liuying Yi, KEKE HUANG, Yangyang Wang, HUIPING WANG, Zhimin Zhai","doi":"10.32604/biocell.2024.047871","DOIUrl":"https://doi.org/10.32604/biocell.2024.047871","url":null,"abstract":"Background: The primary cause of treatment failure in patients with refractory or relapsed B-cell non-Hodgkin lymphoma (r/r B-NHL) is resistance to current therapies, and therapy-induced senescence (TIS) stands out as a crucial mechanism contributing to tumor drug resistance. Here, we analyzed SENEX/Rho GTPase Activating Protein 18 (ARHGAP18) expression and prognostic significance in doxorubicin-induced B-NHL-TIS model and r/r B-NHL patients, investigating its target in B-NHL cell senescence and the effect of combining specific inhibitors on apoptosis resistance in B-NHL-TIS cells. Methods: Raji cells were transfected with the human SENEX shRNA recombinant lentiviral vector (Sh-SENEX) and the empty vector negative (NC) to construct a stable transfection cell line with knockdown of SENEX. Effect of SENEX-silencing on B-NHL-TIS formation, cell function and cell cycle-related pathways was analyzed. Using doxorubicin (DOX)-inducible senescent B-NHL cells combined with the specific cyclin dependent kinase 4/6 (CDK4/6) inhibitor Palbociclib to observe that blocking CDK4/6 effects on TIS formation. SENEX expression of 21 B-NHL patients and 8 healthy controls were analyzed by qRT-PCR, and the correlation between its expression and clinical indicators were evaluated. Results: The downregulation of SENEX expression promotes G1-S phase transition and apoptosis while inhibiting cell proliferation, collectively suppressing the formation of TIS in B-NHL. Blockade of CDK4/6 promotes the DOX-induced G1 phase arrest to enhance TIS formation in B-NHL cells which can reverse the regulatory effect of silencing SENEX on B-NHL cell cycle regulation and senescence. The expression levels of SENEX were notably elevated in B-NHL patients compared to healthy controls, and Elevated expression levels of SENEX were associated with poor prognosis of B-NHL patients. Conclusion: SENEX enhances apoptosis resistance in B-NHL by inhibiting CDK4/6, thereby preventing G1-S phase transition and promoting TIS formation.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 3","pages":"453-462"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19976/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147891179","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":"MAD2L2 overexpression attenuates the effects of TNF-α-induced migration and invasion capabilities in colorectal cancer cells","authors":"Haotong Sun, HEYING WANG, YANJIE HAO, Xin Li, JUN LING, Huan Wang, FEIMIAO WANG, Fang Xu","doi":"10.32604/biocell.2024.052451","DOIUrl":"https://doi.org/10.32604/biocell.2024.052451","url":null,"abstract":"Background: Colorectal cancer is a major global health concern, exacerbated by tumor necrosis factor-alpha(TNF-α) and its role in inflammation, with the effects of Mitotic Arrest Deficient 2 Like 2 (MAD2L2) in this context still unclear. Methods: The colorectal carcinoma cell lines HCT116 and SW620 were exposed to TNF-α for a period of 24 h to instigate an inflammatory response. Subsequent assessments were conducted to measure the expression of inflammatory cytokines, the activity within the p38 mitogen-activated protein kinase (p38 MAPK) and Phosphoinositide 3-Kinase/AKT Serine/Threonine Kinase pathway (PI3K/AKT) signaling cascades. Transcriptome sequencing and subsequent integrative analysis with the Cancer Genome Atlas (TCGA) program database revealed a significant downregulation of the key factor MAD2L2. Enhancement of MAD2L2 expression was facilitated via lentiviral vector-mediated transfection. The influence of this overexpression on TNF-α-prompted inflammation, intracellular signaling pathways, and the migratory and invasive behaviors of the colorectal cancer cells was then scrutinized. Results: TNF-α treatment significantly increased the expression of Interleukin-1 beta (IL-1β) and Interleukin-6 (IL-6), activated the MAPK p38 and PI3K/AKT signaling pathways, and enhanced cell migration and invasion. A decrease in MAD2L2 expression was observed following TNF-α treatment. However, overexpression of MAD2L2 reversed the effects of TNF-α, reducing IL-1β and IL-6 levels, attenuating PI3K/AKT pathway activation, and inhibiting cell migration and invasion. Conclusions: Overexpression of MAD2L2 attenuates the pro-inflammatory effects of TNF-α, suggesting that MAD2L2 plays a protective role against TNF-α-induced migration and invasion of colorectal carcinoma cells. Therefore, MAD2L2 holds potential as a therapeutic target in the treatment of colorectal cancer.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 9","pages":"1311-1322"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147877634","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":"Lysine demethylase 5B transcriptionally regulates TREM1 in human cardiac fibroblasts","authors":"CHUNLING LIANG, Jing Chen, XIAOJIE CHEN, Wei Yan, Jie Yu","doi":"10.32604/biocell.2024.050509","DOIUrl":"https://doi.org/10.32604/biocell.2024.050509","url":null,"abstract":"Background: A differential gene, triggering receptor expressed on myeloid cells 1 (TREM1), was identified in blood sequencing datasets from myocardial infarction patients and healthy controls. Myocardial fibrosis following myocardial infarction significantly contributes to cardiac dysfunction. Objectives: This study aimed to unveil the intrinsic regulatory mechanism of TREM1 in myocardial fibrosis. Methods: Mimicking pathology by angiotensin II (Ang II) treatment of human cardiac fibroblasts (HCFs), the impacts of TREM1 knockdown on its proliferation, migration, and secretion of the pro-fibrotic matrix were identified. Using the Human Transcription Factor Database (HumanTFDB) website, lysine-specific demethylase 5B (KDM5B) was found to bind to the TREM1 promoter, which was further validated through luciferase reporter and chromatin immunoprecipitation (ChIP). By promoting KDM5B overexpression, its effect on the regulation of TREM1 was examined. Results: TREM1 knockdown suppressed the proliferation, migration, and secretion of the pro-fibrotic matrix in HCFs upon Ang II treatment. KDM5B bound to the TREM1 promoter and upregulated its transcriptional expression. Furthermore, KDM5B overexpression reversed the regulation of the above cellular phenotypes by TREM1 knockdown. Conclusion: This study sheds light on the positive regulation of TREM1 by KDM5B, demonstrating their role in promoting myocardial fibrosis. This finding provides a theoretical foundation for understanding disease pathology and potentially advancing the development of new targeted therapies.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 7","pages":"1105-1113"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20719/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905217","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":"Analysis of large datasets for identifying molecular targets in intestinal polyps and metabolic disorders","authors":"S.-H.I. Ou, Yun Xu, QINGLAN LIU, TIANWEN YANG, Wei Chen, XIU YUAN, Xin Zuo, Peng Shi, JIE YAO","doi":"10.32604/biocell.2024.046178","DOIUrl":"https://doi.org/10.32604/biocell.2024.046178","url":null,"abstract":"Background: The interrelation between intestinal polyps, metabolic syndrome (MetS), and colorectal cancer (CRC) is a critical area of study. This research focuses on pinpointing potential molecular targets to understand the link between intestinal polyp formation, metabolic irregularities, and CRC progression. Methods: We examined clinical samples from patients with intestinal polyps coexisting with MetS and compared them with samples from patients with standard intestinal polyps. Transcriptome sequencing and public database analysis were employed to identify significant pathways and genes. These targets were then validated through immunohistochemistry (IHC). Following the RNA interference of key target expression, a series of experiments, including the cell counting kit-8 assay, colony formation, wound healing, and Transwell assays, were conducted. Results: Comparative analysis revealed 75 up-regulated and 61 down-regulated differentially expressed genes (DEGs) in the MetS polyp group vs. the control. Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment suggested these DEGs were primarily associated with cell cycle and mitosis. Integration with comparative toxicogenomics database (CTD) and the cancer genome atlas (TCGA) databases highlighted 44 key CRC-related genes. Protein interaction networks indicated connections of purkinje cell protein 4 (PCP4), olfactomedin 1 (OLFM1), fibronectin 1 (FN1), and transforming growth factor beta 3 (TGF-β3) with the mitogen-activated protein kinase (MAPK) pathway. Tumor correlation studies suggested higher risk associations with FN1, PCP4, and TGF-β3, while OLFM1 was identified as a lower risk gene. Immunohistochemical analysis revealed a decrease in OLFM1 in MetS-associated intestinal polyps. Upon interference with OLFM1 in polyp epithelial cells, there was a significant enhancement in cell proliferation, colony formation, and cell migration and invasion capabilities. Conclusion: Our study highlights a significant decrease in OLFM1 expression in MetS-associated intestinal polyps. And, this reduction in OLFM1 is associated with enhanced cell proliferation, colony formation, and increased cell migration and invasion capabilities. These findings underscore the reduced OLFM1 expression in MetS-associated intestinal polyps may play a crucial role in promoting tumorigenic processes in colorectal pathology. Further research on OLFM1 may provide valuable insights into understanding and targeting MetS-associated intestinal polyps.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 3","pages":"415-429"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19975/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905311","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":"BTG2 interference ameliorates high glucose-caused oxidative stress, cell apoptosis, and lipid deposition in HK-2 cells","authors":"Wenjuan Zhu, Zhengzheng Ju, Fan Cui","doi":"10.32604/biocell.2024.052205","DOIUrl":"https://doi.org/10.32604/biocell.2024.052205","url":null,"abstract":"Objective: Diabetic nephropathy (DN) is a deleterious microangiopathy of diabetes, constituting a critical determinant of fatality in diabetic patients. This work is purposed to disclose the effects and modulatory mechanism of BTG anti-proliferation factor 2 (BTG2) during the pathological process of DN. Methods: BTG2 expression in kidney tissues of diabetic mice and high glucose (HG)-exposed human proximal tubular cell line HK-2 was assessed with Western blot and RT-qPCR. The diabetic mice model was constructed by streptozotocin injection and confirmed by the blood glucose level beyond 16.7 mmol/L. Hematoxylin and eosin (H&E) staining and measurement of kidney function hallmarks were conducted to assess kidney injury. Cell counting kit (CCK)-8 method and TUNEL assay appraised cell activity and apoptosis. Oil red O staining assayed lipid accumulation. Relevant commercial kits were used to estimate oxidative stress-related factors. Co-immunoprecipitation (Co-IP) assay testified the binding relationship of BTG2 with protein arginine methyltransferase 1 (PRMT1). Results: BTG2 expression was significantly raised in renal tissues of diabetic mice and HK-2 cells exposed to HG. BTG2 deficiency improved viability and extenuated the apoptosis, lipid deposition as well as oxidative stress in HK-2 cells following HG exposure. In addition, PRMT1 was also overexpressed in HK-2 cells exposed to HG. BTG2 interacted with PRMT1 and positively modulated PRMT1 expression. The effects of BTG2 interference on viability, apoptosis, lipid deposition, and oxidative stress in HG-challenged HK-2 cells were partially abrogated by PRMT1 overexpression. Conclusion: Altogether, BTG2 might aggravate HK-2 cell injury in response to HG by binding with PRMT1, providing a novel target for the therapeutic strategy of DN.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 9","pages":"1379-1388"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/21222/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910799","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":"Revealing the role of honokiol in human glioma cells by RNA-seq analysis","authors":"Yunbao Guo, Xu Liu, Qi Xu, XIAOTONG ZHOU, Jiawei Liu, YANYAN XU, Yan Lü, HAIYAN LIU","doi":"10.32604/biocell.2024.049748","DOIUrl":"https://doi.org/10.32604/biocell.2024.049748","url":null,"abstract":"Background: Glioma is a kind of tumor that easily deteriorates and originates from glial cells in nerve tissue. Honokiol is a bisphenol compound that is an essential monomeric compound extracted from the roots and bark of Ma... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 6","pages":"945-958"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147897203","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}