Cell Biochemistry and Biophysics最新文献_第3页

FOXM1, a super enhancer-associated gene, is related to poorer prognosis and gemcitabine resistance in pancreatic cancer. FOXM1是一种超级增强子相关基因，与胰腺癌预后不良和吉西他滨耐药有关。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-02-03 DOI: 10.1007/s12013-024-01653-7

Jian Jiang, Tianci Shen, Dan Chen, Zihao Dai, Xuelong Wang, Qiang Meng, Zhuo Yang, Di Zhang, Xiaoyi Guo, Jianqiang Xu, Jiangning Gu, Changmiao Wang

{"title":"FOXM1, a super enhancer-associated gene, is related to poorer prognosis and gemcitabine resistance in pancreatic cancer.","authors":"Jian Jiang, Tianci Shen, Dan Chen, Zihao Dai, Xuelong Wang, Qiang Meng, Zhuo Yang, Di Zhang, Xiaoyi Guo, Jianqiang Xu, Jiangning Gu, Changmiao Wang","doi":"10.1007/s12013-024-01653-7","DOIUrl":"10.1007/s12013-024-01653-7","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive solid tumor; however, the barrier of chemoresistance has yet to be overcome for longer survival. Aberrant gene expression due to epigenetic modification plays an important role in tumorigenesis and treatment. Super enhancers are epigenetic elements that promote targeted gene transcription and ultimately lead to chemoresistance. This study found that the expression of FOXM1 was higher in PDAC tissues and negatively correlated with prognosis. Through RNA sequencing and chromatin immunoprecipitation-sequencing analyses, FOXM1 was found to be regulated by a BRD4-associated super enhancer, which finally promoted gemcitabine resistance via TGFβ/Smad signaling pathway activation. Both TGFβ/Smad-specific inhibitor LY364947 and the BRD4 inhibitor JQ1 decreased the IC50 value of gemcitabine in vitro. Furthermore, combined gemcitabine and JQ1 therapy could not only enhance the therapeutic effect of gemcitabine but also reverse drug resistance in vivo. In conclusion, the super enhancer-associated gene FOMX1 contributes to gemcitabine resistance and is a promising target in PDAC treatment.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2441-2452"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bioinformatics-based Prognosis Effect of Ferroptosis-related Genes on Gastric Cancer. 基于生物信息学的嗜铁相关基因对胃癌预后的影响。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-02-13 DOI: 10.1007/s12013-024-01634-w

Tao Wang, Aoran Zeng, Lili Zhu, Fengzhi Liu, Bowen Pang, Yan Liu, Zijian Liu, Jing Wang

{"title":"Bioinformatics-based Prognosis Effect of Ferroptosis-related Genes on Gastric Cancer.","authors":"Tao Wang, Aoran Zeng, Lili Zhu, Fengzhi Liu, Bowen Pang, Yan Liu, Zijian Liu, Jing Wang","doi":"10.1007/s12013-024-01634-w","DOIUrl":"10.1007/s12013-024-01634-w","url":null,"abstract":"This study investigated the relationship between ferroptosis related genes and the prognosis of gastric cancer patients. Gene expression and corresponding clinical data were obtained from the TCGA database. Differentially expressed genes in gastric cancer were identified using R software, and prognostic-related genes were screened using univariate Cox regression analysis. Prognostic genes related to ferroptosis were determined using a Venn diagram. A prognostic model was constructed using LASSO-Cox regression analysis. Additionally, the expression of DUSP1 in gastric cancer was validated through immunohistochemistry, Western blot, and qRT-PCR. The impact of DUSP1 on ferroptosis was analyzed by measuring iron and lipid content in gastric cancer cell lines. A total of 407 gastric cancer patients were included as the training cohort. Fifteen prognostic genes related to ferroptosis were identified, and an 11-gene prognostic model was constructed. Risk scores were calculated for each patient, revealing that the overall survival rate was higher in the low-risk group compared to the high-risk group. ROC curves, PCA plots, and Kaplan-Meier survival curves demonstrated the model's efficacy in predicting 5-year survival rates (AUC = 0.716). Increased DUSP1 expression, correlated with higher Fe2+ and lipid ROS levels, was observed in gastric cancer cells with increasing Erastin concentration. The prognostic model effectively predicts gastric cancer patient outcomes. DUSP1 is lowly expressed in gastric cancer tissues and is associated with malignancy and metastasis, playing a role in ferroptosis in gastric cancer cells.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2237-2251"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel Interacting Partners of MGP-40, a Chitinase-Like Protein in Buffalo Mammary Epithelial Cells. 水牛乳腺上皮细胞中几丁质酶样蛋白 MGP-40 的新型相互作用伙伴

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-11-23 DOI: 10.1007/s12013-024-01623-z

J Vijay Anand, Shalini Jaswal, Manoj Kumar Jena, Sudarshan Kumar, Jai Kumar Kaushik, Ashok Kumar Mohanty

{"title":"Novel Interacting Partners of MGP-40, a Chitinase-Like Protein in Buffalo Mammary Epithelial Cells.","authors":"J Vijay Anand, Shalini Jaswal, Manoj Kumar Jena, Sudarshan Kumar, Jai Kumar Kaushik, Ashok Kumar Mohanty","doi":"10.1007/s12013-024-01623-z","DOIUrl":"10.1007/s12013-024-01623-z","url":null,"abstract":"Mammary Gland Protein-40 (MGP-40), also known as chitinase-3-like protein 1 (CHI3L1), is involved in critical biological processes such as inflammation, tissue remodeling, and cell proliferation, especially during the involution phase of the mammary gland. This study aimed to explore the molecular mechanisms of MGP-40 by identifying its novel interacting partners in buffalo mammary epithelial cells (BuMECs). Stable overexpression of MGP-40 in BuMECs was achieved through transfection with the pCIneo-MGP-40 vector, followed by G418 selection and confirmation by Western blot analysis. To identify interacting proteins, Co-immunoprecipitation (Co-IP) of BuMEC lysate using an anti-YKL-40 antibody was performed, and the eluted proteins were analyzed using SDS-PAGE and mass spectrometry (MALDI-TOF/TOF). The analysis revealed several interacting proteins, including synaptotagmin-like 3, Ras-related Rab19, RIB34A-like protein with coiled coils, and ATP synthase subunit g. These interacting partners suggest that MGP-40 is involved in crucial cellular processes like vesicle trafficking, cytoskeletal organization, and energy metabolism, extending its known functions in inflammation and tissue remodeling. Notably, the interactions with synaptotagmin-like 3 and Rab proteins emphasize MGP-40's potential role in vesicular transport, essential for milk production in mammary epithelial cells, while the association with ATP synthase subunit g links MGP-40 to energy regulation during lactation. These findings provide preliminary insights into the potential roles of MGP-40 in mammary gland physiology, particularly in cellular processes such as vesicle trafficking and energy metabolism. Further studies, including in vivo validation, are essential to confirm these interactions and clarify their relevance to mammary gland function and pathology.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2127-2137"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluating the Synergistic Antioxidant, Anti-microbial and Adsorbent Potential of Andrographis Paniculata Extract and Gold Nanoparticles. 穿心莲提取物与金纳米颗粒的协同抗氧化、抗菌和吸附潜力评价。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-25 DOI: 10.1007/s12013-024-01627-9

Hema Chandran, Gnana Sekaran Ramakrishnan, Janaki Ramaiah Mekala, Sai Ramesh Anjaneyulu

{"title":"Evaluating the Synergistic Antioxidant, Anti-microbial and Adsorbent Potential of Andrographis Paniculata Extract and Gold Nanoparticles.","authors":"Hema Chandran, Gnana Sekaran Ramakrishnan, Janaki Ramaiah Mekala, Sai Ramesh Anjaneyulu","doi":"10.1007/s12013-024-01627-9","DOIUrl":"10.1007/s12013-024-01627-9","url":null,"abstract":"The present study introduces a minimalistic and cost-effective approach to synthesising Gold nanoparticles (AuNPs) using aqueous leaf extracts of Andrographis paniculata. In this synthesis, bioactive metabolites in the leaf extract act as reducing agents, converting Au³⁺ ions to metallic Au⁰, while proteins in the extract form a stabilising layer around the nanoparticles to prevent agglomeration and maintain particle size stability. The synthesised AuNPs were systematically characterised using a range of analytical techniques. UV-visible spectroscopy verified the presence of surface plasmon resonance, Fourier-transform infrared (FTIR) spectroscopy identified key functional groups, X-ray diffraction (XRD) revealed high crystallinity, and Transmission Electron Microscopy (TEM) indicated particle sizes ranging from approximately 4-15 nm. Additionally, Energy Dispersive X-ray (EDX) analysis confirmed the elemental composition of the nanoparticles. The biological efficacy of the synthesised AuNPs was rigorously evaluated. Antioxidant activity, assessed via DPPH and ABTS assays, showed notable results, with inhibition rates of 87.35% and 75% at a sample concentration of 100 µg/mL, respectively. In vitro cytotoxicity studies on Vero cells demonstrated a significant reduction in cell viability, reaching a minimum of 18.22% at the highest tested concentration of 100 µg/mL. Antimicrobial assays indicated strong activity against Salmonella typhii and Escherichia coli, with comparatively lower efficacy against Pseudomonas aeruginosa and Bacillus cereus. Furthermore, adsorption studies showed the AuNPs' high efficiency in removing 99% of crystal violet dye (500 mg/L) within 30 min under optimised conditions (pH 4.5, temperature 33 °C, and an AuNP dosage of 200 mg/L). This comprehensive analysis indicates that the synthesised AuNPs from A. paniculata exhibit promising properties for applications in biomedicine and wastewater treatment.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2151-2165"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Total Glycosides of Paeony Activates PI3K/Akt Pathway to Alleviate Cardiomyocyte Hypertrophy Induced by AngII. 白芍总苷激活PI3K/Akt通路减轻AngII诱导的心肌细胞肥大

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-01-16 DOI: 10.1007/s12013-024-01616-y

Letian Sheng, Mengjiao Shen, Danyan Shao

{"title":"Total Glycosides of Paeony Activates PI3K/Akt Pathway to Alleviate Cardiomyocyte Hypertrophy Induced by AngII.","authors":"Letian Sheng, Mengjiao Shen, Danyan Shao","doi":"10.1007/s12013-024-01616-y","DOIUrl":"10.1007/s12013-024-01616-y","url":null,"abstract":"Total glucosides of paeony (TGP) have been investigated for their effects on cardiomyocyte hypertrophy induced by angiotensin II (Ang II). In this study, rat cardiomyocyte H9c2 cells were treated with various doses of TGP (0, 12.5, 25, 50, 100, 200, and 400 μmol/L), and cell viability was assessed using the MTT method to determine an optimal dose. To establish the cardiomyocyte hypertrophy model, Ang II (1 μmol/L) was used. The experimental groups included the control (Ctrl) group, the hypertrophy group (Ang II), the TGP treatment group (TGP+Ang II), and a combined treatment group (TGP+Ang II+LY), where LY294002, a PI3K/Akt inhibitor, was used. The surface area of H9c2 cells was analyzed using image analysis software, and apoptosis was assessed via flow cytometry. Western blotting was employed to evaluate markers related to cell proliferation, cardiac hypertrophy, apoptosis, and autophagy, as well as the phosphorylation of the PI3K/Akt pathway. The results revealed that Ang II inhibited cell viability and increased cell surface area, apoptosis, and autophagy, all of which were significantly reversed by TGP treatment. Moreover, the addition of LY294002 partially attenuated the effects of TGP, reducing cell viability and promoting hypertrophy, apoptosis, and autophagy. Additionally, Ang II reduced PI3K/Akt signaling activity, while TGP restored it. LY treatment reversed the effects of TGP and suppressed the PI3K/Akt pathway. In conclusion, TGP improves cardiomyocyte hypertrophy induced by Ang II by activating the PI3K/Akt signaling pathway.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2059-2066"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Curcumin Alleviates Arecoline-induced Oral Submucous Fibrosis via the FOSL1/MAPK8 Axis. 姜黄素通过 FOSL1/MAPK8 轴缓解阿瑞考林诱导的口腔黏膜下纤维化

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-15 DOI: 10.1007/s12013-024-01633-x

Lifen Yin, Xiao Wang

{"title":"Curcumin Alleviates Arecoline-induced Oral Submucous Fibrosis via the FOSL1/MAPK8 Axis.","authors":"Lifen Yin, Xiao Wang","doi":"10.1007/s12013-024-01633-x","DOIUrl":"10.1007/s12013-024-01633-x","url":null,"abstract":"Oral submucous fibrosis (OSF) is a precancerous lesion of the oral cavity. Areca nut consumption can cause OSF through sustained activation of buccal mucosal fibroblasts (BMFs). This study explored the effect of curcumin on arecoline-induced BMF activation and its mechanism of action. BMFs were isolated and identified by immunofluorescence detection of fibroblast surface markers vimentin and S100A4. After transfection with FOSL1- or MAPK8-related vectors, BMFs were activated by arecoline and treated with curcumin. Scratch and transwell assays were performed to detect cell migration. ChIP and luciferase reporter assays were conducted to detect the binding of FOSL1 to the MAPK8 promoter. RT-qPCR was used to detect FOSL1 and MAPK8 mRNA expression. Western blotting was used to detect FOSL1, MAPK8, COL1A1, α-SMA, Smad2, and p-Smad2 proteins. Curcumin treatment inhibited arecoline-induced fibroblast migration, reduced the expression of myofibroblast markers COL1A1, α-SMA, and p-Smad2, and downregulated the expression of FOSL1 and MAPK8. FOSL1 or MAPK8 overexpression enhanced migration and increased COL1A1, α-SMA, and p-Smad2 expression in curcumin-treated cells. FOSL1 bound to the MAPK8 promoter and promoted MAPK8 expression. Simultaneous FOSL1 overexpression and MAPK8 knockdown, compared to FOSL1 overexpression, reduced cell migration and inhibited COL1A1, α-SMA, and p-Smad2 expression. In conclusion, curcumin targets FOSL1 to reduce MAPK8 expression, thereby suppressing arecoline-induced fibroblast activation.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2227-2236"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142826950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neutrophil Membrane Nanovesicles Alleviate the Renal Function Indicators in Acute Kidney Injury Caused by Septic Rats. 中性粒细胞膜纳米囊泡对脓毒症大鼠急性肾损伤肾功能指标的影响

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-01-14 DOI: 10.1007/s12013-024-01664-4

Junhao Pan, Feifei Shao, Xiaorong Xiao, Xin Ke, Zhihui Guan, Hui Lin, Qingqing Yan, Xinyao Xiang, Jinming Luo

{"title":"Neutrophil Membrane Nanovesicles Alleviate the Renal Function Indicators in Acute Kidney Injury Caused by Septic Rats.","authors":"Junhao Pan, Feifei Shao, Xiaorong Xiao, Xin Ke, Zhihui Guan, Hui Lin, Qingqing Yan, Xinyao Xiang, Jinming Luo","doi":"10.1007/s12013-024-01664-4","DOIUrl":"10.1007/s12013-024-01664-4","url":null,"abstract":"This study aims to explore the efficacy of neutrophil membrane nanovesicles (NMNVs) in the treatment of acute kidney injury caused by sepsis (S-AKI). Moreover, its effects on renal function indicators in plasma [creatinine (CREA), urea (UREA)], oxidative stress factor [malondialdehyde (MDA)], inflammatory factor [myeloperoxidase (MPO), histone H4 (H4), and macrophage inflammatory protein-2 (MIP-2)] are studied. Sixty SPF grade adult male Wistar rats in a healthy state under natural infection were randomly divided into blank, LSP, and experimental groups, with 20 rats in each group. After 7 days of adaptive feeding, a S-AKI model was established in the control group and the experimental group. The control group was treated with red blood cell membrane nanovesicles (RBC-NVs), the experimental group was treated with NMNVs, and the blank group was normal rats. The clinical treatment and changes in renal function indicators of the tested rats were observed and recorded. The total effective rate of treatment in the experimental group was higher than that in the controlling group (P < 0.05). Moreover, 1 h after the construction of the S-AKI model, the CREA, UREA, MDA, MPO, H4, MIP-2 in the controlling group and experimental group were higher than those in the blank group. At 7 and 14 h after constructing S-AKI model, the CREA, UREA, MDA, MPO, H4, and MIP-2 in the controlling and experimental groups decreased. However, the above indicators in the experimental group were lower than those in the controlling group (P < 0.05), and the comparison between this group and the blank group showed P > 0.05. In summary, the efficacy of NMNV in treating S-AKI is significant, as it can reduce CREA, UREA, MDA, MPO, as well as H4 and MIP-2, effectively controlling disease progression.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2553-2565"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Donafenib Induces Mitochondrial Dysfunction in Liver Cancer Cells via DRP1. 多纳非尼通过DRP1诱导肝癌细胞线粒体功能障碍

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-02-12 DOI: 10.1007/s12013-024-01648-4

Yuhua Ma, Yougang Sun, Kayishaer Ailikenjiang, Chuanjiang Lv, Xiang Li, YunQiang Nie, Chang Wang, Yan Xiong, Yong Chen

{"title":"Donafenib Induces Mitochondrial Dysfunction in Liver Cancer Cells via DRP1.","authors":"Yuhua Ma, Yougang Sun, Kayishaer Ailikenjiang, Chuanjiang Lv, Xiang Li, YunQiang Nie, Chang Wang, Yan Xiong, Yong Chen","doi":"10.1007/s12013-024-01648-4","DOIUrl":"10.1007/s12013-024-01648-4","url":null,"abstract":"Hepatocellular carcinoma (HCC) represents a significant global health challenge, characterized by a high incidence rate. Mitochondria have emerged as an important therapeutic target for HCC. Donafenib, a multi-receptor tyrosine kinase inhibitor, has been approved for the treatment of advanced HCC. However, the underlying mechanisms remain to be elucidated. In this study, we aim to investigate the effects of Donafenib on mitochondrial function in HCC cells. Firstly, we show that Donafenib induces mitochondrial oxidative stress in SNU-449 liver cancer cells by increasing mitochondrial ROS while reducing glutathione peroxidase (GPx) activity and the expression of Mn-SOD. We also demonstrate that Donafenib decreases mitochondrial membrane potential (MMP) and induces the opening of the mitochondrial permeability transition pore (mPTP). Furthermore, Donafenib reduces mitochondrial respiratory rate, COX IV activity, and ATP production. Notably, Donafenib induces mitochondrial fragmentation and reduces mitochondrial length by increasing the expression of DRP1, without affecting Mfn1 or Mfn2. Silencing of DRP1 protects against mitochondrial dysfunction induced by Donafenib, indicating that DRP1 plays a key role in mediating Donafenib's effects on mitochondrial function in HCC cells.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2379-2388"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Apoc1 Knockdown Alleviates High Glucose-induced Oxidative Stress and Apoptosis of Renal Tubular Cells by Binding to Clusterin. Apoc1基因敲低可通过结合簇蛋白减轻高糖诱导的肾小管细胞氧化应激和凋亡。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-04 DOI: 10.1007/s12013-024-01636-8

Liyin Chai, Zhengyang Liu, Jun Zeng, Li Gong, Sha Xiang, Jing Yu, Haili Sun, Chaolin Wen, Fang Wang, Ning Li, Bingbing Shen, Mei Mei

{"title":"Apoc1 Knockdown Alleviates High Glucose-induced Oxidative Stress and Apoptosis of Renal Tubular Cells by Binding to Clusterin.","authors":"Liyin Chai, Zhengyang Liu, Jun Zeng, Li Gong, Sha Xiang, Jing Yu, Haili Sun, Chaolin Wen, Fang Wang, Ning Li, Bingbing Shen, Mei Mei","doi":"10.1007/s12013-024-01636-8","DOIUrl":"10.1007/s12013-024-01636-8","url":null,"abstract":"Diabetic nephropathy (DN) is a serious diabetic complication. Renal tubular damage is an important aspect of DN. Increased apolipoprotein C1 (Apoc1) has been confirmed in serum of patients with DN. The exact mechanism of Apoc1 in DN is unclear as yet. We aimed to elaborate the molecular mechanism underlying high glucose (HG)-induced renal tubular epithelial damage. In this content, a DN mouse model was established to assess renal damage. Apoc1 and Clusterin expression in renal tissue was detected using immunoblotting and immunofluorescence staining. In vitro, human kidney proximal tubular epithelial cells (HK-2 cells) were exposed to HG to simulate the DN model. After Apoc1 and/or Clusterin knockdown, HK-2 cell viability under HG conditions was detected using CCK-8 assay. DCFH-DA staining was used to examine the production of intracellular reactive oxygen species (ROS). MDA and SOD levels were tested by kits. Moreover, cell apoptosis was measured using TUNEL staining. Immunoblotting was employed to evaluate the expression of proteins. Additionally, the binding between Apoc1 and Clusterin was analyzed using co-immunoprecipitation experiments. Our data revealed that Apoc1 expression was upregulated while Clusterin expression was downregulated in renal tissue of DN mice and HG-treated HK-2 cells. Apoc1 knockdown alleviated oxidative stress and apoptosis in HG-treated HK-2 cells. Importantly, Apoc1 could bind to Clusterin and regulate Clusterin expression in HK-2 cells. Finally, Clusterin silencing blocked the influences of Apoc1 knockdown on the oxidative stress and apoptosis in HK-2 cells under HG conditions. Collectively, Apoc1 knockdown exerts potential anti-DN effects by binding to Clusterin to alleviate HG-induced renal tubular damage, suggesting that Apoc1/Clusterin can be used as a valuable therapeutic target for DN.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2253-2263"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PI3K/mTOR Inhibitor VS-5584 Alters Expression of WNT Signaling Genes and Induces Apoptosis in Lung Adenocarcinoma Cells: In Vitro and In Silico Insight. PI3K/mTOR抑制剂VS-5584改变WNT信号基因表达并诱导肺腺癌细胞凋亡：体外和计算机研究

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-17 DOI: 10.1007/s12013-024-01643-9

Buket Ozel, Sezgi Kipcak, Hasan Onur Caglar, Cagla Kayabasi, Bakiye Goker Bagca, Cumhur Gunduz, Nur Selvi Gunel, Cigir Biray Avci

{"title":"PI3K/mTOR Inhibitor VS-5584 Alters Expression of WNT Signaling Genes and Induces Apoptosis in Lung Adenocarcinoma Cells: In Vitro and In Silico Insight.","authors":"Buket Ozel, Sezgi Kipcak, Hasan Onur Caglar, Cagla Kayabasi, Bakiye Goker Bagca, Cumhur Gunduz, Nur Selvi Gunel, Cigir Biray Avci","doi":"10.1007/s12013-024-01643-9","DOIUrl":"10.1007/s12013-024-01643-9","url":null,"abstract":"Lung cancer (LC) accounts for approximately 25% of all cancer cases, with 80-85% of these being non-small cell lung cancer (NSCLC). VS-5584 is a novel anti-cancer agent that specifically inhibits mTORC1/2 and class I PI3K isoforms. There is cross-talk between the PI3K-Akt-mTOR and WNT signaling pathways that are abnormally activated in NSCLC. In this study, we aimed to evaluate the anti-cancer effects of VS-5584 on A549 lung adenocarcinoma cells and changes in WNT signaling gene expression in vitro, while also correlating differentially expressed genes in silico. The effect of VS-5584 on A549 cell viability was assessed by the MTT assay. Apoptosis and cell cycle profiles were analyzed by flow cytometry, while WNT signaling gene expression was measured by quantitative RT-PCR. Differentially expressed genes (DEGs) in the TCGA LUAD and LUSC datasets were identified using the GEPIA2 platform. VS-5584 treatment induced apoptosis and caused cell cycle arrest at the G0/G1 phase in A549 cells. The mRNA expression levels of WNT signaling genes significantly decreased in treated cells. The expression of some upregulated DEGs in the datasets decreased in A549 cells treated with VS-5584. VS-5584 shows promise as an anti-cancer agent in the treatment of NSCLC by downregulating the expression of WNT signaling genes.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2313-2322"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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