Biochemistry and Cell Biology最新文献_第4页

Antioxidant and migration-modulating effects of lactoferrin in human keratinocytes. 乳铁蛋白在人角质形成细胞中的抗氧化和迁移调节作用。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0327

Morgana Lüdtke Azevedo, Nathalia Stark Pedra, Roselia Maria Spanevello, Rafael Guerra Lund

{"title":"Antioxidant and migration-modulating effects of lactoferrin in human keratinocytes.","authors":"Morgana Lüdtke Azevedo, Nathalia Stark Pedra, Roselia Maria Spanevello, Rafael Guerra Lund","doi":"10.1139/bcb-2025-0327","DOIUrl":"10.1139/bcb-2025-0327","url":null,"abstract":"Lactoferrin (Lf) is a multifunctional glycoprotein with antimicrobial, anti-inflammatory, and antioxidant properties that have been proposed as a therapeutic adjunct in wound healing. As keratinocytes are key drivers of re-epithelialization, this study investigated the effects of Lf on human keratinocyte cell line (HaCaT) cells with a focus on viability, proliferation, migration, and oxidative stress. HaCaT cells were treated with Lf at concentrations of 5, 7.5, and 10 µg/mL, and outcomes were assessed using metabolic and proliferation assays, a scratch wound healing assay, and measurements of nitrite, thiols, and antioxidant enzyme activities. Lf preserved keratinocyte viability and did not induce uncontrolled proliferation, indicating good cellular tolerance. Migration was not affected at early time-points but showed modest enhancement at 48 h in the 5 and 7.5 µg/mL groups. At the redox level, Lf selectively increased catalase activity across all doses, while nitrite and superoxide dismutase remained unchanged and thiols and glutathione S-transferase decreased at higher concentrations. Together, these findings identify Lf as a redox-centric modulator that enhances hydrogen peroxide detoxification without compromising cell integrity, supporting its potential as a safe adjunctive agent to promote orderly wound repair.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-9"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145653382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

PPP2R2B targets the JAK2-STAT3 signaling pathway to regulate ferroptosis in breast cancer cells. PPP2R2B靶向JAK2-STAT3信号通路调控乳腺癌细胞铁下垂。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0361

Weiming Luo, Mei Yang, Yue Tan, Jing Zhang

{"title":"PPP2R2B targets the JAK2-STAT3 signaling pathway to regulate ferroptosis in breast cancer cells.","authors":"Weiming Luo, Mei Yang, Yue Tan, Jing Zhang","doi":"10.1139/bcb-2025-0361","DOIUrl":"10.1139/bcb-2025-0361","url":null,"abstract":"We aimed to explore the effect and the mechanism of PPP2R2B on cell proliferation, migration, and ferroptosis in breast cancer cells. By bioinformatic analysis and data mining, PPP2R2B was associated with the prognosis and ferroptosis of breast cancer. Breast cancer cells were transfected with PPP2R2B overexpression or PPP2R2B knockdown plasmids, and cell proliferation, apoptosis, migration, and invasion were examined. Moreover, transfected breast cancer cells were treated with ferroptosis inducer, and the relative iron level, Fe2+ level, MDA level, lipid ROS level, MitoSOX intensity, and fluorescence intensity were detected. Protein expressions of GPX4, ACSL4, and SLC7A11 were evaluated by Western blot. The effect of PPP2R2B on JAK2-STAT3 signaling was studied. Finally, the tumor xenograft model in nude mice was constructed to study the PPP2R2B overexpression on tumor growth in vivo. PPP2R2B was down-regulated in the breast cancer tissues and predicted poor prognosis. PPP2R2B inhibited cell proliferation and induced cell apoptosis. PPP2R2B suppressed cell migration and invasion of MCF-7 and MDA-MB-231 cells. PPP2R2B promoted erastin-induced ferroptosis in breast cancer cells and regulated the expression of GPX4, ACSL4, and SLC7A11. In addition, PPP2R2B inhibited the phosphorylation of JAK2 and STAT3. PPP2R2B also inhibited tumor growth in vivo. PPP2R2B targets the JAK2-STAT3 signaling pathway to regulate cell proliferation, apoptosis, migration, invasion, and ferroptosis in breast cancer cells.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"104 ","pages":"1-10"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148040928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Design and biological evaluation of novel biphenyl-dihydropyrimidinone derivatives with selective anticancer and nongenotoxic profiles. 具有选择性抗癌和无基因毒性的新型联苯-二氢嘧啶衍生物的设计和生物学评价。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0370

Mehmet Fidan, Arif Ayar, Aliye Gediz Ertürk, Seda Mesci, Burak Yazgan, Tuba Yıldırım

{"title":"Design and biological evaluation of novel biphenyl-dihydropyrimidinone derivatives with selective anticancer and nongenotoxic profiles.","authors":"Mehmet Fidan, Arif Ayar, Aliye Gediz Ertürk, Seda Mesci, Burak Yazgan, Tuba Yıldırım","doi":"10.1139/bcb-2025-0370","DOIUrl":"10.1139/bcb-2025-0370","url":null,"abstract":"This study reports the p-toluenesulfonic acid-catalyzed synthesis of three novel 3,4-dihydropyrimidin-2(1H)-one derivatives (4a = PMe, 4b = PPh, 4c = PNO2) based on a 1,1'-biphenyl, and the evaluation of their cytotoxic, genotoxic, antioxidant, and apoptosis-related effects in vitro and in vivo. Structural characterization was performed using FT-IR, 1H NMR, APT-13C NMR, and LC/MS-MS. Cytotoxicity was assessed on A549 human lung cancer and MRC-5 normal lung fibroblast cells using the WST-8 assay, while genotoxicity was evaluated using the Drosophila wing SMART assay. qRT-PCR was conducted to analyze gene expression related to cellular stress responses, antioxidant defense, and apoptosis in both cell lines and Drosophila melanogaster. All compounds exhibited dose-dependent cytotoxicity toward A549 cells with low toxicity in MRC-5 cells, indicating selective anticancer activity. Compound 4b showed the strongest cytotoxic effect (highest potency), whereas compound 4c exhibited the highest selectivity index (SI = 1.22), indicating a more favorable therapeutic window. Compound 4a induced a pro-apoptotic shift in the BAX/BCL-2 ratio, and all compounds enhanced antioxidant gene expression, particularly 4a. No significant genotoxic effects were detected. These findings suggest that the synthesized dihydropyrimidinone derivatives possess selective anticancer potential and favorable genotoxic safety profile, with mechanistic diversity supporting their relevance for targeted cancer therapy.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-22"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Exploring metaboloepigenetic variability in bovine fibroblast lines. 探讨牛成纤维细胞系的代谢表观遗传变异性。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0438

Eric Hawrylyshyn, Marcia de A M M Ferraz, Biankha Chan, Gabriela F Mastromonaco

{"title":"Exploring metaboloepigenetic variability in bovine fibroblast lines.","authors":"Eric Hawrylyshyn, Marcia de A M M Ferraz, Biankha Chan, Gabriela F Mastromonaco","doi":"10.1139/bcb-2025-0438","DOIUrl":"10.1139/bcb-2025-0438","url":null,"abstract":"Somatic cell-based reproductive technologies (SCRTs) offer a promising approach for preserving the genetic diversity of threatened species. SCRTs require the nuclear reprogramming of a donor somatic cell, which has low success rates (1%-5%) and can vary significantly between individuals and cell lines derived from the same individual. Somatic and pluripotent cells differ in several key characteristics, and donor cells presenting more pluripotent-like traits have been found to result in improved reprogramming outcomes. Here, we characterized 18 standardized fibroblast cell lines from six Angus bulls for several of these characteristics at the inter- and intra-individual levels: bioenergetic status, targeted metabolite abundance, global DNA methylation levels, and presence of key histone modifications. Differences in the metaboloepigenetic profiles of these cell lines were observed at both inter- and intra-individual levels. By integrating these data, we positioned cell lines along a somatic-to-pluripotent-like continuum and identified a reduced set of features that captured the dominant separation between profiles. Although functional reprogramming outcomes were not assessed here, these results provide a data-driven framework to prioritise donor cell lines for prospective induced pluripotent stem cell/somatic cell nuclear transfer validation and to guide the development of practical biomarker panels for SCRT workflows.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Caspase noncanonical roles in mediating lipid homeostasis. 半胱天冬酶在调节脂质稳态中的非规范作用。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2026-0061

Fan Du, Maotian Wang, Siyu Ji

{"title":"Caspase noncanonical roles in mediating lipid homeostasis.","authors":"Fan Du, Maotian Wang, Siyu Ji","doi":"10.1139/bcb-2026-0061","DOIUrl":"10.1139/bcb-2026-0061","url":null,"abstract":"Caspases are well recognized and studied as the central executioners of apoptosis, while recent studies have unraveled their diverse roles beyond cell apoptotic function. One emerging area of interest is nonapoptotic caspase activity as a potential regulator in lipid metabolism. This review explores the differential nonapoptotic role of caspases in lipid metabolic process, encompassing the influence of caspases on lipid reprogramming, lipid synthesis, degradation, transport, and signaling. We discuss the mechanisms underlying these interactions, their relevance to physiological processes, and their implications for various diseases. This reveals a hidden layer of regulation where the machinery of cell death is repurposed to control the fundamental processes of fat handling in living animal. Dysregulation of this system forms a vicious cycle that propagates cellular dysfunction, directly contributing to the pathogenesis of major human diseases in aging, including redox stress, nonalcoholic steatohepatitis, type 2 diabetes, neurodegenerative disorders, and cancer. Consequently, the caspase-metabolism axis emerges as a compelling therapeutic frontier. However, the clinical translation of caspase modulators is challenged by the context-dependent duality of caspase functions. Future therapeutic strategies must therefore advance beyond pan-inhibition toward the precise, context-specific modulation of discrete caspase-mediated metabolic events to halt disease progression effectively.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Autologous chylous fat improves hypertrophic scars via TSG-6: association with endoplasmic reticulum stress mediated by IRE1α phosphorylation and JNK activation. 自体乳糜脂肪通过TSG-6改善增生性疤痕：与IRE1α磷酸化和JNK激活介导的内质网应激相关

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0457

Xingwang Deng, Hongwei Ma, Wenjing Pang, Xuhui Qi, Long Zhang, Yanmei Zhang

{"title":"Autologous chylous fat improves hypertrophic scars via TSG-6: association with endoplasmic reticulum stress mediated by IRE1α phosphorylation and JNK activation.","authors":"Xingwang Deng, Hongwei Ma, Wenjing Pang, Xuhui Qi, Long Zhang, Yanmei Zhang","doi":"10.1139/bcb-2025-0457","DOIUrl":"10.1139/bcb-2025-0457","url":null,"abstract":"Hypertrophic scars (HS) represent pathological outcomes of traumatic or surgical injuries with dysregulated wound healing. We investigated the therapeutic effects and underlying mechanism of autologous chyle fat (ALCF) in HS formation. A thermal injury-induced burn wound model was established in mice. Histopathological alterations, fibrotic deposition, the levels of α-smooth muscle actin (α-SMA), collagen I and collagen III were quantified. To elucidate the mechanism, tumor necrosis factor-stimulated gene-6 (TSG-6) was silenced, and TSG-6, binding immunoglobulin protein (Bip), C/EBP homologous protein (CHOP), inositol-requiring enzyme 1α (IRE1α), p-IRE1α, c-Jun N-terminal kinase (JNK), and p-JNK were assessed to evaluate endoplasmic reticulum stress (ERS) and downstream signaling. The JNK signaling pathway was pharmacologically activated to validate the IRE1α/JNK axis. Clinically, ALCF injection yielded favorable outcomes. ALCF markedly alleviated fibrosis in burn wound scar tissues and reduced Bip and CHOP, indicating ERS attenuation. ALCF upregulated TSG-6 expression in healing wound tissues, whereas TSG-6 knockdown partially abolished the antifibrotic effects of ALCF. ALCF suppressed IRE1α phosphorylation and JNK activation. Reactivation of the IRE1α/JNK pathway reversed the inhibitory effects of ALCF on ERS and promoted fibrotic deposition. Collectively, ALCF attenuates burn wound fibrosis through TSG-6-mediated suppression of ERS, associated with reduced IRE1α phosphorylation and JNK signaling inhibition.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Origin of dedifferentiated adipocyte-derived cells (DFAT) during ceiling culture in an Adiponectin Cre-Recombinase mouse model. 在脂肪蛋白 Cre 重组酶小鼠模型的上限培养过程中，已分化脂肪细胞衍生细胞（DFAT）的起源。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-10-30 DOI: 10.1139/bcb-2024-0140

Marie-Frédérique Gauthier, Giada Ostinelli, Mélissa Pelletier, André Tchernof

{"title":"Origin of dedifferentiated adipocyte-derived cells (DFAT) during ceiling culture in an Adiponectin Cre-Recombinase mouse model.","authors":"Marie-Frédérique Gauthier, Giada Ostinelli, Mélissa Pelletier, André Tchernof","doi":"10.1139/bcb-2024-0140","DOIUrl":"10.1139/bcb-2024-0140","url":null,"abstract":"DFAT cells represent an attractive source of stem cells in tissue engineering and in the potential treatment of several clinical conditions. Our objective was to determine whether DFAT cells originate from mature adipocytes and address whether contamination from the stromal vascular fraction (SVF) could be as a source for these cells. A murine adiponectin-creERT;mT/mG model was used with the excision of the cassette induced by tamoxifen injection for the cells expressing adiponectin (adipoq). This model allows distinguishing of mature adipocytes (green fluorescence) from other SVF cell types (red fluorescence) based on the fluorescent protein expressed. Mature adipocytes and SVF cells were isolated from adipose tissues by collagenase digestion. Ceiling cultures were imaged by time-lapse microscopy. Confocal microscopy was used to follow cells over 21 days. Time-lapse microscopy experiments showed liposecretion occurring in mature adipocytes displaying green fluorescence. Confocal imaging allowed the identification of a heterogeneous cell population expressing green but also red fluorescence after 21 days of culture. Asymmetrical division of mature adipocytes was not observed. In conclusion, liposecretion of mature adipocytes is a phenomenon that can be observed in vitro and DFAT cells do originate from mature adipocytes. However, the population of DFAT cells is heterogenous.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

1-Deoxynojirimycin affects high glucose-induced pancreatic beta-cell dysfunction through regulating CEBPA expression and AMPK pathway. 1-脱氧野尻霉素通过调节CEBPA表达和AMPK通路影响高血糖诱导的胰岛β细胞功能障碍

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-15 DOI: 10.1139/bcb-2024-0128

Xiaoying Li, Shenggui Liu, Siqi Wang, Xinghui Ai, Lin Wei

引用次数: 0

Establishment of immortalized porcine intramuscular preadipocytes for the study of lipid metabolism. 永生化猪肌内前体脂肪细胞的建立及脂质代谢研究。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0174

Briana Locke, Ray Lu

引用次数: 0

HOXD-AS1 interacting with AMPK causes a disturbance in mTOR signaling, impairing ferroptosis in glioma. HOXD-AS1与AMPK相互作用导致mTOR信号紊乱，损害胶质瘤中的铁下垂。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0267

Li Zhou, Shijiao Chen, Mingxing Zhang, Xu-Ming Huang, Hai-Yan Li, Ji-Hui Wang, Zhenhua Song, Yunyun Pan, Nan Jiang

{"title":"HOXD-AS1 interacting with AMPK causes a disturbance in mTOR signaling, impairing ferroptosis in glioma.","authors":"Li Zhou, Shijiao Chen, Mingxing Zhang, Xu-Ming Huang, Hai-Yan Li, Ji-Hui Wang, Zhenhua Song, Yunyun Pan, Nan Jiang","doi":"10.1139/bcb-2024-0267","DOIUrl":"10.1139/bcb-2024-0267","url":null,"abstract":"Ferroptosis, a recently discovered form of cell death, plays an important role in cancer progression. It has been reported that ferroptosis plays a complex regulatory role in the biological processes of glioma. In glioma, the long noncoding RNA, HOXD cluster antisense RNA 1 (HOXD-AS1), functions as an oncogene, contributing to glioma progression. However, its potential functions in ferroptosis are unclear. Herein, we aimed to clarify the biological function and detailed molecular mechanism of HOXD-AS1 in regulating ferroptosis in glioma. Firstly, cell viability, reactive oxygen species (ROS), and malondialdehyde (MDA) content assays were detected. The mechanisms of HOXD1-AS1's effect on ferroptosis were evaluated by detecting glutathione, Cys, and solute carrier family 7 member 11 (SLC7A11) levels. RNA immunoprecipitation and RNA pull-down techniques were employed to explore whether HOXD-AS1 can directly bind AMP-activated protein kinase (AMPK). Our findings indicated that HOXD-AS1 levels were augmented significantly in glioma tissue. HOXD-AS1 knockdown induced MDA and ROS accumulation, subsequently resulting in ferroptosis. Further molecular analysis showed that the binding between HOXD-AS1 and AMPK regulated the mechanistic target of rapamycin kinase pathway, inhibit the transport of Cys, and decrease the production of glutathione, eventually resulting in ferroptosis. Our study revealed that HOXD-AS1 regulates cell ferroptosis, thus its downregulation might be an effective strategy to suppress glioma.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"103 ","pages":"1-12"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145376009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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