Applied Biochemistry and Biotechnology最新文献

{"title":"Optimizing Thermal Stability: Evaluating the Impact of Heterofunctional Hydrophobic Supports on Immobilized Flaxseed Lipase.","authors":"Nicole Novelli do Nascimento, Janaína Cejudo-Sanches, Paulo Waldir Tardioli, José Manuel Guisan, Angélica Marquetotti Salcedo Vieira","doi":"10.1007/s12010-024-05175-z","DOIUrl":"https://doi.org/10.1007/s12010-024-05175-z","url":null,"abstract":"<p><p>Lipases have catalytic capacity in various processes such as hydrolysis. Those derived from plant sources, such as linseed, offer an economical alternative. The immobilization process facilitates the recovery and reuse of lipase, providing advantages such as resistance to high temperatures and difficulties in recovering and reusing free lipases, which makes product separation difficult. This study presents the immobilization of lipases extracted from flax seeds on octylfunctional hydrophobic supports. Additionally, the thermal stability of the derived products was evaluated in comparison with freely soluble lipase. The lipase exhibited a strong affinity for the evaluated heterofunctional hydrophobic supports, with DVS-activated octylagarose emerging as the most efficient method for immobilization, thus increasing catalytic activity upon resuspension. Furthermore, the octylagarose derivative demonstrated a notable increase in thermal stability. The main results of the study include that the soluble enzyme showed greater activity after 24 h, regardless of the temperature evaluated. The benzamide extract showed greater thermal stability, and all supports evaluated showed greater activity than the soluble enzyme after immobilization. Notably, lipase immobilized on octyl glyoxyl agarose showed the highest activity, demonstrated stability for 840 h at 60 °C, and had a half-life of 1242 h. Furthermore, the lipase immobilized in octyl glyoxyl agarose showed a stabilization factor approximately nine times greater than the free enzyme. These results suggest that immobilization, probably achieved through interfacial activation and multipoint covalent bonds, prevented the release of the enzyme into the medium with increasing temperature. This study thus highlights the significant potential of immobilizing flaxseed-derived lipase.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997846","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}

{"title":"Circ-NMNAT1 Drives Tumor Progression in Bladder Cancer by Modulating the miR-370-3p/ATXN2L Axis.","authors":"ChenHui Zhu, LiJuan Lin, ChangQing Huang, ZhaoGuan Li","doi":"10.1007/s12010-024-05162-4","DOIUrl":"https://doi.org/10.1007/s12010-024-05162-4","url":null,"abstract":"<p><p>The relationship between circular RNAs (circRNAs) and tumor growth and metastasis is increasingly well-established. In this study, we sought to shed light on circ-NMNAT1's potential molecular mechanisms in bladder cancer (BCa). circ-NMNAT1, miR-370-3p, and ATXN2L expression profiles were explored using RT-qPCR and/or Western blot techniques. Cell proliferation was detected by MTT and colony formation assay. Transwell assay was used to detect the migration and invasion ability of cells. Western Blot was used to detect the protein expression level of ATXN2L. The targeting relationship between miR-370-3p and circ-NMNAT1 or ATXN2L was confirmed by dual luciferase reporter gene and RIP assay. A xenograft tumor model was created to investigate circ-NMNAT1's function in BCa in vivo. The high expression of circ-NMNAT1 was measured in BCa. circ-NMNAT1 bound competitively to miR-370-3p and downregulated miR-370-3p expression. After knocking down circ-NMNAT1, the proliferation ability of EJ cells was significantly inhibited, and the number of cell colonies was (80.00 ± 7.10). The number of migrated and invaded cells was significantly reduced by (35.49 ± 0.05)% and (59.00 ± 0.04)%, respectively, after silencing circ-NMNAT1. In addition, downregulation of circ-NMNAT1 also significantly increased the apoptosis rate of EJ cells by (23.55 ± 2.95)%. Knockdown of miR-370-3p or overexpression of ATXN2L reduced the effect of circ-NMNAT1 silencing on BCa cells. The promoting effect of circ-NMNAT1 on BCa progression was further validated in vivo tumor models. The weight and volume of the tumor were significantly inhibited after circ-NMNAT1 knockdown, which were (87.50 ± 20.40) mg and (238.90 ± 21.38) mm³, respectively. Circ-NMNAT1 is highly expressed in BCa and promotes the proliferation, migration, and invasion of BCa cells by regulating the miR-370-3p/ATXN2L axis, thereby accelerating the progression of BCa. Our results suggest that circ-NMNAT1 may be a new therapeutic target for BCa.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998230","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}

{"title":"Prediction of Multi-targeting Pharmacological Activity of Bioactive Compounds from Medicinal Plants Against Hepatocellular Carcinoma Through Advanced Network Pharmacology and Bioinformatics-Based Investigation.","authors":"Hema Priya Manivannan, Vishnu Priya Veeraraghavan, Arul Prakash Francis","doi":"10.1007/s12010-024-05150-8","DOIUrl":"https://doi.org/10.1007/s12010-024-05150-8","url":null,"abstract":"<p><p>The primary objective of this study was to identify bioactive compounds from four medicinal plants with multi-targeting activity against hepatocellular carcinoma (HCC). A comprehensive analysis led to the identification of a subset of compounds possessing favorable drug-likeness, pharmacokinetics, and absence of toxicity profiles. Target analysis for 42 phytochemicals revealed 210 potential targets associated with HCC. Protein-protein interaction (PPI) analysis of these targets uncovered five critical hub genes, STAT3, SRC, AKT1, MAPK3, and EGFR, in our study. Correlation analysis of these hub genes indicated a strong positive correlation between EGFR, MAPK3, and SRC expression highlighting their interconnected roles in HCC. Survival analysis underscored the significant prognostic role of these hub genes in HCC underscoring their potential as biomarkers. The co-expression analysis unveiled an intricate network of interactions among the hub genes, while the enrichment analysis demonstrated their enrichment in diverse biological and signaling pathways related to HCC. Molecular docking analysis between the seven phytochemicals and five identified targets revealed that bauerenol exhibited good affinity towards all the targets. Subsequent molecular dynamics (MD) simulations demonstrated that bauerenol formed stable complexes with STAT3, AKT1, EGFR, and MAPK3, suggesting its potential as a multi-targeted inhibitor. Our research suggests that bauerenol shows promise as an inhibitor for HCC targets and stands out as a notable lead compound. However, further experimental studies are necessary to confirm its activity and to evaluate its potential as a therapeutic agent for HCC.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998027","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}

{"title":"Comprehensive Review on Bio-Based Treatments for Polyvinyl Chloride Plastic.","authors":"Neha Hatwar, Asifa Qureshi","doi":"10.1007/s12010-024-05174-0","DOIUrl":"https://doi.org/10.1007/s12010-024-05174-0","url":null,"abstract":"<p><p>Polyvinyl chloride (PVC) plastics are widespread around the globe, and each year, thousands of tons of PVC end up in the environment in the form of micro-/nanoplastics. Literature has reported extensively on the biodegradation of its PVC additives/plasticizers; however, bio-based treatment approaches for its polymers have been scanty. The current review has discussed elaborately all possible PVC degradation processes and the toxicity challenges faced during its mitigation. This review has also delineated and assessed all physical, chemical, and biological approaches reported for PVC treatments. All the biodeterioration, biocatalysis, and biodegradation mechanisms reported for PVC have been comprehensively discussed. Recent advances have also been highlighted like the direct application of invertebrate species and selective enzymes like peroxidases, alkane monooxygenase, and laccase during PVC treatment. Insights of functional genomes/genes and OMICS have been recommended, which might help predict and address any future issues during the mitigation of PVC pollution in the environment.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998232","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}

{"title":"Long Noncoding RNA SNHG12 Regulates Ischemia/reperfusion (I/R)-mediated Acute Kidney Injury (AKI) Through miR-129-1-3p/Ubiquitin Specific Peptidase 25 axis.","authors":"Peng Huang, Lingzhang Meng, Jun Pang, Haiting Huang, Jing Ma, Linlin He, Xu Lin","doi":"10.1007/s12010-024-05148-2","DOIUrl":"https://doi.org/10.1007/s12010-024-05148-2","url":null,"abstract":"<p><strong>Objective: </strong>A growing body of evidence suggests the involvement of long noncoding ribose nucleic acids (lncRNAs) in acute kidney injury (AKI). This study focused on the mechanistic role of lncRNA small nucleolar RNA host gene 12 (SNHG12) in ischemia/reperfusion (I/R)-mediated AKI. A model of hypoxia/reoxygenation (H/R) was created using human kidney cells (HK-2). Expression levels of SNHG12 and miR-129-1-3p mRNAs, and USP25 protein were determined through quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting analyses, respectively. Furthermore, the relationship between SNHG12 and miR-129-1-3p, as well as miR-129-1-3p and Ubiquitin Specific Peptidase 25 (USP25), was investigated using dual-luciferase reporter gene, RNA pull-down, and immunoprecipitation assays. To further evaluate the role of SNHG12 in AKI, a mouse model was established to study the pathological changes in kidney tissues after SNHG12 knockdown. SNHG12 was upregulated in H/R-induced HK-2 cells and I/R-induced AKI mouse model. Conversely, the expression of miR-129-1-3p showed a significant downregulation. Through dual-luciferase assay and RNA pull-down analysis, it was demonstrated that SNHG12 interacted with miR-129-1-3p, and miR-129-1-3p acted as a negative regulator of USP25. Silencing SNHG12 attenuated the detrimental effect of H/R on HK-2 cells, which was counteracted by miR-129-1-3p antagomir. USP25 overexpression also reversed the effect of miR-129-1-3p on H/R-induced HK-2 cells. SNHG12 knockdown was further found to ameliorate I/R-induced renal injury, apoptosis, oxidative stress, and inflammation in AKI mouse model. SNHG12 was upregulated in I/R-induced AKI and its knockdown ameliorated AKI through the miR-129-1-3p/USP25 axis. SNHG12/miR-129-1-3p/USP25 axis serves as a potential therapeutic target for I/R-related renal injury.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142996680","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}

{"title":"Nicotine Ameliorates α-Synuclein Preformed Fibril-Induced Behavioral Deficits and Pathological Features in Mice.","authors":"Zhangqiong Huang, Yue Pan, Kaili Ma, Haiyu Luo, Qinglan Zong, Zhengcun Wu, Zhouhai Zhu, Ying Guan","doi":"10.1007/s12010-024-05086-z","DOIUrl":"https://doi.org/10.1007/s12010-024-05086-z","url":null,"abstract":"<p><p>Epidemiologic study suggests that nicotine reduces the risk of Parkinson's disease (PD) and thus could serve as a potential treatment. In this study, we aimed to investigate the effect of nicotine on the behavioral phenotypes and pathological characteristics of mice induced by human alpha-synuclein preformed fibers (α-syn-PFF). Mice were injected with 5 µg of human α-syn-PFF in the hippocampus while administering nicotine-containing drinking water (200 µg/mL). After 1 month, the motor ability, mood, spatial learning, and memory ability of the PD phenotype-like model mice were detected using open field, rotarod, Y maze, and O maze tests. The expression of pathological α-syn and apoptotic proteins, as well as the number of glial and neural stem cells in the hippocampus of mice, was detected using western blot and immunofluorescence. The results demonstrated that nicotine significantly reduced pathological α-syn accumulation, α-syn serine 129 phosphorylation, and apoptosis induced by α-syn-PFF injection in the hippocampus of mice. Nicotine also inhibited the increase in the number of glia, microglia, and neuronal apoptotic cells, and it decreased the expression of PI3K and Akt while also exhibiting significant memory impairment, motor deficits, and anxiety-like behavior. In conclusion, our findings suggest that nicotine ameliorates behavioral deficits and pathological changes in mice by inhibiting human α-syn-PFF-induced neuroinflammation and apoptosis.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997821","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}

{"title":"¹³C-metabolic flux analysis of respiratory chain disrupted strain ΔndhF1 of Synechocystis sp. PCC 6803.","authors":"Keisuke Wada, Yoshihiro Toya, Fumio Matsuda, Hiroshi Shimizu","doi":"10.1007/s12010-024-05138-4","DOIUrl":"https://doi.org/10.1007/s12010-024-05138-4","url":null,"abstract":"<p><p>Cyanobacteria are advantageous hosts for industrial applications toward achieving sustainable society due to their unique and superior properties such as atmospheric CO₂ fixation via photosynthesis. However, cyanobacterial productivities tend to be weak compared to heterotrophic microbes. To enhance them, it is necessary to understand the fundamental metabolic mechanisms unique to cyanobacteria. In cyanobacteria, NADPH and ATP regenerated by linear and cyclic electron transfers using light energy are consumed by CO₂ fixation in a central metabolic pathway. The previous study demonstrated that the strain deleted a part of respiratory chain complex (ΔndhF1) perturbed NADPH levels and photosynthetic activity in Synechocystis sp. PCC 6803. It is expected that disruption of ndhF1 would result in a decrease in the function of cyclic electron transfer, which controls the ATP/NAD(P)H production ratio properly. In this study, we evaluated the effects of ndhF1 deletion on central metabolism and photosynthesis by ¹³C-metabolic flux analysis. As results of culturing the control and ΔndhF1 strains in a medium containing [1,2-¹³C] glucose and estimating the flux distribution, CO₂ fixation rate by RuBisCO was decreased to be less than half in the ΔndhF1 strain. In addition, the regeneration rate of NAD(P)H and ATP by the photosystem, which can be estimated from the flux distribution, also decreased to be less than half in the ΔndhF1 strain, whereas no significant difference was observed in ATP/NAD(P)H production ratio between the control and the ΔndhF1 strains. Our result suggests that the ratio of utilization of cyclic electron transfer is not reduced in the ΔndhF1 strain unexpectedly.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982309","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}

{"title":"CircZMYM2 Alleviates TGF-β1-Induced Proliferation, Migration and Activation of Fibroblasts via Targeting miR-199b-5p/KLF13 Axis.","authors":"Yu Han, Jun Zhao, Xiuge Liao, Ruifeng Wang, Lixia Dong","doi":"10.1007/s12010-024-05168-y","DOIUrl":"https://doi.org/10.1007/s12010-024-05168-y","url":null,"abstract":"<p><p>Dysregulated circular RNAs (circRNAs) has been revealed to be involved in pulmonary fibrosis progression. Herein, this study focused on exploring the function and mechanism of circRNA Zinc Finger MYM-Type Containing 2 (circZMYM2) on idiopathic pulmonary fibrosis (IPF) using transforming growth factor (TGF)-β1-stimulated fibroblasts. Human fibroblast cell lines IMR-90 and HFL1 were stimulated with TGF-β1 to mimic fibrosis condition in vitro. Levels of genes and proteins were detected by qRT-PCR and western blotting. Cell proliferation and migration were analyzed using cell counting kit-8 assay, 5-Ethynyl-2'-deoxyuridine (EdU) and wound healing assays. The fibrosis progression was determined by the change of E-cadherin, α-smooth muscle actin (α-SMA), collagen type I α 1 (COL1A1) and collagen type III α 1 (COL3A1). The interaction between miR-199b-5p and circZMYM2 or KLF13 (Kruppel Like Factor 13) was analyzed using dual-luciferase reporter, RIP and RNA-pull-down assays. CircZMYM2 was decreased in TGF-β1-induced IMR-90 and HFL1 fibroblasts. Functionally, re-expression of circZMYM2 in IMR-90 and HFL1 cells could attenuate TGF-β1-evoked proliferation, migration and fibrosis in cells. Mechanistically, the circZMYM2/miR-199b-5p/KLF13 constituted a competing endogenous RNA (ceRNA). TGF-β1 reduced KLF13 expression and increased miR-199b-5p expression in IMR-90 and HFL1 cells. Further rescue experiments suggested that miR-199b-5p up-regulation or KLF13 knockdown reversed the anti-fibrotic effects of circZMYM2; moreover, silencing of miR-199b-5p exhibited anti-fibrotic effects, which was counteracted by KLF13 knockdown. CircZMYM2 had an anti-fibrotic effect that could suppress fibroblast activation via miR-199b-5p/KLF13 axis, pointing a novel perspective into the potential action pattern of circ_0022383 in IPF.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976776","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}

{"title":"Study on the Synergistic Effect of Klotho and KRAS on Reducing Ferroptosis After Myocardial Infarction by Regulating RAP1/ERK Signaling Pathway.","authors":"ChengZhe Cai, YiQin Wu, XiaoQian Feng, XianQu Ye, PingFang Liu, XiangJin Huang, ZhiJun Li, ZhuoFan Xu","doi":"10.1007/s12010-024-05171-3","DOIUrl":"https://doi.org/10.1007/s12010-024-05171-3","url":null,"abstract":"<p><p>Myocardial infarction (MI) is a coronary artery-related disease that seriously threatens human life and is the leading cause of sudden death worldwide, where a lack of nutrients and oxygen leads to an inflammatory response and death of cardiomyocytes. Ferroptosis is a form of non-apoptotic cell death associated with metabolic dysfunction, resulting in abnormal breakdown of glutamine and iron-dependent accumulation of reactive oxygen species (ROS) during metabolism. However, the molecular mechanism of ferroptosis in the pathogenesis of MI and the function of Klotho and KRAS on ferroptosis during MI remain unclear. The MI rat model was established by LAD ligation with a 6-0 suture. H9c2 cells were placed in glucose-deficient DMEM (Thermo) and cultured in an anaerobic environment (1% CO₂ and 5% CO) to establish an in vitro OGD cell model. The damage to rat heart tissue was detected by HE staining, and Klotho and KRAS were determined by RT-qPCR, Western Blot, and IHC. TUNEL staining was used to determine apoptosis in rat heart tissue samples. The interaction between Klotho and KRAS was verified by co-immunoprecipitation and Western Blot. The cardiomyocyte activity was measured by CCK-8 assay. LDH, CK-MB, cTnT, and Fe²⁺ markers were detected by the kits. For the assessment of ferroptosis, GSH and ROS in cardiomyocytes and serum were detected by kits, and PTSG was detected by Western Blot. IL-1β and IL-6 in cardiomyocytes and serum were determined by ELISA. Klotho was downregulated in MI. Downregulation of Klotho promoted myocardial injury; increased apoptosis of cardiomyocytes; promoted LDH, CK-MB, and cTnT concentrations; inhibited GSH; and promoted ROS levels, PTGS2 expression, and ferroptosis in rats. The same results were obtained in vitro. Klotho and KRAS had endogenous interactions. KRAS knockdown can reverse Klotho knockdown-mediated MI and ferroptosis. RAP1/ERK pathway was highly expressed in MI, and inhibiting RAP1/ERK pathway activation can reverse the promoting effect of overexpressed KRAS on MI progression and ferroptosis. Klotho interacts with KRAS and inhibits ferroptosis after MI by regulating the RAP1/ERK pathway.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976784","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}

{"title":"In Vitro Cytotoxic Potential and Integrated Network Pharmacology, Molecular Docking and Molecular Dynamic Approaches to Decipher the Mechanism of Gymnostachyum febrifugum Benth., in the Treatment of Breast Cancer.","authors":"K J Spandana, Wilson Joel Rodrigues, Sudeep D Ghate, R Shyama Prasad Rao, K R Chandrashekar, N Bhagya","doi":"10.1007/s12010-024-05173-1","DOIUrl":"https://doi.org/10.1007/s12010-024-05173-1","url":null,"abstract":"<p><p>Gymnostachyum febrifugum, a less-known ethnomedicinal plant from the Western Ghats of India, is used to treat various diseases and serves as an antioxidant and antibacterial herb. The present study aims to profile the cytotoxic phytochemicals in G. febrifugum roots using GC-MS/MS, in vitro confirmation of cytotoxic potential against breast cancer and an in silico study to understand the mechanism of action. Phytochemical profiling using GC-MS/MS showed the presence of eight cytotoxic molecules with lupeol in high abundance. A potent cytotoxic effect of G. febrifugum roots against breast cancer was also observed with antiproliferation, antimigration, inhibition in colony formation and death of breast cancer cells. Further, the cytotoxic potential of the plant was confirmed with the apoptosis of cells as observed in the flow cytometry. In silico network pharmacology, GO and KEGG analysis suggested the modulation of proteins of MAPK, PI3K-AKT and apoptosis pathways by lupeol to induce cytotoxicity in breast cancer. Further, dynamic simulation revealed MAPK and AKT as the major targets for lupeol. Our studies comprehensively elucidated the role of lupeol, a major phytochemical in G. febrifugum to induce cytotoxicity against breast cancer by targeting major cancer signaling pathways, providing a promising strategy and scientific basis to explore lupeol in targeted cancer therapy.</p>","PeriodicalId":465,"journal":{"name":"Applied Biochemistry and Biotechnology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963402","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}