BIOLOGICAL PROCEDURES ONLINE生物学实验方法在线
BIOLOGICAL PROCEDURES ONLINE(英文缩写 BIOL PROCED ONLINE),ISSN 1480-9222,eISSN 1480-9222,中文译名:生物学实验方法在线 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
BIOLOGICAL PROCEDURES ONLINE 最新收录文献
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2. Identification and Validation of Genes Involved in Immune and Ferroptosis in Polycystic Ovarian Syndrome Using Bioinformatics and Experimental Approach.
PMID:日期:2026-07-22Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine and metabolic disease. This study aimed to investigate the synergistic role of immune dysregulation and ferroptosis during the pathogenesis of PCOS. Through integrating multiple Gene Expression Omnibus (GEO) datasets, differentially expressed genes (DEGs) were screened and subjected to functional enrichment analysis; weighted gene co‑expression network analysis combined with LASSO, RandomForest, and support vector machine‑recursive feature elimination algorithms were employed to identify key candidate genes; in vitro, human ovarian granulosa cells (KGN) were treated with dihydrotestosterone (DHT), NNMT expression was regulated via lentiviral vectors together with ferroptosis inhibitor intervention, and cell viability, cytotoxicity, and ferroptosis‑related indicators were examined; in vivo, a PCOS mouse model was established using dehydroepiandrosterone, and ovarian pathology, hormone levels, as well as molecular expression of the ferroptosis pathway were analyzed. DEGs in PCOS were significantly enriched in immune response and ferroptosis pathways. Twelve candidate genes were identified through screening multiple GEO datasets and demonstrated diagnostic potential. DHT induced ferroptosis in KGN cells by upregulating NNMT, manifesting as reduced cell viability, increased LDH release, accompanied by Fe²⁺ accumulation, enhanced lipid peroxidation, downregulation of SLC7A11/GPX4, and upregulation of ACSL4. This process could be partially reversed by ferroptosis inhibitors. Knockdown of NNMT effectively alleviated the DHT‑induced ferroptosis phenotype. Ovaries from PCOS mice exhibited typical pathological alterations, concurrent with elevated NNMT expression and abnormal activation of the ferroptosis pathway. This study has uncovered novel mechanisms underlying the development and progression of PCOS, offering potential targets for its diagnosis and treatment.
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3. Huangjing Jiangzhi Granules Ameliorate Nonalcoholic Fatty Liver Disease by Activating the FOXA1-DERL1 Regulatory Axis to Suppress Lipid Accumulation, Endoplasmic Reticulum Stress, and Apoptosis.
3. 黄精降脂颗粒通过激活FOXA1-DERL1调节轴抑制脂质积聚、内质网应激和细胞凋亡来改善非酒精性脂肪肝PMID:日期:2026-07-21Nonalcoholic fatty liver disease (NAFLD) is an emerging health issue worldwide. It involves intrahepatic lipid accumulation that is potentially deleterious. Traditional Chinese Medicine called Huangjing Jiangzhi (HJJZ) granules holds promise for NAFLD treatment. This study explored the mechanism by which HJJZ granules improve NAFLD in male C57BL/6 mice and oleic acid-induced HepG2 cells.H&E staining, Oil Red O staining, the TUNEL assay, and Western blotting were employed. Chromatin immunoprecipitation and dual-luciferase reporter assays were used to examine transcriptional regulation.HJJZ granules alleviated hepatic steatosis, reduced serum ALT/AST levels, improved lipid profiles, suppressed hepatocyte apoptosis, and inhibited the PERK-eIF2α-CHOP pathway in high-fat diet-fed mice and oleic acid-treated cells. These granules specifically upregulated the expression of the transcription factor FOXA1. FOXA1 knockdown abolished all protective effects of HJJZ granules. Mechanistically, FOXA1 was shown to transcriptionally activate DERL1 expression. DERL1 overexpression rescued the steatotic, apoptotic, and endoplasmic reticulum (ER) stress phenotypes in FOXA1-deficient cells.HJJZ granules ameliorate NAFLD by attenuating lipid accumulation, apoptosis, and ER stress. This protective effect is mediated through FOXA1 upregulation, which, in turn, transcriptionally enhances DERL1 expression, thereby mitigating ER stress. The FOXA1/DERL1 axis is a critical mechanistic pathway for HJJZ granule action.
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4. Therapeutic Mechanisms of Ruangan Huayu Formula in Liver Cirrhosis: Network Pharmacology, Molecular Docking and Experimental Validation.
PMID:日期:2026-07-18Liver cirrhosis remains a challenging global health issue for which current treatment options are largely limited to managing acute liver failure, with no definitive curative therapies available. The Ruangan Huayu Formula (RGHY) has shown promising clinical effects in recent years; however, its comprehensive chemical profile and the specific mechanisms underlying its anti-cirrhotic activity remain to be fully elucidated. Ultra-high-performance liquid chromatography-Orbitrap-explorative mass spectrometry (UHPLC-OE-MS) was performed to characterize the chemical profile of the RGHY. Network pharmacology and molecular docking were leveraged to identify potential targets and pathways. Antifibrotic efficacy and underlying mechanisms of RGHY were evaluated using a thioacetamide (TAA)-induced liver fibrosis model in male Sprague-Dawley rats, along with transforming growth factor-beta (TGF-β)-stimulated human hepatic stellate cells (LX-2) in vitro. UHPLC-OE-MS study showed various chemical components of RGHY. Network pharmacology analysis revealed 57 intersecting targets, with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway standing out. Molecular docking studies returned strong binding scores for AKT1, SRC, PIK3CA, and STAT3 as core targets key to RGHY compounds. RGHY was shown to significantly alleviate TAA-induced liver injury and fibrosis by down-regulating the PI3K/AKT pathway. In vitro, RGHY-containing serum and its key bioactive compounds (7,3',4'-trihydroxyflavone and sulfuretin) disrupted TGF-β-induced LX-2 cell activation, migration, and fibrogenesis. The PI3K/AKT signaling pathway was confirmed to involve in mediating the antifibrotic effects of RGHY. RGHY and its bioactive compounds 7,3',4'-trihydroxyflavone and effectively attenuated liver fibrosis and hepatic stellate cell activation through multicomponent, multitarget actions, primarily by modulating the PI3K/AKT pathway. These findings provide mechanistic evidence supporting its traditional use and its potential as a therapeutic candidate for liver cirrhosis.
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5. High Expression of SAMM50 Indicates Poor Clinical Prognosis in Hepatocellular Carcinoma and Represents a Potential Novel Biomarker.
PMID:日期:2026-07-11Identifying diagnostic and prognostic biomarkers and therapeutic targets for hepatocellular carcinoma (HCC) is essential to improve risk stratification, guide individualized treatment, and enhance therapeutic efficacy.The expression of SAMM50 (Sorting and Assembly Machinery Component 50) was initially analyzed in publicly accessible curated genomic and proteomic databases, such as the Cancer Cell Line Encyclopedia, the Human Protein Atlas, and other HCC-specific repositories. This analysis revealed differential expression patterns between HCC and non-neoplastic liver tissue. Subsequently, clinicopathological data and tissue specimens were collected from 200 HCC patients who underwent treatment at our institution. The protein and transcript levels of SAMM50 were experimentally measured in paired HCC and adjacent non-tumorous tissues using immunohistochemistry (IHC) and quantitative reverse transcription polymerase chain reaction (qRT-PCR). The association between SAMM50 expression and key clinicopathological features was further evaluated. Univariate and multivariate Cox proportional hazards analyses were performed to determine the independent prognostic value of SAMM50 expression in HCC. Based on these results, a reproducible and clinically applicable nomogram, supported by a forest plot, was constructed to facilitate prognostic prediction and support individualized therapeutic decision-making. Finally, in vitro and in vivo experiments were conducted to characterize the phenotypic alterations in HCC cells after SAMM50 knockdown, thereby confirming its involvement in critical oncogenic behaviors.This research demonstrated that the mRNA and protein levels of SAMM50 in HCC tissues were elevated compared to those in normal liver and adjacent tissues. Immunohistochemistry findings confirmed that SAMM50 protein levels were persistently higher in HCC tissues than in paired adjacent tissues. High expression of SAMM50 was correlated with unfavorable clinicopathological factors, encompassing pretreatment alpha-fetoprotein (AFP) levels, tumor size, T stage, American Joint Committee on Cancer (AJCC) stage, histological grade, and worse overall survival.Specifically, high expression of SAMM50 was linked to shorter overall survival (OS), progression-free survival (PFS), and disease-free survival (DFS). Moreover, univariate and multivariate Cox analyses were conducted to investigate the association between SAMM50 expression and clinicopathological features in HCC patients and to identify independent prognostic factors. The area under the receiver operating characteristic (ROC) curve (AUC) for SAMM50 was 0.863, suggesting its potential as a diagnostic marker for HCC, though further validation in independent cohorts is needed. Silencing of SAMM50 inhibited HCC cell proliferation, migration, and invasion, promoted apoptosis in vitro, and suppressed HCC growth in vivo.This research demonstrates that SAMM50 shows potential diagnostic value for HCC, though this observation requires further validation in larger, independent, and prospective cohorts. The results of this study not only contribute to the evaluation of baseline data and risk stratification in HCC but also offer novel approaches for the development of precise treatment strategies and targeted therapies.
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6. MKRN1 suppresses cuproptosis in colorectal cancer through ubiquitin-dependent regulation of SLC31A1.
PMID:日期:2026-07-07Despite the emerging role of cuproptosis in cancer biology, the regulatory mechanism by which ubiquitination modulates this process through MKRN1 and SLC31A1 in colorectal cancer (CRC) progression remains unclear. This study aimed to elucidate the functional relationship between MKRN1, SLC31A1, and cuproptosis in CRC. Stable MKRN1-knockdown and MKRN1-overexpressing colorectal cancer (CRC) cell lines were established. Cuproptosis was induced using elesclomol and copper sulfate, and assessed by cell viability assays,, measurement of intracellular copper levels, and western blot analysis of hallmark proteins (HSP70 and DLAT). The MKRN1-SLC31A1 interaction was examined by co-immunofluorescence, ubiquitination assays (employing MG132, CHX, and linkage-specific ubiquitin mutants), and quantitative real-time PCR (q-PCR). Mitochondrial function was evaluated via JC-1 staining and transmission electron microscopy. Rescue experiments were conducted using dual genetic manipulation of MKRN1 and SLC31A1. Finally, in vivo validation was performed using a xenograft model in NOD-SCID mice. MKRN1 overexpression significantly attenuated cuproptosis agonist-induced cytotoxicity and reduced intracellular copper accumulation. Mechanistically, MKRN1 directly interacts with SLC31A1 and promotes its polyubiquitination and subsequent proteasomal degradation. This degradation prevents copper overload, helping to maintain mitochondrial integrity.(as evidenced by maintained mitochondrial membrane potential and Tomm20 expression) and suppressing key cuproptosis hallmarks, including HSP70 induction and DLAT oligomerization. Genetic rescue experiments confirmed that SLC31A1 knockdown reversed the cuproptosis sensitivity conferred by MKRN1 depletion. Consistently, MKRN1 overexpression promoted tumor growth in vivo while concurrently suppressing cuproptosis. In summary, MKRN1 suppresses copper-induced cell death in colorectal cancer by promoting the ubiquitination and proteasomal degradation of the copper transporter SLC31A1, thus limiting copper accumulation and mitochondrial toxicity. This mechanism confers resistance to copper-induced cell death and facilitates tumor progression, establishing the MKRN1/SLC31A1 axis as a promising therapeutic target.
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7. Ethacrynic Oxadiazole 6u Induces Apoptosis by Targeting mTOR/c-Flip Axis and Noxa in Lymphoma Cells.
PMID:日期:2026-07-03Evasion of apoptosis is a major cause of therapy failure in lymphoma. We studied a covalent compound 6u with an α, β-saturated carbonyl group derived from the diuretic drug ethacrynic acid to induce apoptosis of lymphoma cells by targeting antiapoptotic proteins. We found that 6u induces apoptosis in 4 lymphoma cell lines, Daudi, Romas, Jeko-1 and Jurkat, accompanied by down-regulation of c-Flip and Mcl-1, as well as upregulation of Noxa. The down-regulation of Mcl-1 relies on Noxa induction and that the down-regulation of c-Flip is mediated by inhibiting protein synthesis pathway through covalent binding to mTOR complexes. Overexpression of c-Flip and silencing Noxa attenuate 6u-induced apoptosis. 6u modified with the saturated carbonyl structure loses the mTOR inhibition and apoptosis induction abilities. 6u exhibits potent anti-lymphoma effects in mantle cell lymphoma Jeko-1 xenografts without causing toxicity. 6u functions as an apoptosis inducer through the α, β-saturated carbonyl group to decrease c-Flip and to induce Noxa. 6u represents a new type of covalent agent for targeting lymphoma by inducing apoptosis.
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8. Development and Comparison of Two Rabbit Tibiofemoral Joint Replacement Models.
PMID:日期:2026-07-03Joint arthroplasty, replacement of damaged articular surfaces with a prosthetic component, is an increasingly common orthopaedic procedure. Despite the overall success of arthroplasty, complications such as periprosthetic joint infection remain a persistent problem with severe consequences. With increasing clinical demands, the need for a reliable, reproducible model for testing therapeutic strategies for arthroplasty complications is fundamental. In this study, a novel small animal model was designed and evaluated for downstream investigations. Two different implant designs (tibial vs. femoral) and surgical approaches were compared. The femoral implant resulted in fewer complications such as knee joint destabilization, severe swelling, and erosion of articular cartilage and subchondral bone. Rabbit care methodology was also optimized during model development, and both the process and results are presented to promote ethical and reproducible preclinical model research. The custom porous coated unicondylar femoral implant with a polished condylar surface demonstrated far fewer complications and adverse events than the tibial implant, as well as robust osseointegration. This will serve as a model for future investigations in preventing and treating joint arthroplasty complications.
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9. A novel prognostic model based on MVIRGs identifies ANGPT2 as a key target driving the malignant progression of HCC.
9. 一种基于MVIRGs的新型预后模型将ANGPT2确定为驱动HCC恶性进展的关键靶点PMID:日期:2026-05-29Hepatocellular carcinoma (HCC) is a highly lethal malignancy with high recurrence and limited therapies. Microvascular invasion (MVI) is a critical prognostic factor, but its molecular mechanisms and precise predictive tools are lacking. This study aimed to identify key MVI-associated genes (MVIRGs), develop a prognostic model, and elucidate the role of ANGPT2 in HCC progression and therapeutic responses. Machine learning on multi-cohort data (TCGA, ICGC) identified MVIRGs and constructed a prognostic model. ANGPT2, the core oncogenic MVIRG, was validated clinically (IHC) and functionally (in vitro and in vivo). We analyzed its association with the tumor immune microenvironment (TIME), immune checkpoint inhibitors (ICIs), and drug sensitivity. A powerful six-MVIRG prognostic model was developed, with ANGPT2 identified as the sole oncogenic gene. Clinically, ANGPT2 was significantly overexpressed, correlating strongly with aggressive features like MVI, vascular invasion, and advanced stages, serving as a robust poor prognostic biomarker for OS and PFS. Functionally, ANGPT2 knockdown significantly inhibited HCC cell growth and migration in vitro, and inhibited tumor growth in vivo. Bioinformatics revealed ANGPT2 fosters an immunosuppressive TIME, upregulating immune checkpoints (e.g., PD-L1) to mediate resistance to ICIs. High ANGPT2 expression showed a differential drug response: resistance to targeted therapies (e.g., EGFR-TKIs) but paradoxically increased sensitivity to chemotherapies (e.g., docetaxel, paclitaxel). This study constructed a powerful MVIRG model and identified ANGPT2 as a core oncogenic molecule. ANGPT2 drives HCC progression, mediates immune resistance, and differentially regulates drug sensitivity, making it a key biomarker for prognosis and treatment guidance.
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10. Lipid Metabolic Rewiring During Continuous Prostate Cancer Progression Defines a Biologically Relevant Four-Gene Prognostic Signature.
10. 癌症持续进展过程中的脂质代谢再配线定义了生物学相关的四基因预后特征PMID:日期:2026-05-25Lipid metabolic reprogramming is increasingly recognized as a critical feature of prostate cancer progression, but the lipid metabolism-related genes that remain continuously dysregulated from normal tissue to primary tumor and metastatic disease have not been systematically characterized, and their biological and prognostic relevance remains incompletely understood. To identify lipid metabolism-related genes associated with continuous prostate cancer progression and develop a prognostic signature for survival stratification. Clinical prostate cancer specimens and a high-fat diet (HFD)-driven RM-1 tumor model were first used to evaluate lipid metabolic alterations in vivo. GSE6919 transcriptomic data were used to identify genes shared between the Normal-Primary and Primary-Metastatic transitions. These genes were intersected with a curated lipid metabolism-related gene set, followed by GO and KEGG enrichment analyses. TCGA prostate adenocarcinoma expression and clinical data were used for LASSO regression to construct a prognostic model. The four core genes were further evaluated by clinicopathological correlation analysis, protein- and transcript-level validation in clinical tissues and prostate cancer cell lines, and functional assays under oleic acid-induced lipid stress. Immune infiltration analysis, ssGSEA, and nomogram analysis were performed to assess the biological and clinical relevance of the model. Clinical tissues showed increased PLIN3 expression, and HFD feeding promoted tumor growth and reinforced lipid metabolic alterations in vivo. A total of 44 lipid metabolism-related genes were identified as continuously dysregulated during prostate cancer progression. These genes were mainly enriched in fatty acid metabolism, lipid catabolism, peroxisome, lipid droplet, glycolysis/gluconeogenesis, arachidonic acid metabolism, and PPAR signaling. Eight genes were significantly associated with overall survival in TCGA, and a four-gene signature comprising ALDH3A2, ENO2, PPP1CB, and PTGIS was established. This model effectively stratified patients into high- and low-risk groups with significantly different survival outcomes. The risk score was positively associated with clinical T stage and Gleason score. The four core genes were also associated with lipid metabolic enzymes, immune infiltration patterns, and multiple metabolism-related pathways. Protein- and transcript-level validation in clinical tissues and prostate cancer cell lines supported the biological relevance of the signature, although PTGIS showed a more context-dependent pattern. Functionally, silencing ENO2 reduced oleic acid-induced lipid peroxidation, whereas silencing PPP1CB enhanced it, while ALDH3A2 showed a more context-dependent effect. A nomogram integrating the risk score with clinical variables improved individualized survival prediction. We identified lipid metabolism-related genes continuously dysregulated during prostate cancer progression and established a four-gene prognostic signature with potential value for survival prediction and risk assessment. These findings highlight lipid metabolic rewiring as an important component of prostate cancer evolution and provide candidate biomarkers for future mechanistic and translational studies.