MOLECULAR AND CELLULAR BIOCHEMISTRY分子与细胞生物化学
MOLECULAR AND CELLULAR BIOCHEMISTRY(英文缩写 MOL CELL BIOCHEM),ISSN 0300-8177,eISSN 1573-4919,中文译名:分子与细胞生物化学 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：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.842 | Q3 |
| 2022 | 4.300 | Q2 |
| 2023 | 3.500 | Q3 |
| 2024 | 3.700 | Q2 |
| 2025 | 4.700 | Q2 |
MOLECULAR AND CELLULAR BIOCHEMISTRY 最新收录文献
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1. Anti-inflammatory activity of Chlorella polysaccharide AHP.
1. 小球藻多糖AHP的抗炎活性PMID:日期:2026-09-30Current medications for inflammatory bowel disease (IBD) are associated with various side effects. Researches had shown that bioactive substances (such as polysaccharides) exhibited anti-inflammatory activity, immunomodulatory activity and the property of the regulation of gut microbiota, which could contribute to the repair of colonic tissue and the improvement of intestinal health. The bioactive substances provided a new direction for developing safe, effective and novel therapeutic strategies. Therefore, the objective of this study was to evaluate the efficacy and safety of Chlorella polysaccharide AHP for the treatment of Caco-2 cell injury and ulcerative colitis in mice. This study investigated the anti-inflammatory activity of polysaccharide extracted from Chlorella (AHP) and its mechanisms through in vitro and in vivo experiments. In vitro, AHP significantly reduced reactive oxygen species (ROS) level, suppressed apoptosis and downregulated the levels of proinflammatory factors in dextran sulfate sodium (DSS)-induced Caco-2 cells, demonstrating antioxidant and anti-inflammatory effects. In vivo, AHP alleviated pathological damage of colon, decreased oxidative stress and levels of pro-inflammatory cytokines, enhanced expression of tight junction proteins and repaired intestinal mucosal barrier in mice with DSS-induced colitis. Furthermore, AHP modulated gut microbiota composition and levels of related metabolites, contributing to its anti-inflammatory activity through microecological regulation. These findings indicated that AHP mitigated DSS-induced cell injury and colonic damage via multiple pathways, confirming its potent anti-inflammatory properties through in vitro and in vivo experiments. This study provided important theoretical basis for exploring new treatments of IBD with bioactive substance AHP and developing functional foods based on AHP.
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2. Phytoestrogens and related microbial metabolites remodel aberrant prostate transcriptomic profiles generated upon exposure to oxidative stress.
PMID:日期:2026-09-24Dietary phytoestrogens, including pterostilbene (PTS) from berries and genistein (GEN) from soybeans, exert anti-oxidant and anti-inflammatory effects in prostate cancer. However, the specific actions in regulation of cell biology and homeostasis in normal prostate epithelial cells remain unknown and a prominent research gap refers to the effects of related microbial metabolites of phytoestrogens. We therefore explored effects of distinct phytoestrogens, PTS and GEN, and PTS microbial metabolite, pinostilbene (PNS), in healthy cells with disrupted homeostasis. Human RWPE-1 prostate epithelial cells were treated with 100 µM concentration of hydrogen peroxide (HO). The HO-challenged cells were then exposed to phytoestrogens, followed by RNA sequencing. Transcriptomics revealed 1,770 differentially expressed genes (DEGs) upon HO exposure. Upregulated genes were functionally implicated in immune signaling and inflammatory pathways, whereas downregulated genes were linked to autophagy, homeostasis, and cellular architecture. A quantitative metric termed the Weighted Recovery Ratio (WRR) was developed to quantify the extent that the treatment reversed gene expression change induced upon H₂O₂ challenge. WRR indicated that PNS recovered the highest number of HO-responsive genes. Among all PTS and PNS DEGs, 47% and 69%, respectively, constituted partially or fully recovered HO-responsive genes. This fraction was only 9% for GEN. PTS and PNS, but not GEN, recovered genes involved in DNA methylation/demethylation, which suggests restoration of DNA methylation equilibrium that was disrupted by HO. Our findings provide a novel tool to quantify the relative efficacy of phytoestrogens in attenuating alterations caused by an oxidative stressor. We present evidence for differential action of phytoestrogens with distinct chemical structures and for more potent action of microbial metabolites derived from phytoestrogens.
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3. METTL3‑mediated OTUB1 sustains PD‑L1 protein stability via deubiquitination and promotes immune evasion in oral squamous cell carcinoma.
PMID:日期:2026-09-23Immune evasion facilitates the progression of oral squamous cell carcinoma (OSCC). This study investigates how METTL3-mediated OTUB1 modulates PD-L1 ubiquitination and promotes immune evasion in OSCC. OTUB1 expression was analyzed in tumor and adjacent normal tissues from OSCC patients. OTUB1 knockdown experiments were performed in HN-6 cells. The relationship between OTUB1 and PD-L1 was detected. OTUB1-knockdown HN-6 cells were co-cultured with activated PBMCs, and tumor immunity was subsequently assessed. Tumor growth and immunity were observed in a mouse model injected with HN-6 cells transfected with si-OTUB1 and oe-PD-L1. The mechanistic interaction among METTL3, YTHDF1, and OTUB1 was determined, as well as their action in mouse tumor models. OTUB1 was upregulated in OSCC and correlated with poor prognosis. Knocking down OTUB1 directly increased PD-L1 ubiquitination levels, downregulated PD-L1 protein abundance, and weakened the binding between tumor cells and PD-1. OSCC cells with OTUB1 knockdown were co-incubated with PBMCs, resulting in enhanced apoptosis of OSCC cells, increased CD4⁺/CD8⁺ T cell infiltration, reduced FoxP3⁺ Tregs, exhausted CD8⁺ T cell subsets, and elevated GzmB/IFN-γ production. METTL3 mediated m⁶A modification of OTUB1 mRNA, which enhanced the stability of OTUB1 mRNA and upregulated OTUB1 expression through the reader protein YTHDF1. In vivo experiments confirmed that METTL3 promoted OSCC progression and immune evasion via mA-dependent OTUB1 regulation and subsequent PD-L1-mediated CD8⁺ T cell suppression. METTL3 stabilizes OTUB1 mRNA through mA methylation, upregulates PD-L1 expression, and promotes immune evasion, thereby accelerating OSCC progression.
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4. 18β-glycyrrhetinic acid ameliorates ifosfamide-induced nephrotoxicity by suppressing Wnt3a/IL-17A-driven inflammatory signaling, ER stress, and apoptosis while preserving ZO-1 integrity.
4. 18β-甘草次酸通过抑制Wnt3a/IL-17A驱动的炎症信号、内质网应激和细胞凋亡，同时维持ZO-1完整性，改善异环磷酰胺诱导的肾毒性PMID:日期:2026-09-21Ifosfamide (IFO) is an effective chemotherapeutic agent, but its clinical use is limited by dose-dependent nephrotoxicity. This study investigated the protective effects of 18β-glycyrrhetinic acid (18β-GA) against IFO-induced acute renal injury and explored the underlying molecular mechanisms. Twenty-eight male Wistar albino rats were divided into four groups: Control, 18β-GA, IFO, and IFO+18β-GA. 18β-GA was administered orally at 100 mg/kg/day for two consecutive days, while nephrotoxicity was induced by a single intraperitoneal injection of IFO at 500 mg/kg. Renal function markers, oxidative stress parameters, inflammatory and apoptotic gene expression, Wnt3a/IL-17 A/ACT1/TRAF6 and Notch/HES1 signaling pathways, histopathological alterations, ZO-1 integrity, and CHOP expression were evaluated. IFO markedly impaired renal function, increased serum urea and creatinine levels, enhanced lipid peroxidation, depleted antioxidant defenses, and induced severe histopathological damage. IFO also upregulated NF-κB, TNF-α, Bax, Caspase-3, Wnt3a, IL-17 A, ACT1, TRAF6, Notch, and HES1 expression, while reducing Bcl-2 expression. In addition, IFO increased CHOP immunoreactivity and disrupted ZO-1 expression in tubular epithelial cells. Co-treatment with 18β-GA significantly improved renal function, restored antioxidant capacity, and was associated with the suppression of inflammatory and apoptotic signaling, downregulation of Wnt3a/IL-17 A/ACT1/TRAF6 and Notch/HES1 activation, reduced CHOP expression, preserved ZO-1 immunoreactivity, and ameliorated renal histological injury. These findings suggest that 18β-GA exerts potential multi-target renoprotective effects against IFO-induced nephrotoxicity by modulating oxidative stress, inflammation, ER stress, apoptosis, developmental signaling, and epithelial junctional integrity.
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5. Itaconate metabolism in regulated cell death.
PMID:日期:2026-09-21Itaconate, a metabolite generated from the tricarboxylic acid cycle through aconitate decarboxylase 1 (ACOD1, also known as IRG1), has emerged as a key link between cellular metabolism, immunity, and regulated cell death. Although initially recognized for its anti-inflammatory properties, accumulating evidence indicates that the biological functions of itaconate extend far beyond immunomodulation to encompass multiple forms of regulated cell death. The ACOD1-itaconate axis regulates apoptosis, ferroptosis, pyroptosis, necroptosis, and other emerging cell-death programs through coordinated control of mitochondrial metabolism, redox homeostasis, inflammatory signaling, and covalent protein modification. These effects are context dependent and are further shaped by the distinct biological activities of endogenous itaconate, synthetic derivatives, and the recently recognized itaconate-independent functions of ACOD1. In this review, we summarize recent advances in immunometabolism and regulated cell death, discuss the mechanistic basis by which the ACOD1-itaconate axis governs cell fate, and highlight how intercellular metabolic communication and non-canonical ACOD1 signaling expand its biological functions. We also highlight unresolved questions regarding target selectivity, context-dependent signaling, and therapeutic translation. A deeper understanding of the ACOD1-itaconate network may provide new insights into therapeutic strategies targeting regulated cell death in inflammatory diseases, infection, and cancer.
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6. Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.
6. 癌症基因治疗的机会：抑制MDM2并恢复p14ARF以激活p53PMID:日期:2026-09-21The MDM2/p53/p14ARF axis represents a central regulatory network controlling cell-cycle progression, genomic stability, and tumor suppression, and is frequently deregulated in human cancers. In many malignancies, particularly those retaining wild-type TP53, p53 activity is functionally suppressed through MDM2 overexpression or CDKN2A (p14ARF) loss, events that may be reversed in order to activate this pathway. This review explores the biological basis of the MDM2/p53/p14ARF axis and its relevance as a target for gene therapy and multimodal treatment strategies. While gene therapy for the restoration of p53 has been extensively explored, the use of genetic interventions for the inhibition of MDM2 or the restoration of p14ARF is underrepresented, though they have the potential to re-establish DNA damage responses, promote apoptosis, and enhance tumor sensitivity to chemotherapy and radiotherapy. In addition, p53 activation is now recognized as a contributor to immunogenic cell death and modulation of the tumor microenvironment. Laboratory and early clinical studies demonstrate that inhibition of MDM2 and restoration of p14ARF by gene transfer can integrate tumor cytotoxicity with immune activation. Although large-scale clinical validation remains limited, current evidence supports the MDM2/p53/p14ARF axis as a promising, context-dependent target within biomarker-driven combination therapies rather than a standalone approach.
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7. NRF2 signaling drives chemoresistance in NSCLC and glioblastoma.
PMID:日期:2026-09-19Although great advances have been made in cancer treatment, lung cancer and glioblastoma patients continue to present a dismal prognosis, mainly due to drug resistance. Evidence suggests that NRF2 and glutathione (GSH) play a fundamental role in chemotherapy resistance. Notably, GSH depletion by buthionine sulfoximine (BSO) has been demonstrated to sensitize human tumor cells to a wide variety of chemotherapeutic agents. However, the incorporation of BSO into standard chemotherapy regimens lacks a robust clinical rationale. In this study, we aimed to investigate the mechanisms governing differential sensitivity to chemotherapy in lung cancer and glioblastoma cells to identify novel strategies to enhance outcomes in these malignancies. For this purpose, we analyzed several cellular responses in cell lines exhibiting distinct sensitivities to temozolomide (TMZ) and cisplatin. Our findings indicate that the NRF2/GSH pathway plays a crucial role in TMZ and cisplatin resistance and that pharmacological GSH depletion enhances the sensitivity of NRF2-high, chemotherapy-resistant cells to these agents. Furthermore, BSO in combination with TMZ or cisplatin enhanced chemotherapy-induced cytotoxicity and engaged both apoptotic and ferroptosis-related responses in NSCLC cells. These findings provide preclinical evidence supporting further investigation of NRF2/GSH targeting as a strategy to overcome chemotherapy resistance.
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8. Regulation of the murine preadipocytes differentiation by bitter taste receptor Tas2r108 and Tas2r126.
8. 苦味受体Tas2r108和Tas2r126对小鼠前脂肪细胞分化的调控PMID:日期:2026-09-19Taste 2 receptors (T2Rs) are known as receptors for sensing bitterness, but their gene expressions are observed in various extraoral tissues. T2Rs in adipocytes have attracted attention because bitter compounds influence lipid accumulation. However, the role of T2Rs in adipocytes has not been extensively investigated. This study investigated the functions of Tas2r108 and Tas2r126 in preadipocyte differentiation. Overexpression of Tas2r108 or Tas2r126 inhibited the differentiation of 3T3-L1 cells and mouse primary preadipocytes. Similarly, knockdown of Tas2r108 suppressed the differentiation of these cells. Consistent with the knockdown results, stimulation with T2R agonists during the differentiation of 3T3-L1 cells enhanced adipogenesis. Mechanistic analysis revealed that the suppressed differentiation by T2R overexpression involves the downregulation of Cebpb, while T2R knockdown involves the upregulation of Nr4a2 and Nr4a3 and downregulation of Egr2. Analysis with T2R agonists revealed that T2Rs in preadipocytes couple with inhibitory G-protein to downregulate intracellular cAMP concentrations, which works through ERK to enhance adipogenesis. These results demonstrate the regulation of adipocyte differentiation by T2Rs and suggest that bitter compounds enhance adipogenesis via T2Rs.
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9. Integrative multi-omics analysis identifies LIPA as a prognostic hub and ferroptosis regulator in lung adenocarcinoma.
9. 整合多组学分析确定LIPA作为肺腺癌的预后枢纽和铁死亡调节因子PMID:日期:2026-09-19Lung adenocarcinoma (LUAD) remains one of the leading causes of cancer mortality, underscoring the urgent need for biomarkers and therapeutic targets rooted in metabolic reprogramming. By integrating multi-omics analyses with experimental validation, we identified 67 lipid metabolism-related genes dysregulated in LUAD and constructed a five-gene prognostic signature via LASSO regression; lower expression of the signature genes correlated with poor survival. Single-cell and spatial transcriptomics revealed cell-type-specific dysregulation of the hub gene LIPA, which was upregulated in monocytes but downregulated in macrophages within the tumor microenvironment. Functional assays demonstrated that LIPA overexpression inhibited tumor proliferation in vitro and suppressed orthotopic tumor growth in vivo, at least in part through a ferroptosis-dependent mechanism involving TXNIP and ALOX5. Virtual screening further identified Castanospermine as a potential LIPA activator; treatment elevated LIPA expression, modulated the CD4+/CD8 + T-cell ratio, and attenuated tumor progression in mice. Collectively, these findings establish LIPA as a critical link between lipid metabolism, ferroptosis, and immune modulation in LUAD, and provide a prognostic signature for risk stratification as well as a candidate compound for targeting lipid metabolic vulnerabilities.
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10. SERPINE1 promotes CRC cell invasion and metastasis through resistance to anoikis.
10. SERPINE1通过抵抗失巢凋亡促进结直肠癌细胞的侵袭和转移PMID:日期:2026-09-19Colorectal cancer (CRC) is one of the most common and lethal malignancies worldwide, and its tumor ecosystem remains highly complex and incompletely understood. Here, we analyzed 3,264 single-cell transcriptomes from primary CRC tumors obtained from nine patients in the GSE110009 dataset. We identified 15 distinct cell clusters corresponding to seven major cell types. Trajectory inference (pseudotime analysis) was performed to characterize lineage relationships and cellular developmental trajectories. Genes associated with distinct expression programs were classified into two clusters exhibiting different tumor microenvironment (TME) characteristics. Functional enrichment analysis revealed that epithelial-mesenchymal transition (EMT) plays a critical role in CRC tumorigenesis and metastasis. Moreover, we established a novel three-gene prognostic signature that effectively predicts clinical outcomes in CRC patients. Further analyses revealed that SERPINE1 promotes CRC cell invasion and metastasis by enhancing resistance to anoikis. Furthermore, SERPINE1 was found to enhance the malignant phenotype of metastatic colorectal cancer cells. Collectively, these findings reveal the immunosuppressive landscape of the CRC TME, provide new insights into CRC progression, and identify SERPINE1 as a potential prognostic biomarker and therapeutic target.