Biochimica et biophysica acta. Reviews on cancer最新文献

Cancer-associated fibroblasts-derived exosomes in colorectal cancer progression: Mechanism and therapeutic opportunities 结直肠癌进展中癌症相关成纤维细胞衍生外泌体：机制和治疗机会

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-27 DOI: 10.1016/j.bbcan.2026.189545

Linling Yang , Parastoo Akbarabadi , Sadegh Babashah

Colorectal cancer (CRC) progression is profoundly shaped by the tumor microenvironment. Among stromal components, cancer-associated fibroblasts (CAFs) release small extracellular vesicles (exosomes) that deliver miRNAs, lncRNAs, circRNAs, proteins, and metabolites to malignant and immune cells. In CRC, CAF-derived exosomes (CAF-Exo) drive epithelial–mesenchymal transition, sustain stemness, stimulate angiogenesis, suppress antitumor immunity, and promote resistance to fluoropyrimidines and oxaliplatin. Representative mechanisms include exosomal miR-92a-3p activation of Wnt/β-catenin signaling, the lncRNA WEE2-AS1–mediated suppression of Hippo restraint with YAP activation, and circRNA cargos that reprogram autophagy or endothelial dynamics. Circulating CAF-Exo signatures are emerging as minimally invasive biomarkers for diagnosis, prognosis, and therapy stratification. However, translation remains limited by CAF heterogeneity, cargo variability, and incomplete in vivo characterization of vesicle dynamics. Therapeutic opportunities include blockade of exosome biogenesis or uptake, pharmacologic reprogramming of CAFs, and engineering vesicles to deliver targeted inhibitors or RNA-based therapeutics. This review synthesizes current mechanistic insights, evaluates biomarker potential, and outlines clinical priorities for targeting CAF-exosomal pathways in CRC.

结直肠癌（CRC）的进展深受肿瘤微环境的影响。在基质成分中，癌症相关成纤维细胞（CAFs）释放小的细胞外囊泡（外泌体），将mirna、lncrna、circrna、蛋白质和代谢物传递给恶性细胞和免疫细胞。在结直肠癌中，cafo衍生外泌体（cafo - exo）驱动上皮-间质转化，维持干细胞，刺激血管生成，抑制抗肿瘤免疫，促进对氟嘧啶和奥沙利铂的耐药性。具有代表性的机制包括外泌体miR-92a-3p激活Wnt/β-catenin信号，lncRNA wee2 - as1介导的Hippo抑制与YAP激活，以及重编程自噬或内皮动力学的circRNA载体。循环ca - exo标记正在成为诊断、预后和治疗分层的微创生物标志物。然而，翻译仍然受到CAF异质性、货物可变性和囊泡动力学的不完整体内表征的限制。治疗机会包括阻断外泌体的生物发生或摄取，对CAFs进行药理学重编程，以及设计囊泡以传递靶向抑制剂或基于rna的治疗方法。这篇综述综合了目前的机制见解，评估了生物标志物的潜力，并概述了针对CRC中ca -外泌体途径的临床重点。

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引用次数: 0

Precision cytokine modulation to overcome tumor microenvironment-driven resistance to immune checkpoint blockade 精确的细胞因子调节克服肿瘤微环境驱动的免疫检查点阻断抗性。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-23 DOI: 10.1016/j.bbcan.2026.189536

Xiaodong Wang , Junjie Wang , Qianqian Wang , Gouping Ding , Yiping Huang , Yeqian Feng

Immune checkpoint inhibitors (ICIs) can elicit durable remissions, yet most solid tumors show primary non-response or acquired resistance because the tumor microenvironment (TME) limits T-cell priming, trafficking and effector fitness. Cytokines orchestrate these barriers by shaping spatial immune architecture, regulating suppressive myeloid programmes and inducing inhibitory ligands such as PD-L1. In this Review, we synthesize mechanistic and clinical evidence and propose a push–pull framework for cytokine modulation during checkpoint blockade: locally amplifying Th1/CTL-supporting signals (IL-2/IL-12/IL-15 and type I/II interferons) while selectively attenuating dominant suppressive circuits (TGF-β, IL-6/STAT3, IL-8–CXCR1/2, IL-10 and TNF-driven exhaustion). We critically contrast successful and failed cytokine–ICI combinations, highlighting how systemic exposure, network redundancy and counter-regulatory feedback have constrained several engineered agonists and explain why certain blockade strategies can improve efficacy while reducing immune-related toxicity. We discuss next-generation solutions—tumor-activated pro-cytokines, intratumoral gene delivery and immunocytokines—that concentrate activity within resistant niches and widen the therapeutic window. Finally, we outline actionable biomarkers, including transcriptomic signatures, plasma cytokine kinetics, myeloid/neutrophil metrics and spatial TME profiling, to stratify patients and guide dosing, sequencing and adaptive add-on strategies. Rational, biomarker-guided cytokine modulation offers a path to convert immune-excluded tumors into durable ICI responders.

免疫检查点抑制剂（ICIs）可以引起持久的缓解，但大多数实体瘤表现为原发性无反应或获得性耐药，因为肿瘤微环境（TME）限制了t细胞的启动、运输和效应适应度。细胞因子通过塑造空间免疫结构、调节抑制性骨髓程序和诱导抑制性配体（如PD-L1）来协调这些屏障。在这篇综述中，我们综合了机制和临床证据，并提出了检查点阻断期间细胞因子调节的推挽框架：局部放大Th1/ ctl支持信号（IL-2/IL-12/IL-15和I/II型干扰素），同时选择性地减弱显性抑制回路（TGF-β、IL-6/STAT3、IL-8-CXCR1/2、IL-10和tnf驱动的衰竭）。我们对成功和失败的细胞因子- ici组合进行了批判性对比，强调了系统暴露、网络冗余和反调节反馈如何限制了几种工程激动剂，并解释了为什么某些阻断策略可以在降低免疫相关毒性的同时提高疗效。我们讨论了下一代解决方案-肿瘤激活的前细胞因子，肿瘤内基因传递和免疫细胞因子-集中活性在耐药壁龛和扩大治疗窗口。最后，我们概述了可操作的生物标志物，包括转录组特征，血浆细胞因子动力学，骨髓/中性粒细胞指标和空间TME分析，以对患者进行分层并指导剂量，测序和适应性附加策略。合理的、生物标志物引导的细胞因子调节为将免疫排斥肿瘤转化为持久的ICI应答提供了一条途径。

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引用次数: 0

Current landscape of PDT-based combination therapy for cutaneous squamous cell carcinoma: From molecular mechanisms to clinical practice 基于pdp的皮肤鳞状细胞癌联合治疗的现状：从分子机制到临床实践。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-22 DOI: 10.1016/j.bbcan.2026.189541

Ziwei Kang , Guorong Yan , Guolong Zhang

Photodynamic therapy (PDT) has been extensively applied in the management of superficial cutaneous squamous cell carcinoma (cSCC). However, the efficacy of PDT was limited by issues including poor tissue penetration and hypoxia. In recent years, to enhance the effectiveness of PDT in cSCC, various combination strategies have been derived. Here, we revisit the basic mechanism of PDT and summarize clinical and basic researches of PDT-based combination strategies in treating cSCC, including topical agents, systemic therapies, and physical interventions. Evidences indicate that most of these combination approaches significantly enhanced the efficacy of PDT and leveraged three primary synergistic mechanisms: enhanced photosensitizer accumulation and delivery, potentiated tumor cell death, and augmented anti-tumor immunity. Future research should focus on optimizing light dosimetry, validating combination protocols in large clinical trials, and developing more tumor-targeted photosensitizers to improve PDT's clinical outcomes.

光动力疗法（PDT）已广泛应用于浅表皮肤鳞状细胞癌（cSCC）的治疗。然而，PDT的疗效受到组织穿透性差和缺氧等问题的限制。近年来，为了提高PDT在cSCC中的有效性，人们衍生出了各种组合策略。在此，我们回顾了PDT的基本机制，并总结了PDT联合治疗cSCC的临床和基础研究，包括局部药物、全身治疗和物理干预。有证据表明，这些联合方法中的大多数都显著提高了PDT的疗效，并利用了三个主要的协同机制：增强光敏剂的积累和传递，增强肿瘤细胞死亡，增强抗肿瘤免疫。未来的研究应该集中在优化光剂量学，在大型临床试验中验证联合方案，以及开发更多的肿瘤靶向光敏剂来改善PDT的临床结果。

引用次数: 0

Harnessing microRNAs in lung cancer: The future of diagnosis and precision therapy 在肺癌中利用微小rna：诊断和精确治疗的未来。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-22 DOI: 10.1016/j.bbcan.2026.189535

Daniela Alexandre , Pedro V. Baptista , Carla Cruz

Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related death, driven by late diagnosis and therapeutic resistance. microRNAs (miRs) regulate post-transcriptional networks across cancer hallmarks and are unusually stable in biofluids, positioning them as powerful, minimally invasive biomarkers and therapeutic targets. This review summarizes current knowledge on miR biogenesis, regulation, and function in NSCLC; critically evaluates circulating and compartment-specific biomarkers (plasma/serum, sputum, and peripheral blood mononuclear cells (PBMCs); and appraises translational advances in oncomiR inhibition and tumor-suppressor restoration using modern delivery systems. We also analyze methodological progress, highlight persistent pre-analytical and normalization challenges, and outline practical routes toward regulatory-grade standardization. Convergent evidence indicates that circulating and exosomal miR panels can improve early detection and malignant-nodule triage, particularly when integrated with imaging and proteomic markers, and provide independent prognostic and treatment-monitoring value, often anticipating radiographic response or resistance. Despite strong pre-clinical efficacy, the clinical translation of miR mimics and inhibitors has been limited by delivery barriers and immunotoxicity, constraining progress into late-phase development. Unstandardized workflows and incomplete attribution of tumor-derived signals remain key barriers to clinical adoption. Overall, miRs hold strong potential to advance precision oncology in NSCLC through real-time disease monitoring and pathway-level targeting. Progress will likely depend on multimodal integration with circulating tumor DNA (ctDNA), proteomics, and imaging, alongside optimized delivery strategies, improved immunosafety, and rigorous multicenter validation to enable translation into routine care.

非小细胞肺癌（NSCLC）仍然是癌症相关死亡的主要原因，其原因是晚期诊断和治疗耐药性。microrna （miRs）调节跨越癌症特征的转录后网络，在生物体液中异常稳定，使其成为强大的微创生物标志物和治疗靶点。本文综述了miR在非小细胞肺癌中的生物发生、调控和功能；严格评估循环和室特异性生物标志物（血浆/血清、痰和外周血单个核细胞（pbmc））；并评估了使用现代递送系统的肿瘤抑制和肿瘤抑制因子恢复的转化进展。我们还分析了方法上的进展，强调了持续的分析前和规范化挑战，并概述了实现监管级标准化的实用路线。越来越多的证据表明，循环和外泌体miR检测可以改善早期发现和恶性结节分类，特别是当与影像学和蛋白质组学标志物结合使用时，并提供独立的预后和治疗监测价值，通常可以预测影像学反应或耐药性。尽管具有很强的临床前疗效，但miR模拟物和抑制剂的临床转化受到递送障碍和免疫毒性的限制，限制了其进入后期开发。不标准化的工作流程和肿瘤来源信号的不完整归属仍然是临床应用的主要障碍。总的来说，miRs通过实时疾病监测和通路水平靶向，在推进非小细胞肺癌的精确肿瘤学方面具有强大的潜力。进展可能取决于与循环肿瘤DNA （ctDNA）、蛋白质组学和成像的多模式整合，以及优化的递送策略、改进的免疫安全性和严格的多中心验证，以便转化为常规护理。

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引用次数: 0

The interplay between cytokines and immune checkpoints in breast cancer therapy 细胞因子与免疫检查点在乳腺癌治疗中的相互作用。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-21 DOI: 10.1016/j.bbcan.2026.189539

Ying Wu , Yin Zhu , Qing Cang , Zakari Shaibu , Lifeng Kong , Qi Zhou , Xinxin Li , Liang Yin

Breast cancer (BC) immunotherapy has transformed treatment paradigms, yet response rates remain limited by the complex interplay between cytokine networks and immune checkpoints. This review synthesizes emerging evidence on how cytokines dynamically regulate immune checkpoint expression and function within the breast tumor microenvironment. We examine pro-tumorigenic cytokine circuits alongside immunostimulatory pathways. A key focus is the subtype-specific nature of these interactions, with triple-negative breast cancers (TNBC) exhibiting distinct cytokine-checkpoint crosstalk compared to hormone receptor-positive subtypes. The review highlights innovative therapeutic strategies, including cytokine-targeting agents in clinical trials and engineered approaches like spatial-targeted nanocarriers. We further discuss how cutting-edge technologies from single-cell RNA sequencing to spatial proteomics are revealing novel biomarker opportunities. By decoding these intricate immune dialogues, this review provides a framework for developing precision immunotherapy combinations tailored to BC immunological heterogeneity.

乳腺癌（BC）免疫治疗已经改变了治疗模式，但应答率仍然受到细胞因子网络和免疫检查点之间复杂相互作用的限制。本综述综合了细胞因子如何动态调节乳腺肿瘤微环境中免疫检查点表达和功能的新证据。我们检查促肿瘤细胞因子回路与免疫刺激途径。一个关键的焦点是这些相互作用的亚型特异性，与激素受体阳性亚型相比，三阴性乳腺癌（TNBC）表现出不同的细胞因子检查点串扰。这篇综述强调了创新的治疗策略，包括临床试验中的细胞因子靶向药物和工程方法，如空间靶向纳米载体。我们进一步讨论了从单细胞RNA测序到空间蛋白质组学的尖端技术如何揭示新的生物标志物机会。通过解码这些复杂的免疫对话，本综述为开发针对BC免疫异质性的精确免疫治疗组合提供了框架。

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引用次数: 0

Emerging multi-omics biomarkers in glioblastoma: Integrative insights from genomics to metabolomics 胶质母细胞瘤中新兴的多组学生物标志物：从基因组学到代谢组学的综合见解

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-21 DOI: 10.1016/j.bbcan.2026.189540

Ganesh S. Kakde , Tikam Chand Dakal , Pawan Kumar Maurya

Glioblastoma (GBM) is the most malignant form of primary brain tumor in adults, described by profound molecular heterogeneity, rapid progression, and limited therapeutic response. Despite advances in chemotherapy (TMZ), radiotherapy, and surgery, patient outcomes remain poor, with a median survival of 12–15 months. Traditional single-omics studies have identified critical biomarkers such as IDH mutations, MGMT promoter methylation, and EGFR alterations; however, these provide only partial insight into the disease's complexity. Recent integrative multi-omics approaches encompassing genomics, transcriptomics, epigenomics, proteomics, metabolomics, and non-coding RNAs have transformed the landscape of biomarker discovery in GBM. Genomic profiling has revealed recurrent mutations and subtype-specific aberrations, while transcriptomic analyses refine molecular classification and uncover alternative splicing and fusion events. Epigenomic markers, particularly MGMT methylation and G-CIMP status, are now central to prognosis and therapy stratification. Proteomic and metabolomic studies highlight dysregulated pathways, metabolic vulnerabilities, and non-invasive biomarkers in cerebrospinal fluid and plasma. Integrating multi-omics data not only improves diagnostic and prognostic accuracy but also unveils therapeutic targets, offering opportunities for precision oncology. Furthermore, liquid biopsy and single-cell/spatial omics enhance real-time monitoring of disease progression and treatment response, addressing challenges posed by intratumoral heterogeneity. This review synthesizes recent advances in GBM biomarker research across multiple omics layers, emphasizing their complementary roles in unravelling tumor biology, guiding personalized treatment, and shaping future therapeutic strategies.

胶质母细胞瘤（GBM）是成人原发性脑肿瘤中最恶性的形式，具有深刻的分子异质性，快速进展和有限的治疗反应。尽管在化疗（TMZ）、放疗和手术方面取得了进展，但患者的预后仍然很差，中位生存期为12-15个月。传统的单组学研究已经确定了关键的生物标志物，如IDH突变、MGMT启动子甲基化和EGFR改变；然而，这些只提供了对这种疾病复杂性的部分了解。最近，包括基因组学、转录组学、表观基因组学、蛋白质组学、代谢组学和非编码rna在内的综合多组学方法已经改变了GBM生物标志物发现的格局。基因组分析揭示了复发性突变和亚型特异性畸变，而转录组学分析改进了分子分类并揭示了可选择的剪接和融合事件。表观基因组标记，特别是MGMT甲基化和G-CIMP状态，现在是预后和治疗分层的核心。蛋白质组学和代谢组学研究强调了脑脊液和血浆中的失调途径、代谢脆弱性和非侵入性生物标志物。整合多组学数据不仅提高了诊断和预后的准确性，而且揭示了治疗靶点，为精确肿瘤学提供了机会。此外，液体活检和单细胞/空间组学增强了疾病进展和治疗反应的实时监测，解决了肿瘤内异质性带来的挑战。本文综述了GBM生物标志物在多个组学层面的最新研究进展，强调了它们在揭示肿瘤生物学、指导个性化治疗和塑造未来治疗策略方面的互补作用。

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引用次数: 0

Heterogeneous neutrophils: Key players in regulating tumor immunity 异质中性粒细胞：调节肿瘤免疫的关键角色。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-20 DOI: 10.1016/j.bbcan.2026.189538

Wenchao Bi , Xue Li , Huajun Zhao , Qiuju Han , Jian Zhang

As the most abundant innate immune cells in bone marrow and peripheral blood, neutrophils were once considered functionally homogeneous and exerted inflammatory and anti-infection functions. However, emerging evidence reshapes the perception of neutrophils from passive effectors to dynamic regulators with high plasticity and heterogeneity, especially within the tumor microenvironment (TME). This review summarizes recent advances, particularly driven by single-cell technologies, demonstrating that tumor-associated neutrophils (TANs) represent a continuum of distinct functional states originating from heterogeneous developmental pathways in bone marrow, circulation and spleen. We classified TANs into diverse subsets based on unique molecular signatures and functions, including pro-tumor, inflammatory, interferon-stimulated genes (ISGs)^high, and antigen-presenting subsets, and highlighted that TANs profoundly impacting tumor progression through distinct molecular mechanisms. Importantly, we delineate how TANs functionally interact with T cells, NK cells, macrophages and other immune cells, revealing the pivotal role of TANs in reconfiguring immune response networks to modulate tumor progression. Lastly, we discuss emerging therapeutic strategies targeting TAN recruitment, reprogramming, or specific pro-tumor subsets to overcome therapy resistance, aiming to provide insights for future research directions on neutrophils and the development of neutrophil-targeted cancer therapeutic strategies.

中性粒细胞作为骨髓和外周血中最丰富的先天免疫细胞，曾被认为功能同质，具有炎症和抗感染功能。然而，新出现的证据将中性粒细胞从被动效应器重塑为具有高可塑性和异质性的动态调节剂，特别是在肿瘤微环境（TME）中。这篇综述总结了最近的进展，特别是单细胞技术的推动下，证明肿瘤相关中性粒细胞（TANs）代表了来自骨髓、循环和脾脏异质发育途径的不同功能状态的连续体。我们根据独特的分子特征和功能将TANs分为不同的亚群，包括促肿瘤、炎症、干扰素刺激基因（ISGs）高和抗原呈递亚群，并强调TANs通过不同的分子机制深刻影响肿瘤进展。重要的是，我们描述了TANs如何与T细胞，NK细胞，巨噬细胞和其他免疫细胞相互作用，揭示了TANs在重新配置免疫反应网络以调节肿瘤进展中的关键作用。最后，我们讨论了针对TAN募集、重编程或特异性促肿瘤亚群来克服治疗耐药的新兴治疗策略，旨在为中性粒细胞的未来研究方向和中性粒细胞靶向癌症治疗策略的发展提供见解。

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引用次数: 0

Histone acetyltransferase HBO1 in cancer biology: Essential mechanisms and implications for targeted therapeutics 组蛋白乙酰转移酶HBO1在癌症生物学中的作用：靶向治疗的基本机制和意义。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-18 DOI: 10.1016/j.bbcan.2026.189533

Alissa D. Marchione, Katie L. Kathrein

The histone acetyltransferase complex HBO1 (KAT7) is an oncogenic regulator across multiple cancers, promoting cell proliferation and migration. Though clinically important, no targeted therapies address HBO1 dysregulation. HBO1 forms complexes with MEAF6, JADE(1/2/3), ING(ING4/5), and BRPF1/2/3 to acetylate histones H3 and H4, especially at H3K14, promoting transcriptional activation and genomic stability. It colocalizes with active transcriptional sites and participates in gene regulation, DNA repair and replication. Most HBO1-associated cancer mutations are missense, though their effects remain unclear. Silencing HBO1 restores normal proliferation and gene expression, underscoring its oncogenic role. HBO1 activity supports cancer pathways, including apoptosis resistance, DNA damage response, and cell cycle regulation. The HBO1 inhibitor WM-3835 disrupts H3K14 acetylation, reducing tumor growth in several cancers. This review provides insights into the function of HBO1 in cancer, especially in histone acetylation, ubiquitination, stem cell maintenance, and pro- and anti-oncogenic signaling. Understanding the roles of HBO1 may guide new epigenetic therapies for HBO1-driven malignancies.

组蛋白乙酰转移酶复合物HBO1 （KAT7）是多种癌症的致癌调节剂，促进细胞增殖和迁移。尽管具有重要的临床意义，但目前还没有针对HBO1失调的靶向治疗。HBO1与MEAF6、JADE（1/2/3）、ING（ING4/5）和BRPF1/2/3形成复合物，使组蛋白H3和H4乙酰化，特别是在H3K14位点，促进转录激活和基因组稳定性。它与活跃的转录位点共定位，参与基因调控、DNA修复和复制。大多数与hbo1相关的癌症突变是错误的，尽管它们的影响尚不清楚。沉默HBO1可以恢复正常的增殖和基因表达，强调其致癌作用。HBO1活性支持癌症途径，包括细胞凋亡抵抗、DNA损伤反应和细胞周期调节。HBO1抑制剂WM-3835破坏H3K14乙酰化，减少几种癌症的肿瘤生长。本文综述了HBO1在癌症中的作用，特别是在组蛋白乙酰化、泛素化、干细胞维持以及促癌和抗癌信号传导方面的作用。了解HBO1的作用可能会指导HBO1驱动的恶性肿瘤的新表观遗传治疗。

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引用次数: 0

SCF-FBXO31 E3 ubiquitin ligase in cancer: Molecular insights and clinical implications SCF-FBXO31 E3泛素连接酶在癌症中的作用：分子见解和临床意义。

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-17 DOI: 10.1016/j.bbcan.2026.189534

Osheen Sahay , Abhayananda Behera , Chandra Biswas , Ganesh Kumar Barik , Sehbanul Islam

F-box only protein 31 (FBXO31), a substrate adapter of SKP1-Cullin1-F-box (SCF) E3 ubiquitin ligase, was first identified as a candidate tumor suppressor in breast cancer due to its role in inducing senescence. Over the past two decades, FBXO31 has emerged as a crucial regulator in several human cancers, where it promotes the proteasomal degradation of various oncoproteins. FBXO31 plays a crucial role in regulating the cell cycle to maintain genomic integrity and inhibits processes such as epithelial-to-mesenchymal transition (EMT), invasion, and metastasis. This review examines the molecular mechanisms underlying the potent tumor-suppressive functions of FBXO31 in diverse human cancers. We also discuss the underlying causes of FBXO31 deregulation in cancer, providing insights into the intricate regulatory networks governing its expression. Additionally, we also examine the unexpected oncogenic functions of FBXO31 in certain cellular contexts. Finally, we highlight the clinical potential of FBXO31 in human malignancies, discussing its implications as both a biomarker and a therapeutic target. In conclusion, understanding the nuanced biology of FBXO31 is crucial for unravelling its role in tumorigenesis and advancing future therapeutic strategies.

F-box only protein 31 （FBXO31）是SKP1-Cullin1-F-box (SCF) E3泛素连接酶的底物适配器，由于其在诱导衰老中的作用，首次被发现是乳腺癌的候选肿瘤抑制因子。在过去的二十年中，FBXO31已经成为几种人类癌症的关键调节因子，它促进各种癌蛋白的蛋白酶体降解。FBXO31在调节细胞周期以维持基因组完整性和抑制上皮-间质转化（EMT）、侵袭和转移等过程中起着至关重要的作用。本文综述了FBXO31在多种人类癌症中有效肿瘤抑制功能的分子机制。我们还讨论了FBXO31在癌症中解除调控的潜在原因，提供了对控制其表达的复杂调控网络的见解。此外，我们还研究了FBXO31在某些细胞环境下意想不到的致癌功能。最后，我们强调了FBXO31在人类恶性肿瘤中的临床潜力，讨论了它作为生物标志物和治疗靶点的意义。总之，了解FBXO31的微妙生物学对于揭示其在肿瘤发生中的作用和推进未来的治疗策略至关重要。

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引用次数: 0

Targeting glycolysis in prostate cancer: Molecular mechanisms and therapeutic advances 靶向糖酵解治疗前列腺癌：分子机制和治疗进展

IF 9.7 1区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Reviews on cancer

Pub Date : 2026-01-16 DOI: 10.1016/j.bbcan.2026.189537

Jiexiang Zhang , Tongtong Zhang , Dexin Song , Dongliang Xu

Prostate cancer (PCa) is the second most common cancer among men worldwide and poses a significant threat to male health. A key feature of tumor progression is metabolic reprogramming, which involves the abnormal activation of glycolysis. This metabolic process supports PCa proliferation, metastasis, and drug resistance through rapid energy production, the provision of biosynthetic precursors, and the remodeling of the tumor microenvironment (TME). Key enzymes such as hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase M2 (PKM2), glucose transporters (GLUTs), and lactate dehydrogenase A (LDHA) play pivotal roles in regulating aerobic glycolysis in PCa cells. Glycolytic enzymes are modulated by a variety of mechanisms, including the PI3K/AKT and AMPK signaling pathways, hypoxia-inducible factor 1α (HIF-1α), c-Myc, and non-coding RNAs. Current therapeutic strategies targeting glycolysis include natural products and small-molecule inhibitors. Targeting glycolysis presents novel opportunities to address existing limitations in PCa management. This review discusses the advances, challenges, and future research directions in glycolysis-focused PCa studies, providing a theoretical foundation for the development of precise metabolic interventions.

前列腺癌（PCa）是全球男性中第二大常见癌症，对男性健康构成重大威胁。肿瘤进展的一个关键特征是代谢重编程，它涉及糖酵解的异常激活。这种代谢过程通过快速的能量产生、生物合成前体的提供和肿瘤微环境（TME）的重塑来支持前列腺癌的增殖、转移和耐药。己糖激酶2 （HK2）、磷酸果糖激酶（PFK）、丙酮酸激酶M2 （PKM2）、葡萄糖转运蛋白（GLUTs）和乳酸脱氢酶A （LDHA）等关键酶在调节PCa细胞的有氧糖酵解中起关键作用。糖酵解酶受多种机制调节，包括PI3K/AKT和AMPK信号通路、缺氧诱导因子1α (HIF-1α)、c-Myc和非编码rna。目前针对糖酵解的治疗策略包括天然产物和小分子抑制剂。靶向糖酵解为解决PCa管理的现有局限性提供了新的机会。本文综述了以糖酵解为重点的PCa研究的进展、挑战和未来的研究方向，为开发精确的代谢干预提供理论基础。

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引用次数: 0