Liposomes, as one of the most established nanocarriers, have been widely employed in lung cancer therapy, which remains the leading cause of cancer-related mortality worldwide. However, the current landscape of liposomal...Liposomes, as one of the most established nanocarriers, have been widely employed in lung cancer therapy, which remains the leading cause of cancer-related mortality worldwide. However, the current landscape of liposomal formulations and the principles guiding their rational design remain insufficiently defined. This review provides a comprehensive analysis of how liposomal delivery systems have been engineered to address biological and therapeutic challenges in lung cancer. We analyze liposome-based delivery of chemotherapeutic agents, including formulations that have advanced to clinical trials, with particular emphasis on strategies developed to overcome multidrug resistance (MDR). Surface engineering and functionalization strategies that enable active targeting and enhance therapeutic efficacy are also reviewed. Liposomal platforms for immunotherapy are examined, alongside their application in delivering phytochemicals, nucleic acid therapeutics, and photo-enabled modalities, including photothermal and photodynamic therapies, which are discussed in dedicated sections. Cutting-edge innovations, such as biomimetic liposomes, stimuli-responsive smart systems, and theranostic designs integrating diagnostic and therapeutic functions, are highlighted. Finally, pulmonary delivery of anticancer agents is evaluated, focusing on formulation parameters informed by current liposome-based evidence and broader lessons from nanomedicine. By providing mechanistic insights, design principles, and translational perspectives, this review offers a unified framework for liposome-based platforms in lung cancer therapy.
Bone metastasis is a pivotal hallmark of advanced malignant tumors. It severely impairs the therapeutic efficacy of immune checkpoint inhibitors (ICIs) and serves as an independent risk factor for poor prognosis of immun...Bone metastasis is a pivotal hallmark of advanced malignant tumors. It severely impairs the therapeutic efficacy of immune checkpoint inhibitors (ICIs) and serves as an independent risk factor for poor prognosis of immunotherapy in solid tumors. Most existing reviews are confined to traditional research frameworks and have not yet resolved this clinical dilemma. This paper systematically elaborates on the core mechanisms underlying the poor efficacy of immunotherapy for bone metastasis. It clarifies that the immune suppression mediated by the bone metastatic microenvironment (BME) is not induced by a single factor, but rather a consequence of the cross-regulation of immunity, metabolism, bone matrix, blood vessels, epigenetics, microbiota, and nerves. From seven dimensions-immune cell-mediated immune escape, bone matrix-immune cell crosstalk, vascular-mediated immune suppression, metabolic-immune cross-regulation, epigenetic disorders, microbiota-osteoimmune axis imbalance, and neuro-immune-bone metastasis regulation-the study comprehensively sorts out the key nodes of immunotherapy resistance and clarifies the core cellular, molecular, and microenvironmental interaction mechanisms of this cross-regulatory network. On this basis, this paper explores a multi-target combined therapeutic strategy of "breaking the vicious cycle by targeting key nodes, restoring anti-tumor immunity with ICIs, and realizing local-systemic synergism", including combined bone matrix-immune targeted therapy, immune phenotype-based precise treatment, local-systemic synergistic immunotherapy and multi-dimensional microenvironment remodeling regimens.Finally, the paper prospects future research directions, including in-depth mechanism analysis, new target development, precision diagnosis and treatment innovation, and clinical translation. It aims to systematically summarize current mechanisms and provide theoretical reference and novel insights for developing precise immunotherapeutic strategies against bone metastasis.
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) growth and metastasis are influenced by the tumor microenvironment (TME), which includes immune cells, endothelial cells, macrophages, and cancer-associated fibroblasts...BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) growth and metastasis are influenced by the tumor microenvironment (TME), which includes immune cells, endothelial cells, macrophages, and cancer-associated fibroblasts (CAFs). Since the novel integrin-targeted cytotoxin ProAgio can inhibit activated CAFs and endothelial cells, we investigated its combination with standard of care chemotherapies in genetically engineered mouse (GEM) and orthotopic murine models of PDAC. METHODS: We established metastatic murine KPC-Ganji & Bassel-Luc (mKPC-GB-Luc) cell lines and validated them using bulk RNA sequencing. Two in vivo orthotopic mouse model were used to evaluate ProAgio with chemotherapy. mKPC-GB-Luc was used to evaluate the 5FU, oxaliplatin, and irinotecan (FOI combination), and KPC-ML1-Luc was used to evaluate the gemcitabine, nab-paclitaxel (GPTx combination). Immunohistochemistry was used to measure integrin β3, E-cadherin, and HIF-1α. Hypoxia was evaluated using pimonidazole. Stem cells, CAFs, and immune cell subtypes were quantified by flow cytometry. We evaluated the combination of ProAgio plus gemcitabine in a KPC genetically engineered mouse model (KPC GEM). Two sets of KPC GEM were developed. The first set was used for a survival study. The second set was terminated early and tumors were used for single-cell RNA seq and sequential multiplex immunofluorescence (COMET). RESULTS: Compared with the chemo regimen (GPTx or FOI), ProAgio, or sham, the combination of ProAgio plus chemo significantly modulated the TME, reduced tumor weight, reduced hypoxia, and eliminated metastasis to the lungs and liver. The combination of ProAgio and gemcitabine increased overall survival in KPC GEM mice compared with either treatment alone. Single-cell RNA sequencing, flow cytometry, immunofluorescence, immunohistochemistry, and COMET analyses demonstrated that ProAgio plus chemotherapy reprogrammed the PDAC-TME by changing activated CAFs toward a qCAFs (quiescent CAFs), macrophages from protumor to proinflammatory polarization, and activating natural killer (NK) cells, CD4⁺, and CD8⁺ T cells. Combination therapy inhibited PDAC stemness. ProAgio-treated CAFs in vitro exhibited reduced secretion of glycine and cysteine, vital metabolites that support stemness and tumor progression. CONCLUSIONS: These results confirm the novel mechanism of action of ProAgio, which includes reducing hypoxia and modulating TME. The current data provide evidence for potentiation of chemotherapy efficacy by ProAgio.
Murakami K, Takamura S, Miyagawa C
… +13 more, Takamatsu S, Kashima Y, Nagaoka K, Kobayashi Y, Hakata Y, Kato S, Tsuji-Kawahara S, Nan D, Chandler R, Takahashi S, Miyazawa M, Kakimi K, Matsumura N
BACKGROUND: While immune checkpoint inhibitors (ICIs) have failed to improve outcomes in unselected ovarian cancer populations, objective responses are observed in a minority of ovarian clear cell carcinoma (OCCC) cases,...BACKGROUND: While immune checkpoint inhibitors (ICIs) have failed to improve outcomes in unselected ovarian cancer populations, objective responses are observed in a minority of ovarian clear cell carcinoma (OCCC) cases, implying biological heterogeneity and a yet-undefined immunologically responsive subset within this histotype. METHODS: We performed immunohistochemical profiling of tumor-infiltrating immune cells and analyzed transcriptomic data from human OCCC cohorts. Functional studies were conducted using an immunocompetent syngeneic OCCC mouse model to assess the effects of IL-17 on tumor cell inflammatory signaling, immune microenvironment remodeling, and responsiveness to immune checkpoint blockade, including single-cell RNA sequencing of tumor-infiltrating T cells. RESULTS: OCCC exhibited an immune-sparse tumor microenvironment with relative enrichment of CD4⁺ T cells. RORC expression was elevated in OCCC but showed intertumoral heterogeneity. In the transcriptome data (n = 180), an IL17A subset (5%), enriched within the RORC fraction, exhibited a T cell-inflamed gene expression profile independent of microsatellite instability and tumor mutational burden, yet was not associated with survival. Mechanistically, IL-17 directly activated NF-κB-dependent inflammatory programs in OCCC tumor cells, inducing cytokines and chemokines involved in T-cell recruitment and activation. In the syngeneic model, IL-17 exposure increased intratumoral CD4⁺ and CD8⁺ T-cell infiltration and activation. Single-cell profiling further revealed expansion of Th17/Tfh-like CD4⁺ T cells and cytotoxic, non-terminally exhausted CD8⁺ T cells. Consistent with these changes, anti-PD-L1 therapy improved survival in Th17-biased partial chimera mice. CONCLUSIONS: IL-17-responsive, tumor cell-intrinsic inflammatory programming remodels the tumor immune microenvironment toward an immunotherapy-permissive state. These findings establish IL-17-responsive tumor cell inflammatory programming as a mechanistic axis shaping immune checkpoint sensitivity and provide a rationale for biomarker-guided immunotherapy strategies.
Oral potentially malignant disorder (OPMD) remains a critical clinical challenge for cancer interception. However, the progression of OPMD toward oral squamous cell carcinoma (OSCC) is driven by profound cellular heterog...Oral potentially malignant disorder (OPMD) remains a critical clinical challenge for cancer interception. However, the progression of OPMD toward oral squamous cell carcinoma (OSCC) is driven by profound cellular heterogeneity and dynamic microenvironmental remodeling. The mechanisms underlying these processes are not yet fully understood. Recent advancements in single-cell and spatial omics have facilitated high-resolution decoding of the precancerous landscape, unveiling multistep epithelial cell plasticity, fibroblast heterogeneity with extracellular matrix remodeling, immune suppression, and inflammatory reprogramming, as well as coupled metabolic and redox alterations that govern malignant transformation. These insights into the cellular mechanisms have led to a paradigm shift in the understanding of OPMD, reclassifying it as an ecosystem-level disease rather than a purely epithelial pathology. Nanomedicine is a potent platform for translating mechanistic knowledge into precision diagnostics and interventions at the precancerous stage. Nanomaterial-based strategies have been demonstrated to facilitate several critical processes, including enabling early lesion visualization and risk stratification, immune microenvironment reactivation, anti-fibrotic and anti-inflammatory remodeling, and targeted regulation of metabolic and oxidative stress pathways. A mounting body of evidence from preclinical and clinical studies lends support to the notion that nanotechnology-assisted early detection, microenvironmental reprogramming, and the interception of malignant transformation across oral and other precancerous conditions are indeed feasible. This review integrates single-cell-resolved mechanisms of OPMD progression with state-of-the-art nanomedicine-based diagnostic and therapeutic strategies, highlighting convergent biological axes and translational opportunities. By integrating single-cell biology with nanotechnology-driven precision medicine, this work is expected to improve the development of a nanomedicine framework for early cancer detection and treatment and outline future directions and challenges toward clinical implementation.
Dall'Olio FG, Zrafi WS, Song X
… +24 more, Lawrance L, Shalimanova E, Schwager A, Myszka N, Chen F, Ibrahim R, Guinhut M, Busson P, Brenner C, Benihoud K, Barlesi F, Even C, Brempou D, Lassau N, Nicotra C, Camus MN, Aglave M, Loriot Y, Cardenas D, Jamal-Hanjani M, Prado CM, Italiano A, Vassetzky Y, Besse B
BACKGROUND: Cancer-related sarcopenia is associated with poor clinical outcomes but remains difficult to define and quantify in routine oncology practice. Current assessments rely on imaging and functional scales that ar...BACKGROUND: Cancer-related sarcopenia is associated with poor clinical outcomes but remains difficult to define and quantify in routine oncology practice. Current assessments rely on imaging and functional scales that are time-consuming and provide limited biological insight. We aimed to identify a plasma proteomic signature of cancer-related sarcopenia and to uncover circulating mediators involved in its pathophysiology. METHODS: Patients were included from two cohorts of the MATCH-R study (NCT02517892): a discovery cohort of advanced cancer patients treated with immunotherapy and an independent validation cohort of metastatic castration-resistant prostate cancer (mCRPC) patients treated with androgen-receptor pathway inhibitors. External validation was performed in the TRACERx cohort of non-small cell lung cancer. Skeletal muscle index at third lumbar vertebra (L3) was quantified using imaging, and ECOG performance status served as a functional proxy. Plasma proteomics was performed using the Olink Explore platform. An extreme gradient boosting (XGBoost) model was trained on a high-contrast subset using a neuromuscular-focused protein panel and validated across cohorts. Functional effects of candidate mediators were assessed in differentiating human myoblasts. RESULTS: The model generated a continuous sarcopenia probability (SP) score that correlated with muscle mass and functional status and consistently stratified overall survival across cohorts. A reduced four-protein model retained comparable performance, supporting translational applicability. Proteins associated with SP included insulin-like growth factor binding protein 1 and 2 (IGFBP1, IGFBP2), and interleukin-6 (IL6). IGFBP1 and IGFBP2 impaired myoblast differentiation, while IL6 induced IGFBP1 expression in liver cells. CONCLUSIONS: Plasma proteomics enables scalable and biologically informed assessment of cancer-related sarcopenia, identifies tumor-host mediators of muscle dysfunction, and supports objective patient stratification for therapeutic intervention.
WD40-repeat (WDR) proteins constitute one of the largest and most functionally diverse scaffold families in eukaryotes. By folding tandem WD repeats into β-propeller domains, they provide modular interaction surfaces tha...WD40-repeat (WDR) proteins constitute one of the largest and most functionally diverse scaffold families in eukaryotes. By folding tandem WD repeats into β-propeller domains, they provide modular interaction surfaces that assemble multi-protein complexes governing transcription and epigenetic control, ubiquitin-dependent proteostasis, RNA metabolism, and cell-cycle progression. Despite their pervasive involvement in oncogenic signaling and hallmark cancer phenotypes, the cancer field still lacks an integrated framework that connects WDR structural logic to context-dependent mechanisms and, critically, to actionable biomarkers and therapeutic strategies; existing evidence remains dispersed across tumor types and molecular pathways. This review synthesizes current knowledge to address that gap. We first summarize core structural principles of WD40 β-propellers and explain how multivalent binding and partner selection enable WDR proteins to function as assembly platforms in oncogenic networks. We then consolidate mechanistic evidence showing how representative WDR proteins shape malignant state transitions, including sustained proliferation, survival under stress, epigenetic plasticity, invasion and metastasis, and therapy resistance, by rewiring chromatin programs, ubiquitination circuits, and RNA and translation outputs across cancers. Finally, we highlight translational progress and opportunities. Overall, this review integrates the fragmented WDR research into a clinically oriented framework that clarifies their potential as biomarkers for early detection, stratified diagnosis, and treatment-response prediction, and delineates druggable entry points and rational combination strategies, thereby providing a translational roadmap to enable more precise cancer diagnosis and more effective targeted therapies in the future.
Pouyan A, Ghorbanlo M, Eslami M
… +11 more, Jahanshahi M, Ziaei E, Salami A, Mokhtari K, Shahpasand K, Farahani N, Meybodi TE, Entezari M, Taheriazam A, Hushmandi K, Hashemi M
The advent of antibody-drug conjugates (ADCs) has caused a paradigm shift in breast cancer management, transforming the treatment landscape from advanced lines to curative-intent settings. By integrating the specificity...The advent of antibody-drug conjugates (ADCs) has caused a paradigm shift in breast cancer management, transforming the treatment landscape from advanced lines to curative-intent settings. By integrating the specificity of monoclonal antibodies with the potency of cytotoxic payloads, ADCs have broken the limitations of traditional chemotherapy. This review aims to provide a comprehensive overview of the current state of ADCs in breast cancer, concentrating on targets under development, toxicity, and the challenges that remain to be overcome. Distinct from conventional classifications, we propose a framework categorizing ADC targets into three dimensions based on biological features: oncogenic driver antigens, lineage and oncofetal antigens, and tumor microenvironment antigens. Meanwhile, we discuss the structural evolution of ADCs, the management of toxicity, and the mechanism-based resistance. The future of treatment calls for precise ADC management, the use of next-generation bispecific ADCs and immune-oncology combinations, and the imperative of biomarker-guided sequencing.
Extracellular vesicles (EVs) are important mediators of intercellular communication in solid tumors. Released by malignant, stromal, immune, and microbial cells, they influence tumor evolution by transferring proteins, n...Extracellular vesicles (EVs) are important mediators of intercellular communication in solid tumors. Released by malignant, stromal, immune, and microbial cells, they influence tumor evolution by transferring proteins, nucleic acids, lipids, and metabolites that reshape local and systemic signaling. Current evidence implicates EVs in tumor microenvironment remodeling, metastatic niche formation, immune regulation, and adaptive responses to metabolic and therapeutic stress. However, these functions are highly context-dependent and remain unevenly supported across tumor types, disease stages, and experimental systems. Mechanistically, EV production is increasingly understood not as a constitutive secretory event, but as an adaptive output of intracellular trafficking and metabolic programs that govern vesicle fate, cargo selection, and release under stress. The same properties that complicate biological interpretation-including heterogeneity, membrane plasticity, and context-dependent cargo sorting-also make EVs attractive candidates for therapeutic engineering. In this Review, we critically examine EV biology in solid tumors by connecting biogenesis, trafficking control, lipid metabolism, and functional heterogeneity with emerging engineering strategies, including source selection, surface modification, cargo loading, and hybrid engineering strategies. We further discuss the major barriers that continue to limit clinical translation, particularly biological heterogeneity, isolation-dependent variability, incomplete mechanistic resolution, manufacturing scalability, and regulatory standardization. By distinguishing more established principles from emerging or model-restricted findings, this Review aims to provide a balanced assessment of both the opportunities and the current limitations of EV-based diagnostics and therapeutics.
Tumor neuron hijack is a malignant adaptive program whereby tumor cells recruit, physically engage and functionally reprogram the peripheral and central nervous system within the local microenvironment and host macroenvi...Tumor neuron hijack is a malignant adaptive program whereby tumor cells recruit, physically engage and functionally reprogram the peripheral and central nervous system within the local microenvironment and host macroenvironment; this process not only exploits neuro-immune regulatory machineries, neural endocrine signaling, and nutrient supply for sustaining tumor growth, invasion, metastasis, immune escape and treatment resistance, but also closely involves the induction and amplification of cancer-associated pain, a common and debilitating manifestation of the host's pathological response to tumor-neural crosstalk, which further perturbs the host macroenvironment and facilitates tumor progression. Neoplastic cells employ context-dependent strategies: central nervous system tumors (e.g., gliomas) integrate into existing neuronal circuits via synaptogenesis and metabolic coupling, while peripheral solid tumors induce de novo innervation via neurotrophic factors, axon guidance cues regulating angiogenesis, and perineural invasion. Sympathetic, parasympathetic, and sensory nerves modulate tumor behavior via neurotransmitters or neuropeptides, with autonomic nerves also regulating endocrine glands to reprogram tumor metabolism. Pivotal to this regulation is the tripartite crosstalk among nerves, immune cells, and tumor cells, which establishes an immunosuppressive tumor microenvironment and drives progression from immune equilibrium to escape. These mechanisms have spurred therapeutic avenues such as neurotrophic agent repurposing, synaptic blockade, and neural-signal reprogramming, particularly in combination with immunotherapy, with promising preclinical and translational potential for precision oncology and cancer pain management.
Zhao F, Zeng F, Zhou P
… +22 more, Zheng H, Hu Y, Tang J, Hu Y, Li G, Feng Y, Wang X, Yu J, Li Y, Yue C, Liu X, Zhang T, Huang N, Sun X, Wang X, Huang S, He M, Zeng X, Wu W, Cui X, Cui K, Li J
Metabolic reprogramming, particularly aberrant glycolysis, is a hallmark of NSCLC progression; however, the regulatory mechanisms remain incompletely understood. Here, we identify SerpinB7, an endogenous serine protease...Metabolic reprogramming, particularly aberrant glycolysis, is a hallmark of NSCLC progression; however, the regulatory mechanisms remain incompletely understood. Here, we identify SerpinB7, an endogenous serine protease inhibitor, as a novel oncogenic regulator of glycolytic reprogramming in NSCLC. SerpinB7 is significantly overexpressed in NSCLC tissues and correlates with poor prognosis. Mechanistically, SerpinB7 functions in a non-canonical, protease-independent manner by directly binding to Annexin A2 (ANXA2), protecting it from NEDD4L-mediated ubiquitination and degradation, thereby stabilizing ANXA2 protein levels.As an RNA-binding protein, ANXA2 interacts with c-Myc via its C-terminal domain, enhancing c-Myc driven transcription of glycolytic genes. This establishes a previously unrecognized SerpinB7-ANXA2-c-Myc regulatory axis that promotes glycolytic activation and malignant transformation in NSCLC cells. Importantly, immunohistochemical analysis of clinical specimens confirms the co-overexpression of SerpinB7 and ANXA2 in tumors, underscoring the clinical relevance of this pathway. Targeting SerpinB7 using siRNAs encapsulated in ferritin protein shells effectively suppresses NSCLC tumor growth and metastasis. These findings reveal SerpinB7 as a tumor-specific modulator of glycolysis and a potential metabolic target in NSCLC.
Zhang W, Yao Y, Wang Y
… +26 more, Shen L, Ding J, Zhu Y, Xu H, Shao Y, Gu X, Lu H, Zhou J, Deng H, Zhou J, Chen W, Xia W, Jiang J, Yu X, Sun S, Chen J, Liu J, Wang D, Liu W, Lin Z, Xu K, Wu Q, Huang J, Li H, Yu Z, Ni C
Despite widespread use of ultrasound and mammography, the accuracy of early breast cancer detection remains suboptimal, particularly in Asian women with dense breast tissue, underscoring the unmet need for biologically i...Despite widespread use of ultrasound and mammography, the accuracy of early breast cancer detection remains suboptimal, particularly in Asian women with dense breast tissue, underscoring the unmet need for biologically informed, non-invasive diagnostic approaches. Notably, systematic characterization of circulating proteomic and metabolomic alterations in early-stage breast cancer remains limited, especially in large, well-validated cohorts. Here, leveraging a registered multicenter prospective study (NCT06016790) together with an independent external validation cohort, we enrolled 662 participants across nine healthcare institutions to evaluate a plasma-based multi-omics liquid-biopsy framework for non-invasive detection. Data-independent acquisition proteomics and untargeted metabolomics profiled 5,549 proteins and 630 metabolites, with targeted validation performed in independent cohorts. Integrated analyses revealed coordinated molecular remodeling characterized by enrichment of cytoskeleton- and adhesion-associated proteins (for example ACTN1, VCL, ITGA2B and MYH9) together with rewiring of lipid-metabolic pathways. Network and trajectory modeling further identified 13 malignancy-associated protein modules and two progression-linked metabolic trajectories. Based on these features, we developed ProMeta-BC, a combined plasma proteome-metabolome model incorporating 15 proteins and 5 metabolites, which achieved robust discrimination between benign and malignant lesions (AUC 0.973 and 0.951 in training and validation cohorts, respectively), and ProMeta-BC-LN for prediction of axillary lymph-node metastasis (AUC 0.841 and 0.753). Notably, in cases with discordant radiological and pathological findings, the model detected 8 of 9 imaging-negative cancers and correctly reclassified 38 of 56 patients with inconsistent lymph-node calls, indicating complementary clinical utility. Together, these findings show that coordinated molecular signatures encoded in the circulating proteome-metabolome capture disease-relevant biology and provide a scalable, interpretable framework for non-invasive detection and stratification in breast cancer.
Cancer immunotherapy has revolutionized oncology, yet its efficacy remains frequently constrained by the immunosuppressive tumor microenvironment (TME). Circular RNAs (circRNAs) are covalently closed RNA molecules genera...Cancer immunotherapy has revolutionized oncology, yet its efficacy remains frequently constrained by the immunosuppressive tumor microenvironment (TME). Circular RNAs (circRNAs) are covalently closed RNA molecules generated through back-splicing. Their lack of free ends confers strong resistance to exonuclease degradation and high molecular stability. Within tumor cells, circRNAs govern multiple cancer hallmarks via diverse regulatory mechanisms. Beyond these cell-intrinsic functions, circRNAs can be secreted as intercellular messengers that enter and reshape the TME by modulating antitumor immunity. Clinically, the high stability of circRNAs in body fluids highlights their potential as non-invasive liquid biopsy biomarkers for cancer diagnosis and prognosis. Furthermore, beyond targeting endogenous circRNAs, engineered circRNAs encoding tumor antigens or immunomodulatory proteins represent a promising platform for cancer immunotherapy. In this article, we briefly summarize recent advances in the understanding of circRNAs in tumor biology and immunology.
RNA methylation represents a critical epi-transcriptomic modification that regulates cell fate by modulating diverse aspects of RNA metabolism, including splicing, export, translation, and degradation. Among the best-cha...RNA methylation represents a critical epi-transcriptomic modification that regulates cell fate by modulating diverse aspects of RNA metabolism, including splicing, export, translation, and degradation. Among the best-characterized modifications are N-methyladenosine (mA), 5-methylcytosine (mC), N-methylguanosine (mG), and N-methyladenosine (mA), which are dynamically regulated by specific writer, eraser and reader proteins. Dysregulation of these modifications perturbs multiple regulated cell death pathways, such as apoptosis, autophagy, pyroptosis, necroptosis, ferroptosis, and cuproptosis, thereby promoting tumor progression, immune evasion, and therapeutic resistance. In this review, we summarize the molecular mechanisms by which RNA methylation shapes cell death programs and highlight its potential as a biomarker for cancer diagnosis and prognosis, as well as a promising target for therapeutic intervention.
Nanomedicine has revolutionized oncology through targeted drug delivery and theranostic applications. However, its clinical translation remains a formidable challenge, primarily due to the translational gap created by co...Nanomedicine has revolutionized oncology through targeted drug delivery and theranostic applications. However, its clinical translation remains a formidable challenge, primarily due to the translational gap created by conventional preclinical models. These models often fail to recapitulate patient-specific tumor heterogeneity and the complex dynamics of the tumor microenvironment. This review posits that emerging tumor organoid platforms, particularly tumor organoid-on-a-chip systems, represent a transformative solution. A key contribution of this review is the introduction of a comprehensive evaluation framework for assessing nanomedicine efficacy, safety and clinical correlation using organoid platforms, offering a critical comparison with conventional models. Furthermore, we identify pivotal challenges including simulation of tumor immune microenvironment, material compatibility, and integration with artificial intelligence, and propose innovative bioengineering approaches to address them. By faithfully bridging the gap between in vitro models and human pathophysiology, tumor organoid platforms are poised to unlock the full clinical potential of next-generation cancer nanomedicine.
Jiang M, Zhang K, Li M
… +17 more, Tian Y, Wang T, Rodríguez RA, Lin Z, Meng J, Li C, Wang Z, Wu S, Cai Y, Zhang W, Guo R, Liu Y, Bai Y, Lai G, Zhang C, Bo Z, Wei R