Cancer Cell International最新文献

Leukemia survivorship presents ongoing clinical and functional challenges, including persistent fatigue, metabolic disturbances, and reduced quality of life. Integrative, non-pharmacologic strategies that combine exercise and targeted nutrition may help address these late effects. This narrative review synthesizes current evidence on the physiological, molecular, and clinical impact of exercise training and nutritional interventions among leukemia survivors. Exercise programs, ranging from aerobic and resistance training to high-intensity interval and mobile health-based formats, consistently improve cardiorespiratory fitness, muscular strength, and fatigue outcomes, while modulating inflammatory cytokines such as interleukin-6 and tumor necrosis factor-α. Nutritional components including polyphenol-rich functional foods, omega-3 fatty acids, and microbiota-supportive diets contribute anti-inflammatory and antioxidant effects that may complement exercise in restoring immune and metabolic balance. Together, these approaches form a promising foundation for personalized supportive care in leukemia survivorship. Yet, most studies remain limited by small sample sizes, heterogeneous protocols, and short follow-ups. Future research should prioritize larger, leukemia-specific clinical trials integrating exercise and nutrition components, with standardized outcome measures to enable evidence-based recommendations for survivorship care.

Background: Breast cancer (BC) remains a leading cause of cancer-related mortality among women globally, especially among women aged 45-55 years. A key driver of tumor progression, metastasis, and therapy resistance in BC is the aberrant activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), a proinflammatory transcription factor. Concurrently, microRNAs (miRNAs), a class of small non-coding RNAs, have emerged as critical post-transcriptional regulators of gene expression, influencing oncogenesis, immune response, apoptosis, and therapeutic outcomes.

Main body: Studies have revealed a complex interplay between miRNAs and NF-κB, wherein miRNAs exhibit context-dependent roles, functioning as either tumor suppressors or oncogenic regulators that modulate NF-κB signaling through direct or indirect mechanisms, modulating NF-κB signaling via direct or indirect mechanisms. This dual regulatory capacity presents unique therapeutic opportunities to either suppress oncogenic NF-κB signaling through tumor suppressor miRNAs (TS-miRs) or inhibit oncogenic miRNAs (OncomiRs) that potentiate NF-κB activity. This review presents a comprehensive overview of how miRNAs modulate NF-κB pathways in BC, outlines recent preclinical advances in miRNA delivery technologies, and discusses the clinical implications of miRNA-based therapeutics.

Conclusion: We emphasize the translational potential of miRNAs as emerging therapeutic modalities and predictive biomarkers for the personalized management of BC.

TAGLN is identified as a key prognostic gene in colorectal cancer through TCGA-COAD analysis, with high expression correlating with poor survival and advanced tumor stage. Functionally, TAGLN overexpression promotes epithelial-mesenchymal transition and enhances cancer cell migration. Transcriptomic profiling reveals its involvement in extracellular matrix remodeling and cell adhesion pathways. Mechanistically, TAGLN expression is upregulated by stiff tumor-mimicking extracellular matrix and is correlated with key mediators of collagen crosslinking and EMT. Clinically, TAGLN exhibits progressive overexpression from normal epithelium to primary tumors and metastatic lesions. These findings establish TAGLN as a stiffness-responsive regulator of ECM remodeling and EMT, driving colorectal cancer metastasis and serving as a potential therapeutic target.

Renal cell carcinoma (RCC), the most common type of kidney cancer, is characterized by a poor prognosis due to its aggressive metastasis and resistance to treatment. Long non-coding RNAs (lncRNAs) have emerged as key regulators of RCC progression, influencing cellular processes such as proliferation, migration, invasion, and apoptosis. LncRNA biogenesis occurs through both canonical and non-canonical pathways, involving RNA Polymerase II-mediated transcription and alternative splicing. LncRNAs like HOTAIR, MALAT1, and GAS5 regulate critical signaling pathways, including the PI3K/AKT/mTOR axis, Wnt/β-catenin, and JAK/STAT, while others, such as RCAT1, DUXAP9, and Lnc-LSG1, modulate protein degradation, impacting tumor growth and metastasis. Additionally, lncRNAs like EGFR-AS1 and MALAT1 enhance the EGFR/AKT and VEGF/Akt pathways, driving RCC cell proliferation and migration. LncRNAs such as HOTAIR and TCL6 also promote epithelial-to-mesenchymal transition, contributing to tumor invasion and therapy resistance. Furthermore, lncRNAs regulate the p53 pathway, with some, like MEG3, acting as tumor suppressors, while others, like SNHG3, suppress p53 activity, accelerating RCC progression. These insights into lncRNA-mediated regulatory mechanisms provide promising therapeutic targets for RCC, suggesting that modulating specific lncRNAs or their associated pathways could offer innovative strategies for treatment and prognosis. This review presents a comprehensive analysis of the biogenesis, functions, and regulatory roles of lncRNAs in RCC, emphasizing their potential as diagnostic biomarkers and therapeutic targets to improve patient outcomes.

Non-small cell lung cancer (NSCLC) is currently the most prevalent malignancy worldwide, and its therapeutic resistance poses an enormous challenge to current therapeutic efforts. As the most common internal modification of RNA molecules, n6-methyladenosine (m6A) affects RNA structure and function and regulates gene expression. It is widely acknowledged that this modification contributes to progression and resistance to drug therapy in NSCLC. Because tumors exhibit heterogeneous characteristics, the functional expression of m6A-modifying enzymes and the molecular mechanisms and downstream pathways they regulate exhibit distinct phenotypic characteristics. By precisely controlling the methylation process, understanding the specific regulatory mechanisms involved in m6A modification may result in more effective treatments for NSCLC progression and drug resistance. This review summarizes recent functional analyses of m6A modifications in NSCLC, focusing on their impact on therapeutic responses via modulation of specific gene expression levels. Furthermore, we examined the potential of m6A modifications as therapeutic interventions and predictive biomarkers for drug resistance, aiming to enable individualized and precise therapeutic strategies to treat NSCLC.

In recent years, RNA modifications have been shown to play a key role in regulating immune cell functions, reshaping the tumor immune microenvironment (TIME), mediating immune escape, and influencing the efficacy of immunotherapy. These processes are central to the field of epitranscriptomics. Researchers have discovered various RNA modifications, such as N6-methyladenosine (m⁶A), 5-methylcytosine (m⁵C), N1-methyladenosine (m¹A), N7-methylguanosine (m⁷G), and N4-acetylcytosine (ac⁴C), that dynamically regulate the development, differentiation, activation, and functional state of immune cells through the " writers-readers-erasers " system-a set of enzymes that add, recognize, and remove these modifications-thus contributing to the formation and evolution of the TIME. Furthermore, RNA modification enzymes can serve as predictive markers of general immune responses and are also closely linked to responses to immunotherapy. Accordingly, they have become potential targets for combination therapies. As RNA modification detection technologies advance, researchers are uncovering the spatial heterogeneity and cell-specific regulatory mechanisms of RNA modifications in tumor immunity, which provides new strategies for targeted immunotherapy. However, the regulatory mechanisms of certain RNA modifications on specific immune cells remain unclear, and how to translate research findings into clinical applications also requires further exploration.