MedComm最新文献

{"title":"Heat Shock Protein Family A Member 1A Attenuates Apoptosis and Oxidative Stress via ERK/JNK Pathway in Hyperplastic Prostate","authors":"Huan Liu,&nbsp;Yongying Zhou,&nbsp;Zhen Wang,&nbsp;Daoquan Liu,&nbsp;Yan Li,&nbsp;Huan Lai,&nbsp;Jizhang Qiu,&nbsp;Shidong Shan,&nbsp;Feng Guo,&nbsp;Ping Chen,&nbsp;Yuming Guo,&nbsp;Guang Zeng,&nbsp;Michael E. DiSanto,&nbsp;Xinhua Zhang","doi":"10.1002/mco2.70129","DOIUrl":"https://doi.org/10.1002/mco2.70129","url":null,"abstract":"<p>Benign prostatic hyperplasia (BPH) is a prevalent disorder in aging males. It is investigated whether heat shock protein family A member 1A (HSPA1A), a cytoprotective chaperone induced under stress, has been implicated in the development of BPH. RNA-sequencing and single-cell sequencing analyses revealed significant upregulation of HSPA1A in BPH compared to controls. In vitro experiments elucidated that HSPA1A was localized in prostatic epithelium and stroma, with upregulated expression in BPH tissues. Moreover, HSPA1A silencing augmented apoptosis and reactive oxygen species (ROS) accumulation, inhibiting proliferation via ERK/JNK activation, while overexpression reversed these effects in prostatic BPH-1 and WPMY-1 cells. Additionally, ERK1/2 suppression with U0126 rescued the effects of HSPA1A silencing. In vivo, testosterone-induced BPH (T-BPH) rat models treated with the HSPA1A antagonist KNK437 exhibited prostatic atrophy and molecular changes consistent with reduced HSPA1A activity. Finally, we conducted a tissue microarray (TMA) analysis of 139 BPH specimens from Zhongnan Hospital of Wuhan University, which revealed a positive correlation between HSPA1A expression and clinical parameters, including prostate volume (PV), tPSA, fPSA, and IPSS. In conclusion, our findings suggested that HSPA1A attenuated apoptosis and oxidative stress through the ERK/JNK signaling pathway, contributing to BPH pathogenesis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70129","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep Disorders: Pathogenesis and Therapeutic Interventions","authors":"Cheng Liu,&nbsp;Zhigang He,&nbsp;Yanqiong Wu,&nbsp;Yanbo Liu,&nbsp;Zhixiao Li,&nbsp;Yifan Jia,&nbsp;Hongbing Xiang","doi":"10.1002/mco2.70130","DOIUrl":"https://doi.org/10.1002/mco2.70130","url":null,"abstract":"<p>Sleep disorder significantly disrupts the quality of life for patients. Although it is clinically acknowledged, the fundamental neuropathological mechanisms are still not understood. Recent preclinical research has been directed toward understanding the fundamental mechanisms underlying the sleep deprivation and sleep/wake dysregulation. Sleep disorder is linked to changes in the structure and function of the neural basis of cognition. We reviewed the neural circuits related to sleep disorders, along with alterations in connectivity and brain region functions, based on advancements in electrophysiology and optogenetic/chemogenetic techniques. We subsequently outline the cellular and molecular modifications linked to sleep disorders in preclinical studies, primarily involving changes in neuronal metabolism, electrophysiological activity, synaptic plasticity, and glial cells. Correspondingly, on the basis of the crosstalk between the brain and peripheral organs, we elucidate the underlying mechanisms of the involvement of celiac disease and hepatic disease in the pathogenesis of sleep disorders. In this review, we mainly discussed the pathogenesis at molecular, cellular, and neural circuit levels that contribute to sleep disorder. The review also covered potential strategies for treating sleep disorders and future research avenues.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fusobacterium nucleatum Promotes the Growth and Metastasis of Colorectal Cancer by Activating E-Cadherin/Krüppel-Like Factor 4/Integrin α5 Signaling in a Calcium-Dependent Manner","authors":"Xuebing Yan,&nbsp;Xiao Qu,&nbsp;Jiaxin Wang,&nbsp;Ling Lu,&nbsp;Wenjuan Wu,&nbsp;Jingxian Mao,&nbsp;Donglin Li,&nbsp;Ying Wang,&nbsp;Qing Wei,&nbsp;Jianqiang Liu","doi":"10.1002/mco2.70137","DOIUrl":"https://doi.org/10.1002/mco2.70137","url":null,"abstract":"<p>Gut microbiota and integrins are known to contribute to colorectal cancer (CRC), but whether they interact has been unclear. Here, we provided evidence that <i>Fusobacterium nucleatum</i> upregulated integrin α5 (ITGA5) in CRC in both human patients and murine models. Knocking down <i>ITGA5</i> in CRC cells weakened the ability of <i>F. nucleatum</i> to stimulate their malignant characteristics. <i>Fusobacterium nucleatum</i> increased intracellular Ca²⁺ concentration, which in turn promoted interaction between E-cadherin and Krüppel-like factor 4 (KLF4), resulting in KLF4 phosphorylation and translocation in the nucleus, where it induced <i>ITGA5</i> transcription and activated the downstream signaling. Knocking down E-cadherin or chelating Ca²⁺ with BAPTA-AM antagonized the impact of <i>F. nucleatum</i> on KLF4, whereas knocking down <i>KLF4</i> or chelating Ca²⁺ antagonized the bacteria's oncogenic role. Knocking down <i>KLF4</i> or <i>ITGA5</i> attenuated <i>F. nucleatum–</i>induced growth of patient-derived organoids, subcutaneous xenografts, and orthotopic tumors, as well as liver metastasis in nude mice. Integrin α5 antibody antagonized the oncogenic role of <i>F. nucleatum</i> in vitro and in vivo. These findings suggest that <i>F. nucleatum</i> promotes the growth and metastasis of CRC by activating E-cadherin/KLF4/integrin α5 signaling in a Ca²⁺-dependent manner.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70137","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Utility of 18Fluorine-Fibroblast Activation Protein Inhibitor-04 Positron Emission Tomography/Computed Tomography in the Evaluation of Pancreatic Ductal Adenocarcinoma: Comparison With 18Fluorine-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography","authors":"Lili Lin,&nbsp;Guangfa Wang,&nbsp;Yafei Zhang,&nbsp;Guolin Wang,&nbsp;Kui Zhao,&nbsp;Xinhui Su","doi":"10.1002/mco2.70136","DOIUrl":"https://doi.org/10.1002/mco2.70136","url":null,"abstract":"<p>Pancreatic ductal adenocarcinoma (PDAC) is highly susceptible to metastasis, making early detection of metastases and associated risk factors crucial for effective management. This study aimed to assess the performance of ¹⁸fluorine (¹⁸F)- fibroblast activation protein inhibitor-04 (¹⁸F-FAPI-04) positron emission tomography/computed tomography (PET/CT) in detecting metastasis and predicting pathological characteristics and risk factors in 67 PDAC patients. Comparisons were made with ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) PET/CT. Lesion identifications and radiotracer uptakes were evaluated through visual inspection and semiquantitative analysis using the maximum standardized uptake value (SUVmax). We analyzed the risk factors for metastasis and observed that ¹⁸F-FAPI-04 identified more positive lesions and showed significantly higher SUVmax values than ¹⁸F-FDG in both primary tumors and metastases, leading to upstaging in several cases. In primary tumors, ¹⁸F-FAPI-04 was associated with higher levels of poorly differentiated PDAC, compared to those with moderately differentiated tumors. Notably, the SUVmax of 18F-FAPI-04 in primary tumors demonstrated a significant correlation with pathological differentiation and served as an independent prognostic factor for peritoneal metastasis, rather than lymph node or liver metastasis. Our findings suggested that ¹⁸F-FAPI-04 PET/CT offers superior tumor detectability and improved node-metastasis (NM) staging in PDAC patients, positioning it as a more effective tool than ¹⁸F-FDG PET/CT.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions","authors":"Huimin Yuan,&nbsp;Ruochen Xu,&nbsp;Senlin Li,&nbsp;Mengzhu Zheng,&nbsp;Qingyi Tong,&nbsp;Ming Xiang,&nbsp;Yonghui Zhang","doi":"10.1002/mco2.70121","DOIUrl":"https://doi.org/10.1002/mco2.70121","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality globally, predominantly associated with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. These infections drive persistent liver inflammation, culminating in cellular dysregulation, fibrosis, and cancer. Despite advancements in targeted therapies, drug resistance and the lack of reliable biomarkers for patient stratification still terribly hinder the treatment of viral HCC. To this end, the review delves into the intricate mechanisms underlying the malignant transformation of viral hepatitis to HCC, including viral integration, genomic instability, epigenetic modifications, oxidative stress, gut microbiota dysbiosis, chronic inflammation, immune escape, and abnormal signaling pathways, highlighting their complex interactions and synergies. Cutting-edge preclinical and clinical advancements in HCC management, including lifestyle modifications, drug therapies, immunotherapies, gene-based approaches, and innovative treatments, are further investigated, with particular priority given to their therapeutic potential and future applications in overcoming current limitations. By synthesizing recent scientific and clinical insights, this review aims to deepen the understanding of HCC pathogenesis in the context of chronic viral hepatitis, paving the way for novel therapeutic targets and personalized treatment strategies, ultimately improving patient outcomes.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases","authors":"Liuting Zeng,&nbsp;Wang Xiang,&nbsp;Wei Xiao,&nbsp;Yang Wu,&nbsp;Lingyun Sun","doi":"10.1002/mco2.70101","DOIUrl":"https://doi.org/10.1002/mco2.70101","url":null,"abstract":"<p>Neutrophil extracellular traps (NETs) are unique fibrous structures released by neutrophils in response to various pathogens, exhibiting both anti-inflammatory and proinflammatory effects. In autoimmune conditions, NETs serve as crucial self-antigens triggering inflammatory cascades by activating the inflammasome and complement systems, disrupting self-tolerance mechanisms and accelerating autoimmune responses. Furthermore, NETs play a pivotal role in modulating immune cell activation, affecting adaptive immune responses. This review outlines the intricate relationship between NETs and various diseases, including inflammatory arthritis, systemic autoimmune diseases, Behçet's disease, systemic lupus erythematosus, autoimmune kidney diseases, autoimmune skin conditions, systemic sclerosis, systemic vasculitis, and gouty arthritis. It highlights the potential of targeting NETs as a therapeutic strategy in autoimmune diseases. By examining the dynamic balance between NET formation and clearance in autoimmune conditions, this review offers critical insights and a theoretical foundation for future research on NET-related mechanisms. Advances in systems biology, flow cytometry, and single-cell multiomics sequencing have provided valuable tools for exploring the molecular mechanisms of neutrophils and NETs. These advancements have renewed focus on the role of neutrophils and NETs in autoimmune diseases, offering promising avenues for further investigation into their clinical implications.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143564992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Colorectal Cancer: Pathogenesis and Targeted Therapy","authors":"Jingyuan Li,&nbsp;Jiashu Pan,&nbsp;Lisheng Wang,&nbsp;Guang Ji,&nbsp;Yanqi Dang","doi":"10.1002/mco2.70127","DOIUrl":"https://doi.org/10.1002/mco2.70127","url":null,"abstract":"<p>Colorectal cancer (CRC) ranks among the most prevalent malignant neoplasms globally. A growing body of evidence underscores the pivotal roles of genetic alterations and dysregulated epigenetic modifications in the pathogenesis of CRC. In recent years, the reprogramming of tumor cell metabolism has been increasingly acknowledged as a hallmark of cancer. Substantial evidence suggests a crosstalk between tumor cell metabolic reprogramming and epigenetic modifications, highlighting a complex interplay between metabolism and the epigenetic genome that warrants further investigation. Biomarkers associated with the pathogenesis and metabolic characteristics of CRC hold significant clinical implications. Nevertheless, elucidating the genetic, epigenetic, and metabolic landscapes of CRC continues to pose considerable challenges. Here, we attempt to summarize the key genes driving the onset and progression of CRC and the related epigenetic regulators, clarify the roles of gene expression and signaling pathways in tumor metabolism regulation, and explore the potential crosstalk between epigenetic events and tumor metabolic reprogramming, providing a comprehensive mechanistic explanation for the malignant progression of CRC. Finally, by integrating reliable targets from genetics, epigenetics, and metabolic processes that hold promise for translation into clinical practice, we aim to offer more strategies to overcome the bottlenecks in CRC treatment.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PD-1/PD-L1 Inhibitors Plus Chemotherapy Versus Chemotherapy Alone as First-Line Therapy for Patients With Unfavorable Cancer of Unknown Primary: A Multicenter, Retrospective Cohort Study","authors":"Riqing Huang,&nbsp;Haifeng Li,&nbsp;Shuo Li,&nbsp;Ditian Shu,&nbsp;Rishang Chen,&nbsp;Zhousan Zheng,&nbsp;Tinghua Gao,&nbsp;Meiting Chen,&nbsp;Anqi Hu,&nbsp;Yunjie Huang,&nbsp;Qiufan Zheng,&nbsp;Xin An,&nbsp;Cong Xue,&nbsp;Yuchen Cai,&nbsp;Yanxia Shi","doi":"10.1002/mco2.70124","DOIUrl":"https://doi.org/10.1002/mco2.70124","url":null,"abstract":"<p>This multicenter study aimed to investigate the efficacy and safety of PD-1/PD-L1 inhibitors plus chemotherapy (ICI-Chemo group) versus chemotherapy alone (Chemo group) for patients with cancer of unknown primary (CUP) in the first-line setting. We included patients with unfavorable CUP across four medical centers in China. Between January 2014 and December 2023, 117 patients were enrolled: 46 patients in the ICI-Chemo group and 71 patients in the Chemo group. After a median follow-up of 28.1 months, the ICI-Chemo group exhibited a significant improvement over the Chemo group in median PFS (9.10 months vs. 6.37 months; hazard ratio [HR] 0.46; 95% CI: 0.30–0.71; <i>p</i> &lt; 0.001) and OS (35.67 months vs. 10.2 months; HR 0.37; 95% CI: 0.22–0.64; <i>p</i> &lt; 0.001). Similarly, among patients who received TP (taxane plus platinum)-based chemotherapies, OS and PFS benefits were observed in the ICI-Chemo group. The objective response rate was higher in the ICI-Chemo group than in the Chemo group (54.35% vs. 22.53%, <i>p</i> &lt; 0.001). Grade 3 or higher drug-related adverse events occurred in 11 patients (23.91%) in the ICI-Chemo group and 28 patients (39.44%) in the Chemo group. Thus, PD-1/PD-L1 inhibitors plus chemotherapy could be the preferred first-line treatment for patients with unfavorable CUP, providing improved efficacy and manageable toxicity.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining JAK Inhibitors with Immune Checkpoint Inhibitors: Overcoming Resistance in Cancer Treatment","authors":"Hai-Jing Zhong","doi":"10.1002/mco2.70141","DOIUrl":"https://doi.org/10.1002/mco2.70141","url":null,"abstract":"&lt;p&gt;Balancing acute inflammation and chronic inflammation is challenging in cancer immunotherapy while two recent groundbreaking studies published in &lt;i&gt;Science&lt;/i&gt; have shown a promising strategy to address this challenge by combining Janus kinase (JAK) inhibitors with anti-PD-1 therapy [&lt;span&gt;1, 2&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;One of these studies, Zak et al. [&lt;span&gt;1&lt;/span&gt;] assessed the efficacy of combining the anti-PD-1 antibody nivolumab with ruxolitinib in patients with relapsed or refractory Hodgkin lymphoma. Ruxolitinib, the first JAK inhibitor approved by US Food and Drug Administration, has proven to be clinically useful in treating graft-versus-host disease and myeloproliferative neoplasms [&lt;span&gt;3&lt;/span&gt;]. The combination therapy in the classical Hodgkin lymphoma (CHL) trial demonstrated striking efficacy, achieving a best overall response rate of 53% (10 out of 19). All enrolled patients had previously failed checkpoint inhibitor therapy, with eligibility criteria specifically requiring patients to have exhibited refractory disease, relapsed disease, or stable disease. Notably, significant clinical responses were observed in these patients.&lt;/p&gt;&lt;p&gt;In another clinical trial focusing on metastatic non-small cell lung cancer (NSCLC), the combination of anti-PD-1 therapy (pembrolizumab) and itacitinib, a selective JAK1 inhibitor, demonstrated remarkable efficacy. This study, conducted by Mathew et al., reported an overall response rate of 67% among the 21 treatment-naïve metastatic NSCLC patients with tumor PD-L1 ≥50% [&lt;span&gt;2&lt;/span&gt;]. This response rate significantly surpasses historical response rate of 44.8% to pembrolizumab monotherapy in NSCLC.&lt;/p&gt;&lt;p&gt;Immune checkpoint inhibitors (ICIs) are widely used as standard treatments for various cancer types; however, their overall response rate remains low across the broader patient population [&lt;span&gt;4&lt;/span&gt;]. These two studies in NSCLC and Hodgkin lymphoma show how well the combination works to enhance ICI efficacy and overcome resistance mechanisms (Figure 1).&lt;/p&gt;&lt;p&gt;JAK inhibitors help address the mixed effects of interferon (IFN) signaling, which can both stimulate and suppress antitumor immunity. While IFNs are important for antiviral and antitumor activity, persistent IFN signaling can lead to immunosuppression and resistance to ICIs therapy. This was demonstrated in the NSCLC study, where patients who responded to JAK inhibitor itacitinib addition showed decreased inflammatory signaling and reduced IFN-stimulated gene expression. By carefully timing JAK inhibition, the treatment can block the immunosuppressive effects of chronic inflammation while preserving beneficial acute inflammatory responses that support antitumor immunity. In the Hodgkin lymphoma study, the combination of ruxolitinib and checkpoint inhibitors demonstrated a unique ability to preserve and even enhance essential T cell functions, including cytokine production and proliferation, while carefully modulating chronic IFN signaling w","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic reprogramming in cancer and senescence","authors":"Yuzhu Zhang,&nbsp;Jiaxi Tang,&nbsp;Can Jiang,&nbsp;Hanxi Yi,&nbsp;Shu Guang,&nbsp;Gang Yin,&nbsp;Maonan Wang","doi":"10.1002/mco2.70055","DOIUrl":"https://doi.org/10.1002/mco2.70055","url":null,"abstract":"<p>The rising trend in global cancer incidence has caused widespread concern, one of the main reasons being the aging of the global population. Statistical data show that cancer incidence and mortality rates show a clear upward trend with age. Although there is a commonality between dysregulated nutrient sensing, which is one of the main features of aging, and metabolic reprogramming of tumor cells, the specific regulatory relationship is not clear. This manuscript intends to comprehensively analyze the relationship between senescence and tumor metabolic reprogramming; as well as reveal the impact of key factors leading to cellular senescence on tumorigenesis. In addition, this review summarizes the current intervention strategies targeting nutrient sensing pathways, as well as the clinical cases of treating tumors targeting the characteristics of senescence with the existing nanodelivery research strategies. Finally, it also suggests sensible dietary habits for those who wish to combat aging. In conclusion, this review attempts to sort out the link between aging and metabolism and provide new ideas for cancer treatment.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}