Cancer Biomarkers最新文献

{"title":"Systematic exploration of prognostic alternative splicing events related to tumor immune microenvironment of Clear Cell Renal Cell Carcinoma.","authors":"Hongwei Wu, Yuchuan Zhou, Xi Wang, Chunhan Tang, Fang Yang, Ke Xu, Tao Ren","doi":"10.1177/18758592251317402","DOIUrl":"https://doi.org/10.1177/18758592251317402","url":null,"abstract":"<p><p>BackgroundPathologically, clear cell renal cell carcinoma (ccRCC) is the most common type of renal carcinoma, with high heterogeneity and poor prognosis. There is increasing evidence that alternative splicing (AS) is involved in tumor evolution and tumor immune microenvironment (TIME). However, studies on the exploration of AS events and TIME in ccRCC are still few but needed.MethodsThe transcriptional data and clinicopathological information of patients with ccRCC in The Cancer Genome Atlas (TCGA) database were extracted completely. Patients were grouped according to the ESTIMATE algorithm and differentially expressed AS events (DEASs) were identified. The relationship between AS events and features of TIME were investigated by functional enrichment analysis and unsupervised consensus analysis. Finally, hub splicing factors (SFs) was identified by the regulatory network of survival-related AS events and intersection SFs, and its biological function was further verified in vitro.ResultsIn total, the data of 515 patients with ccRCC were extracted and analyzed. Patients with low immune-score presented longer overall survival (OS) than high immune-score. 861 AS events were identified as DEASs, and they were enriched in immune-related pathways. 3 AS-based clusters were identified and found to have different prognoses and unique immune features. Finally, MBNL1 was identified as a hub SF, and it was shown to inhibit proliferation and metastasis, promote apoptosis, and block cells in G2/M phase in 786O and A498 cells. Mechanistically, MBNL1 regulates QKI expression through AS.ConclusionThe prognostic risk model constructed base on immune-related AS events has good predictive ability for ccRCC. The hub SF MBNL1 identied in the present study could inhibit the progression of ccRCC. This effect is likely due to the regulation of QKI expression through AS.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592251317402"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"External validation of CEA and CA125 prediction model for lymph node metastasis in endometrial cancer: A multi-institute cohort study.","authors":"Hao Lin, Hung-Chun Fu, Szu-Yu Huang, Chen-Hsuan Wu, Szu-Wei Huang, Shao-Chi Wang, Yu-Che Ou","doi":"10.1177/18758592241306265","DOIUrl":"https://doi.org/10.1177/18758592241306265","url":null,"abstract":"<p><p>BackgroundWe previously utilized pretreatment tumor markers Carcinoembryonic Antigen (CEA) and Cancer Antigen 125 (CA125) for predicting lymph node metastasis (LNM) in endometrioid endometrial cancer (EC).ObjectiveThe aim of this study was to externally validate a nomogram developed in our previous single-center retrospective study.MethodsA multi-center validation study was conducted to recruit endometrioid EC patients from four branches of Chang Gung Memorial Hospital between 2009 and 2021, with patients participating in the original research being excluded. The previously established nomogram was applied with optimal cut-off values for CEA 1.4 ng/ml and CA125 40 U/mL identified through receiver operating characteristic (ROC) curves. The concordance index (C-index) was calculated to assess discrimination, and comparative negative predictive value (NPV) and negative likelihood ratio (NLR) were determined. Decision curve analysis (DCA) was plotted to evaluate our predictive model's clinical utility and net benefit.ResultsOverall, 1271 patients were included in this external validation study. The results demonstrated a C-index of 0.727, indicating moderate discrimination ability of the nomogram in predicting LNM in this independent cohort. Comparative analysis of NPV 97.2% and NLR 0.36 revealed performance metrics consistent with the original study, reinforcing the nomogram's potential clinical utility in ruling out the possibility of LNM if both pretreatment CEA and CA125 were less than 1.4 ng/ml and 40 U/mL, respectively. The DCA indicated that the nomogram provided clinical utility.ConclusionThe reproducible performance metrics in the independent large sample cohort underscore the robustness and generalizability of utilizing CEA and CA125 as predictors of LNM in endometrioid EC, suggesting its potential as a simple tool for clinicians in preoperative decision-making regarding lymphadenectomy.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592241306265"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of low-intensity resistance exercise training on Serum tumor biomarkers and quality of life in women with breast cancer: A randomized controlled trial.","authors":"Deniz Kocamaz, Nahide Ayhan Fidancioğlu, Ramazan Cihad Yilmaz, Kübranur Ünal, Tülin Düger, Hüseyin Yüce Bircan, Yavuz Yakut","doi":"10.1177/18758592251329201","DOIUrl":"https://doi.org/10.1177/18758592251329201","url":null,"abstract":"<p><p>BackgroundAs the role of physical activity in breast cancer management gains increasing recognition, understanding the effects of aerobic exercise on patients' quality of life and biological markers has emerged as a critical area of research to inform clinical practices and improve patient outcomes.ObjectiveThis study aims to investigate the impact of low-intensity resistance exercise training on serum tumor biomarkers and quality of life in women with breast cancer, providing evidence for its potential role as an adjunct therapy in improving clinical outcomes and patient well-being.MethodsThis study was carried out on 70 women between the ages of 18 and 65, who were included in the study while receiving chemotherapy treatment. The subject was divided into low-intensity resistance exercise (Group I) and control (Group II). Demographic characteristics, quality of life, and serum tumor biomarkers were evaluated. Participants in group I underwent a 12-week exercise programme of low-intensity resistance exercises three times a week (three metabolic equivalents, approximately 30 min/session).ResultsThe quality of life has been found to be significantly higher in the low-intensity resistance exercise group (p < 0.05). The serum tumor biomarker levels of CEA, CA15-3, and CA19-9 decreased across all participants. However, the reduction in serum tumor biomarker levels was found to be more pronounced in Group 1 (p < 0.05).ConclusionsLow-intensity resistance exercise has demonstrated a positive effect on the quality of life in women with breast cancer. Within the framework of oncological rehabilitation, aerobic exercise regimens may be preferred due to their role in promoting improvements in serum tumor biomarker levels and contributing to enhanced quality of life.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592251329201"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain tumor segmentation and detection in MRI using convolutional neural networks and VGG16.","authors":"Shunmugavel Ganesh, Ramalingam Gomathi, Suriyan Kannadhasan","doi":"10.1177/18758592241311184","DOIUrl":"https://doi.org/10.1177/18758592241311184","url":null,"abstract":"&lt;p&gt;&lt;p&gt;BackgroundIn this research, we explore the application of Convolutional Neural Networks (CNNs) for the development of an automated cancer detection system, particularly for MRI images. By leveraging deep learning and image processing techniques, we aim to build a system that can accurately detect and classify tumors in medical images. The system's performance depends on several stages, including image enhancement, segmentation, data augmentation, feature extraction, and classification. Through these stages, CNNs can be effectively trained to detect tumors in MRI images with high accuracy. This automated cancer detection system can assist healthcare professionals in diagnosing cancer more quickly and accurately, improving patient outcomes. The integration of deep learning and image processing in medical diagnostics has the potential to revolutionize healthcare, making it more efficient and accessible.MethodsIn this paper, we examine the failure of semantic segmentation by predicting the mean intersection over union (mIoU), which is a standard evaluation metric for segmentation tasks. mIoU calculates the overlap between the predicted segmentation map and the ground truth segmentation map, offering a way to evaluate the model's performance. A low mIoU indicates poor segmentation, suggesting that the model has failed to accurately classify parts of the image. To further improve the robustness of the system, we introduce a deep neural network capable of predicting the mIoU of a segmentation map. The key innovation here is the ability to predict the mIoU without needing access to ground truth data during testing. This allows the system to estimate how well the model is performing on a given image and detect potential failure cases early in the process. The proposed method not only predicts the mIoU but also uses the expected mIoU value to detect failure events. For instance, if the predicted mIoU falls below a certain threshold, the system can flag this as a potential failure, prompting further investigation or triggering a safety mechanism in the autonomous vehicle. This mechanism can prevent the vehicle from making decisions based on faulty segmentation, improving safety and performance. Furthermore, the system is designed to handle imbalanced data, which is a common challenge in training deep learning models. In autonomous driving, certain objects, such as pedestrians or cyclists, might appear much less frequently than other objects like vehicles or roads. The imbalance can cause the model to be biased toward the more frequent objects. By leveraging the expected mIoU, the method can effectively balance the influence of different object classes, ensuring that the model does not overlook critical elements in the scene. This approach offers a novel way of not only training the model to be more accurate but also incorporating failure prediction as an additional layer of safety. It is a significant step forward in ensuring that autonomous systems, ","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592241311184"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From discovery to clinical implementation of a pancreatic blood biomarker, apolipoprotein A2 isoform.","authors":"Ayumi Kashiro, Giman Jung, Kazufumi Honda","doi":"10.1177/18758592251317405","DOIUrl":"https://doi.org/10.1177/18758592251317405","url":null,"abstract":"<p><p>Pancreatic cancer is a rare and refractory cancer, and the development of blood biomarkers for the enrichment of high-risk individuals who have risk factors for pancreatic cancer from the asymptomatic population is an unmet medical need. We identified abnormalities in the C-terminal truncation of the apolipoprotein A2 dimer (apoA2-isoforms: apoA2-i) in the blood of pancreatic cancer patients through proteomic analysis, and we have reported the potential for diagnosing resectable pancreatic cancer by detecting these abnormalities. We successfully developed enzyme-linked immunosorbent assay (ELISA) reagents for measuring apoA2-i for research use only, and then the basic data for diagnosing pancreatic cancer were accumulated by several studies using these reagents. In 2023, ELISA for measuring apoA2-i was regenerated by the regulation under the Japanese Quality Management System (QMS), it received marketing approval in Japan as an <i>in vitro</i> diagnostic (IVD) kit to aid in the diagnosis of pancreatic cancer, and it is now used in clinical practice. This review chronicles the journey from the initial discovery through omics research, to demonstrating clinical utility via multicenter studies in Japan and international collaborative research using the research reagent and validating the clinical performance of the IVD ELISA kit through a regulatory, science-guided, clinical trial in Japan, and finally to recent activities in the USA.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592251317405"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the regulatory role of CNPY3 as a prognostic biomarker on human glioma cell migration, invasion and immune infiltration.","authors":"Lu Zhan, Fanyue Zeng, Jie Zheng, Sijing Chen, Zhiyun Zhang, Donghui Ju","doi":"10.1177/18758592251328162","DOIUrl":"https://doi.org/10.1177/18758592251328162","url":null,"abstract":"<p><p>BackgroundCanopy FGF signalling regulator 3 (CNPY3) is involved in immune regulation, tumorigenesis and development, nevertheless, its role in glioma remains largely unexplored. Our study aimed to explore the regulatory role of CNPY3 as a prognostic biomarker in human glioma cell migration, invasion and immune infiltration.MethodsBioinformatics analysis of CNPY3 and clinical relevance of glioma in public databases was performed. COX regression analysis was performed to assess the relationship between CNPY3 and glioma prognosis. GO and Kyoto Encyclopedia of Genes and Genomes analyses were conducted to predict the signaling pathways of CNPY3 in gliomas. Tumor immune infiltration was explored using TIMER, CIBERSORT, and Pearson correlation analysis. GSVA analysis and single-cell sequencing data were employed for further validation. The effects of CNPY3 on the migration and invasion of glioma cells were investigated through cell scratch assay and transwell assay.ResultsCNPY3 was positively correlated with IDH mutation status, 1p/19q status, histopathologic grade, and MGMT promoter methylation status, but negatively with the overall survival of glioma patients (<i>P </i>< 0.05). CNPY3 was significantly associated with tumor immune response, inflammatory response, and lipopolysaccharide-mediated signaling pathway. CNPY3 influenced different types of immune cells which affected the immune microenvironment of glioma. CNPY3 promoted the increase of M2 macrophage and was negatively correlated with the positive regulation of macrophages apoptotic process. In vitro data suggested the promotion of CNPY3 in U87MG cells was associated with an increased capacity for cell migration and invasion (<i>P </i>< 0.05). Tumor drug sensitivity analysis showed more sensitivity towards temozolomide, irinotecan, and cisplatin among high CNPY3 expression patients (<i>P </i>< 0.05).ConclusionIncreased CNPY3 expression impacts the immune microenvironment of glioma and enhances the migration and invasion of glioma. CNPY3 is recommended as a prognostic biomarker for glioma patients.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592251328162"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BUB1, miR-495-3p, and E2F1/E2F8 axis is associated with poor prognosis of breast cancer patients and infiltration of Th2 cells in the tumor microenvironment.","authors":"Rajeev Nema, Ashok Kumar","doi":"10.1177/18758592241310109","DOIUrl":"https://doi.org/10.1177/18758592241310109","url":null,"abstract":"<p><p>Breast cancer, the most common cancer in women, is characterized by cell cycle dysregulation and chromosome segregation errors, leading to mitotic catastrophe and genomic instability. Understanding these molecular mechanisms is crucial for better diagnosis and treatment. We used databases like TIMER 2.0, UALCAN, and Oncomine to determine the differential expression of Budding uninhibited by benzimidazole 1 (BUB1) in normal and pan-cancer tissues. we also used the Kaplan-Meier Plotter database to analyze gene expression associations with survival outcomes, bc-GenExMiner v5.0 to analyze BUB1 gene expression and histological subtypes, and ctcRbase and miR-TV to identify microRNAs associated with BUB1 expression in breast cancer. Our data show that BUB1 expression is overexpressed in breast cancer tumors, metastatic tissues, and circulating tumor cells, leading to <u>shorter</u> overall survival, disease-free survival, and relapse-free survival compared to low-expression patients. BUB1 expression is strongly correlated with E2F1/E2F8 expression, suggesting a potential regulatory relationship between these genes. The study revealed a negative correlation between target miRNA miR-495-3p and BUB1 expression in breast cancer tumors, indicating a potential regulatory relationship between these genes. The BUB1 expression was also strongly correlated with the infiltration of CD4+ T helper 2 (Th2) subtypes in the tumors, suggesting a need for further research.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 3","pages":"18758592241310109"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia inducible factor-1α promotes non-small cell lung cancer progression by activating leptin receptor transcription.","authors":"Yan Li, Bo Chen, Shuangshuang Wu, Yijue Zhong, Yuxing Zhang, Jianqing Wu","doi":"10.1177/18758592251330479","DOIUrl":"https://doi.org/10.1177/18758592251330479","url":null,"abstract":"<p><p>BackgroundHypoxia and leptin receptors (also called obesity receptors, OB-R) are evident markers of tumor progression and have been demonstrated to be essential oncogenes in a variety of cancers. However, the specific role of OB-R in lung cancer, especially non-small cell lung cancer (NSCLC) and its correlation with HIF1α remains unclear. Present study aims to explore the potential functions and mechanisms of OB-R in NSCLC.MethodsThe RNA levels of HIF1α and OB-R in NSCLC cells were detected by quantitative real-time PCR (qRT-PCR) and western blotting. The HIF-1α, OB-R, and Ki67 levels in tumor tissues were detected by immunohistochemistry. CCK8 assays for proliferation, transwell assays for migration were performed to determine the role of HIF-1α and OB-R <i>in vitro</i>, while subcutaneous tumors in nude mice were used for <i>in vivo</i> functional studies. Mechanically, chromatin immunoprecipitation and luciferase reporter gene analyses were executed to determine the relationship between HIF-1α and OB-R.ResultsqRT-PCR and western blotting revealed that HIF-1α and OB-R was highly expressed in NSCLC cells. Moreover, hypoxia up-regulated OB-R expression in NSCLC cells via HIF-1α. Hence, down-regulating HIF-1α significantly reduced the mRNA level of OB-R. In addition, HIF-1α silencing reduced cell proliferation and migration <i>in vitro</i>. Xenograft mouse models indicated that decrease of HIF-1α led to tumor growth by decreasing OB-R <i>in vivo</i>. Mechanically, we unveiled that HIF-1α bound to the promoter region (-831 to -824) and positively regulated OB-R expression by activating its transcription. Additionally, by immunohistochemical staining, we observed that high levels of HIF-1α and OB-R were positively associated with tumor size and lymph node metastasis.ConclusionIn conclusion, our present results demonstrated that HIF-1α positively regulates the expression of OB-R, which acts as an oncogene in NSCLC. HIF-1α and OB-R are potential therapeutic targets in NSCLC.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 2","pages":"18758592251330479"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of key genes related to cancer associated fibroblasts in neuroblastoma: A comprehensive bioinformatics approach.","authors":"Zhao Qianyun, Wang Jianjun, Fan Kaisi, Li Jinhao, Chen Renhai, Ding Xiaoting, Li Yongteng, Yang Liucheng, Wu Kai","doi":"10.1177/18758592251317406","DOIUrl":"https://doi.org/10.1177/18758592251317406","url":null,"abstract":"<p><p>BackgroundNeuroblastoma (NB) is one of the most common and aggressive pediatric solid tumors, characterized by a highly complex pathogenesis. Within the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) constitute a major cell population and play a pivotal role in facilitating communication among various stromal cells. However, the specific functions and contributions of CAFs in NB remain incompletely understood.ObjectiveTo investigate the impact of CAFs-related genes on the prognosis of NB, we developed a risk model to facilitate the diagnosis and prognostication of patients.MethodsIn this study, a CAFs gene prognostic model for NB was established using single-cell analysis and genomic sequencing data. The effectiveness of this prognostic model was subsequently evaluated through the development of a nomogram, immune infiltration analysis, drug prediction, and gene set enrichment analysis. Ultimately, the expression levels of the identified key genes were experimentally validated in NB tissues.ResultsA novel prognostic model for CAFs related to NB prognosis was established through single-cell analysis and transcriptome dataset analysis. The prognosis of the high-risk group was worse than that of the low-risk group. The validity of the model was confirmed by nomogram, drug sensitivity analysis, and immune infiltration methods. Finally, the high expression of the key gene STEAP2 in NB tissues was verified by experiments.ConclusionsThe study introduces a new predictive model that uses CAF markers to forecast the prognosis of NB. STEAP2 plays a key role in identifying high-risk neuroblastoma and may become a potential therapeutic target for NB.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 2","pages":"18758592251317406"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Panax notoginseng improves the sensitivity of non-small cell lung cancer to cisplatin by inhibiting Akt signaling.","authors":"Lizhen Pan, Dandan Zhang, Qiqi Shao, Maohao Cheng, Zhicheng Liao, Lingpei Yu, Yuanyuan Wang, Pengcheng Jia, Jizhou Zhang","doi":"10.1177/18758592241303377","DOIUrl":"https://doi.org/10.1177/18758592241303377","url":null,"abstract":"<p><p>BackgroundCisplatin (DDP) resistance is a major challenge in the management of non-small cell lung cancer (NSCLC). Panax notoginseng has anticancer effects on a variety of solid tumors, but data on NSCLC and DDP resistance are lacking.ObjectiveTo investigate the effect of Panax notoginseng on DDP resistance in NSCLC in vitro and in vivo and explore the mechanisms involved.MethodsA 1 g/mL Panax notoginseng extract was prepared to treat the A549 and DDP-resistant A549/DDP cell lines. Cell proliferation was assessed using the CCK-8 assay, and apoptosis was measured via Annexin V-FITC/PI staining and flow cytometry. Glucose uptake, ATP production, and lactate levels were evaluated. Protein levels of p-AKT, GLUT1, HKII, and cleaved-caspase-3 were analyzed by Western blot. IGF1 was used to activate the Akt pathway. In vivo, A549/DDP cells were inoculated into nude mice to establish subcutaneous tumors, and tumor growth and apoptosis were assessed.ResultsPanax notoginseng inhibited A549/DDP cell proliferation, enhanced DDP-induced apoptosis, and reduced glucose uptake, ATP, and lactate levels (all <i>p</i> < 0.05). Combined treatment decreased p-AKT, GLUT1, and HKII expression while increasing cleaved-caspase-3(<i>p</i> < 0.05). IGF1 reversed these effects, indicating Akt pathway involvement (<i>p</i> < 0.05). In vivo, Panax notoginseng and DDP significantly suppressed tumor growth and increased apoptosis in tumors, confirming enhanced chemosensitivity (<i>p</i> < 0.05).ConclusionPanax notoginseng can improve the sensitivity of A549/DDP cells to DDP by inhibiting the effects of TRIM46 and Akt signaling pathways on glycolysis in vivo and in vitro.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 2","pages":"18758592241303377"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}