Oncology reports最新文献

{"title":"Overexpression of ATP1B2 promotes cancer cell migration and inhibits apoptosis in patients with esophageal squamous cell carcinoma.","authors":"Fang-Fei Liu, Hui Wen, Xiao-Bo Liu, Sheng-Bao Li, Shu Jin, Zi-Ye Gao, Qiang Tong","doi":"10.3892/or.2025.8929","DOIUrl":"10.3892/or.2025.8929","url":null,"abstract":"<p><p>The present study aimed to investigate the expression of ATP1B2 in esophageal squamous cell carcinoma (ESCC) and its biological effects. A total of 44 patients with ESCC who underwent surgical resection at Taihe Hospital between December 1, 2017 and December 1, 2018 were enrolled. The expression levels of ATP1B2 in cancerous and adjacent normal tissues were assessed. The present study also examined the associations between ATP1B2 expression and clinicopathological features and patient prognosis. The influence of ATP1B2 on ESCC cell proliferation, migration, cell cycle progression and apoptosis was evaluated using the methylcyclopentadienyl manganese tricarbonyl assay, plate cloning, scratch assay and flow cytometry. Furthermore, the effects of ouabain on these cellular processes were investigated. The results demonstrated that patients with high ATP1B2 expression exhibited significantly shorter overall survival than did those with low ATP1B2 expression (37.3 months vs. 43.1 months; Z=7.52; P<0.05). ATP1B2 expression, tumor invasion and lymph node metastasis were significantly associated (P<0.05). Notably, the overexpression of ATP1B2 correlated with reduced survival rates. ATP1B2 knockdown hindered cell migration and induced apoptosis, whereas ATP1B2 overexpression facilitated migration and impeded apoptosis. Ouabain treatment suppressed proliferation and migration in cells overexpressing ATP1B2 and caused cell cycle arrest in the G₁/S phase. In conclusion, ATP1B2 overexpression is associated with poor prognosis in patients with ESCC by enhancing cancer cell migration and reducing apoptosis. Ouabain is a potential targeted therapeutic agent for ESCC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HOTTIP suppresses ferroptosis via mediating DGCR8/miR‑214‑3p/GPX4 regulatory axis in osteosarcoma.","authors":"Shou-Chang Ding, Chuan-Jian Shi, Feng-Xiang Pang, Rui-Jia Wen, Nan Li, Yong-Xin Mai, Shu-Ting Zhou, Jin-Fang Zhang","doi":"10.3892/or.2025.8927","DOIUrl":"10.3892/or.2025.8927","url":null,"abstract":"<p><p>Osteosarcoma (OS) is the most common primary bone malignancy in children and adolescents and the current typical strategy remains unsatisfactory in clinical practice. Ferroptosis has been considered as a novel form of programmed cell death in eukaryotic cells, which is characterized by iron‑dependent lipid peroxidation accumulation. The emergence of ferroptosis brings great hope to develop the potential therapeutic targets for OS patients. Long noncoding (lnc)RNA HOXA transcript at the distal tip (HOTTIP) has been identified as an oncogene to facilitate tumorigenesis in OS. Whether ferroptosis participates in this lncRNA mediated OS tumorigenesis is not fully understood. In the present study, HOTTIP was found to be downregulated in the Erastin‑treated OS cells. Silence of HOTTIP promoted, while ectopic expression of HOTTIP suppressed, ferroptosis in OS cells <i>in vitro</i> and <i>in vivo</i>. Mechanically, HOTTIP recruited the RNA binding protein DiGeorge Critical Region 8 (DGCR8) and influenced its protein stability, which disrupted miR‑214‑3p biogenesis and facilitated the de‑repression of glutathione peroxidase 4 transcription, eventually leading to preventing ferroptosis. Taken together, the present study demonstrated that HOTTIP suppressed ferroptosis in OS cells via DGCR8/micro RNA 214‑3p/GPX4 regulatory axis, which might provide insights to develop HOTTIP as a promising therapeutic target for OS patients.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of extracellular vesicles as promotors for activation of leukemia‑derived dendritic cell‑mediated antileukemic immune response against AML‑blasts.","authors":"Lin Li, André Görgens, Veronika Mussack, Elena Pepeldjiyska, Anne Sophie Hartz, Hazal Aslan, Elias Rackl, Tobias Baudrexler, Andreas Rank, Jörg Schmohl, Doris Krämer, Samir El Andaloussi, Michael W Pfaffl, Helga Maria Schmetzer","doi":"10.3892/or.2025.8932","DOIUrl":"10.3892/or.2025.8932","url":null,"abstract":"<p><p>The transformation of myeloid leukemia blasts into leukemia‑derived dendritic cells (DC_leu) is a notable phenomenon. Extracellular vesicles (EVs) play a crucial role in modulating physiological and pathological activities, particularly in immune activation. In the present study, EVs were isolated from DC/DC_leu culture supernatants derived from healthy (H) donors (n=9) and patients with acute myeloid leukemia (AML) (n=9) using whole blood (WB) samples, both with and without Kit M (granulocyte‑macrophage colony‑stimulating factor and prostaglandin E₁). This was followed by T‑cell enriched mixed lymphocyte culture (MLC) with Kit M‑treated and untreated WB. To assess the qualitative and quantitative differences in EVs between Kit M‑treated and untreated samples, transmission electron microscopy, fluorescence nanoparticle tracking analysis and multiplex bead‑based flow cytometry were employed. The present findings indicate that DC/MLC supernatant‑derived EVs can be successfully identified, quantified and characterized. Furthermore, these EVs exhibit regulatory properties in both H and AML samples. Results showed that a higher number of CD8⁺ EVs were detected after DC culture compared with before in both H and AML samples. Thrombocyte‑associated EVs (CD41b⁺, CD42a⁺ and CD62P⁺) significantly increased following DC culture in both groups. While low frequencies of progenitor/blast marker (CD133⁺) associated EVs were detected in H samples before and after DC culture, their frequencies increased after DC culture in AML samples. Additionally, a higher number of CD8⁺ and CD2⁺ EVs were observed after MLC culture compared with before in both H and AML samples. Correlation analyses revealed that improved blast lysis in Kit M‑pretreated samples (normalized to control) associated with the presence of EV subtypes associated with T (CD2⁺), B (CD20⁺, 24⁺), and other cell markers (for example, CD31⁺, CD146⁺, CD44⁺ and CD49e⁺). This comprehensive approach provides insights into the impact of Kit M on DC/DC_leu generation and the subsequent activation of immune cells, leading to differences in EV production between H and AML samples.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between cancer‑associated fibroblasts and inflammation in tumor microenvironment: A novel perspective in cancer therapy (Review).","authors":"Xinyan Liu, Chaofeng Wang, Huijuan Mao, Jianzi Wei","doi":"10.3892/or.2025.8926","DOIUrl":"10.3892/or.2025.8926","url":null,"abstract":"<p><p>Inflammation is a hallmark of cancer, significantly contributing to tumor progression and therapeutic outcomes. Among the diverse cellular components of the tumor microenvironment, fibroblasts have been recognized as key regulators of inflammatory processes. Under tumor‑specific conditions, cancer‑associated fibroblasts (CAFs) undergo differentiation and promote tumor proliferation, metastasis and immune evasion <i>via</i> highly intricate mechanisms. This review provides a comprehensive analysis of the reciprocal interactions between CAFs and inflammation, elucidating the mechanisms by which CAFs induce pro‑inflammatory signaling and how inflammatory mediators, in turn, potentiate CAF activation and function. Furthermore, innovative therapeutic strategies, including the inhibition of stromal proteins, hypoxia‑inducible factor 1α and metabolic pathways associated with CAFs, as well as the application of nanoparticle‑based drug delivery systems, are examined for their potential to impede CAF‑mediated tumor progression. Pharmacological agents targeting CAF‑associated signaling pathways or inflammatory cytokines show dual efficacy by concurrently modulating inflammatory responses and CAF activity. These approaches frequently demonstrate improved therapeutic efficacy compared to interventions solely directed at CAF surface proteins, highlighting the therapeutic potential of concurrently addressing both inflammation and CAFs to enhance cancer treatment efficacy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role and potential mechanisms of miR‑100 in different diseases (Review).","authors":"Jiaqi Liu, Gejile Hu, Hua Du, Yingxu Shi","doi":"10.3892/or.2025.8924","DOIUrl":"10.3892/or.2025.8924","url":null,"abstract":"<p><p>In recent years, the role of microRNAs (miRNAs) in disease has attracted considerable interest, underscoring their potential utility as diagnostic biomarkers. miR‑100, belonging to the miR‑99 family, is integral to the pathophysiological processes underlying numerous diseases. miR‑100 has been found to influence the pathogenesis of a variety of noncancerous diseases. As for cancer, this factor plays a significant role in various tumors throughout diverse systems, influencing essential processes including cell proliferation, invasion, migration and apoptosis of cancerous cells. This review examines the existing literature on miR‑100 in the context of non‑cancerous diseases and cancer, investigates its mechanisms of action across different diseases and considers its potential role as a diagnostic biomarker as well as its involvement in cancer drug resistance.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Goserelin promotes the apoptosis of epithelial ovarian cancer cells by upregulating forkhead box O1 through the PI3K/AKT signaling pathway.","authors":"Ning Zhang, Junjun Qiu, Tingting Zheng, Xiaodan Zhang, Keqin Hua, Ying Zhang","doi":"10.3892/or.2025.8910","DOIUrl":"10.3892/or.2025.8910","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention the fact that six consecutive β‑actin bands looked similar, comparing across panels in Fig. 6A and B on p. 1040, even though different time points were represented in these experiments.  After having re‑examined their original data files, the authors realized that the β‑actin bands shown in Fig. 6A were inadvertently assembled incorrectly. The revised version of Fig. 6, now featuring the correct β‑actin blots for Fig. 6A, is shown on the next page. Note that the corrections made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this further Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 39: 1034‑1042, 2018; DOI: 10.3892/or.2017.6159].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12079634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tryptophan metabolism: From physiological functions to key roles and therapeutic targets in cancer (Review).","authors":"Jiawei Zhao, Xiaohui Bai, Jingjing Du, Yujing Chen, Xiaotong Guo, Juzheng Zhang, Jinfeng Gan, Peitao Wu, Siqi Chen, Xinwen Zhang, Jinfeng Yang, Jiamin Jin, Li Gao","doi":"10.3892/or.2025.8919","DOIUrl":"10.3892/or.2025.8919","url":null,"abstract":"<p><p>Tryptophan (Trp) metabolism is a complex and important biochemical process in humans. It is vital in protein synthesis and is a precursor of various bioactive molecules. Trp is metabolized through the kynurenine, serotonin and indole pathways, mediating diverse physiological functions, including neurotransmitter synthesis, immune regulation, antioxidant effects, and biosynthesis of niacin and melatonin. These metabolic pathways maintain essential functions under normal physiological conditions. However, they are significantly affected by various types of cancers. Trp metabolites regulate tumor angiogenesis, affect the self‑renewal of cancer stem cells, and participate in immune evasion and cell death through complex mechanisms. As the mechanisms underlying Trp metabolism in diseases are increasingly being elucidated, targeting Trp metabolic pathways has emerged as a promising therapeutic strategy. Further investigation of the molecular mechanisms underlying Trp metabolism and its role in diseases may provide new perspectives and approaches for diagnosing and treating diseases.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] MicroRNA‑345 inhibits hepatocellular carcinoma metastasis by inhibiting YAP1.","authors":"Hui Zhang, Hui Liu, Huaqiang Bi","doi":"10.3892/or.2025.8913","DOIUrl":"10.3892/or.2025.8913","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the scratch wound assay data panels shown in Fig. 8B on p. 848 were strikingly similar to data which had appeared several years previously in Fig. 2A in another article written by different authors at different research institutes published in the journal <i>Therapeutics, Targets</i>, and <i>Chemical Biology.</i> In view of the fact that these data had already appeared in another publication prior to its submission to <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 38: 843‑849, 2017; 10.3892/or.2017.5772].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12093927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Hydroxytyrosol inhibits cholangiocarcinoma tumor growth: An <i>in vivo</i> and <i>in vitro</i> study.","authors":"Shuai Li, Zhiyang Han, Yong Ma, Ruipeng Song, Tiemin Pei, Tongsen Zheng, Jiabei Wang, Dongsheng Xu, Xiang Fang, Hongchi Jiang, Lianxin Liu","doi":"10.3892/or.2025.8918","DOIUrl":"10.3892/or.2025.8918","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that unexpected similarities existed among the β‑actin control western blots in Figs. 1B, 3E and 3G, albeit with the protein bands featured in a different orientation, and with different dimensions, in Fig. 3E compared with Figs. 1B and 3E. Furthermore, the two leftmost β‑actin blots in Fig. 3G appeared to show unexpected similarities to the β‑actin blots in Fig. 4F, even though different experimental conditions were reported in these figures. Following an independent assessment of the apparent errors that had been made in assembling the data in the three affected figures, the Editor of <i>Oncology Reports</i> has decided that this article should be retracted from the publication on account of a lack of overall confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes for any inconvenience that might result from this retraction. [Oncology Reports 31: 145‑152, 2014; DOI: 10.3892/or.2013.2853].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DEPP1: A prognostic biomarker linked to stroma‑rich and immunosuppressive microenvironment, promoting oxaliplatin resistance in gastric cancer.","authors":"Xudong Qiu, Tao Pan, Tian Kuang, Yanying Shen, Yihan Zheng, Haigang Geng, Bo Ni, Xiang Xia, Chunchao Zhu, Zizhen Zhang, Hui Cao, Lin Tu","doi":"10.3892/or.2025.8915","DOIUrl":"10.3892/or.2025.8915","url":null,"abstract":"<p><p>Decidual protein induced by progesterone (DEPP1) was identified to exert heterogeneous functions in several cancers, whereas its role in gastric cancer (GC) remains elusive. In the present study, differential expression analysis was conducted using three Gene Expression Omnibus datasets (GSE54129, GSE26942 and GSE3438). Validation of DEPP1 expression was performed using reverse transcription‑quantitative PCR, western blotting and immunofluorescence. Kaplan‑Meier survival and Cox regression analyses were employed to assess the association between DEPP1 expression and the prognosis of patients with GC. Immune infiltration analysis was conducted to explore the correlation between DEPP1 and the tumor microenvironment. The potential of DEPP1 to promote oxaliplatin resistance was assessed using flow cytometry, western blotting, and subcutaneous mouse models. DEPP1 was found to be significantly upregulated in the aforementioned cohorts, which was consistent with the clinical specimens of the present study, and it emerged as an independent risk factor for poor overall survival in patients with GC. A prognostic nomogram was developed to improve prognosis prediction. High DEPP1 expression correlated with increased infiltration of cancer‑associated fibroblasts, endothelial cells, and M2 macrophages, contributing to the development of a stroma‑rich and immunosuppressive microenvironment in GC. Furthermore, high DEPP1 expression was associated with reduced sensitivity to chemotherapy drugs in patients with GC. <i>In vitro</i> and <i>in vivo</i> experiments highlighted DEPP1's crucial role in promoting oxaliplatin resistance in GC. In conclusion, DEPP1 is identified as a promising prognostic biomarker linked to a stroma‑rich and immunosuppressive microenvironment, and it is critical in driving oxaliplatin resistance in GC. These findings may inform personalized therapeutic strategies for patients with GC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12117316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}