Oncology reports最新文献

{"title":"Lactate and lactylation in gastrointestinal cancer: Current progress and perspectives (Review).","authors":"Yufen He, Yaxi Huang, Peng Peng, Qi Yan, Lidan Ran","doi":"10.3892/or.2024.8839","DOIUrl":"10.3892/or.2024.8839","url":null,"abstract":"<p><p>Gastrointestinal (GI) cancers, which have notable incidence and mortality, are impacted by metabolic reprogramming, especially the increased production and accumulation of lactate. Lactylation, a post‑translational modification driven by lactate, is a crucial regulator of gene expression and cellular function in GI cancer. The present review aimed to examine advancements in understanding lactate and lactylation in GI cancer. The mechanisms of lactate production, its influence on the tumor microenvironment and the clinical implications of lactate levels as potential biomarkers were explored. Furthermore, lactylation was investigated, including its biochemical foundation, primary targets and functional outcomes. The present review underscored potential therapeutic strategies targeting lactate metabolism and lactylation. Challenges and future directions emphasize the potential of lactate and lactylation as innovative therapeutic targets in GI cancer to improve clinical outcomes.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605841","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 value of the tumor microenvironment in the progression and treatment resistance of gastric cancer (Review).","authors":"Heng Yun, Fangde Dong, Xiaoqin Wei, Xinyong Yan, Ronglong Zhang, Xiuyu Zhang, Yulin Wang","doi":"10.3892/or.2024.8847","DOIUrl":"10.3892/or.2024.8847","url":null,"abstract":"<p><p>Gastric cancer (GC) is characterized by a complex and heterogeneous tumor microenvironment (TME) that significantly influences disease progression and treatment outcomes. The tumor stroma, which is composed of a variety of cell types such as cancer‑associated fibroblasts, immune cells and vascular components, displays significant spatial and temporal diversity. These stromal elements engage in dynamic crosstalk with cancer cells, shaping their proliferative, invasive and metastatic potential. Furthermore, the TME is instrumental in facilitating resistance to traditional chemotherapy, specific treatments and immunotherapy strategies. Understanding the underlying mechanisms by which the GC microenvironment evolves and supports tumor growth and therapeutic resistance is critical for developing effective treatment strategies. The present review explores the latest progress in understanding the intricate interactions between cancer cells and their immediate environment in GC, highlighting the implications for disease pathogenesis and therapeutic interventions.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751323","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":"Nucleolar casein kinase 2 alpha as a prognostic factor in patients with surgically resected early‑stage lung adenocarcinoma.","authors":"Satoshi Muto, Miwako Kato Homma, Yuichiro Kiko, Yuki Ozaki, Masayuki Watanabe, Naoyuki Okabe, Kazuyuki Hamada, Yuko Hashimoto, Hiroyuki Suzuki","doi":"10.3892/or.2024.8837","DOIUrl":"https://doi.org/10.3892/or.2024.8837","url":null,"abstract":"<p><p>Lung cancer remains a leading cause of global cancer‑related deaths, therefore the identification of prognostic factors for lung cancer is critical. Casein kinase 2 alpha (CK2α) is one of the driver kinases in various cancers, and it was previously demonstrated that CK2α localization was associated with a poor prognosis in invasive breast cancer. In the present study, the importance of CK2α in the nucleolus was explored as a potential prognostic marker for surgically resected early‑stage lung adenocarcinoma. The present study included 118 patients who underwent pulmonary lobectomy between 2014 and 2018 in Fukushima Medical University Hospital (Fukushima, Japan), and in whom CK2α localization in tumor samples was assessed by immunohistochemistry. Patient and tumor characteristics, including pathological stage, histological type and histological grade, were analyzed. Recurrence‑free survival (RFS) and overall survival were evaluated in relation to nucleolar CK2α staining. CK2α staining in the nucleoli was observed in 50.8% of lung adenocarcinoma tumors. Positive nucleolar CK2α staining was independent of pathological stage, histological type and histological grade. Patients with positive nucleolar CK2α staining exhibited significantly worse RFS compared with patients with negative staining. Multivariate analysis identified nucleolar CK2α staining and lymph node metastasis as independent poor prognostic factors. The results of the present study suggested that nucleolar CK2α staining is a novel and independent prognostic factor in surgically resected early‑stage lung adenocarcinoma. These findings indicated the potential of nucleolar CK2α as a predictive biomarker for future recurrence, and a guide to treatment decisions. Further research is required, particularly in understanding the molecular mechanisms linking nucleolar CK2α to recurrence.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605847","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":"Exosome applications for the diagnosis and treatment of pancreatic ductal adenocarcinoma: An update (Review).","authors":"Xinchi Luan, Xuezhe Wang, Gang Bian, Xiaoxuan Li, Ziru Gao, Zijiao Liu, Zhishang Zhang, Tianyue Han, Jinpeng Zhao, Hongjiao Zhao, Xinyue Luan, Wuhui Zhu, Lili Dong, Feifei Guo","doi":"10.3892/or.2024.8846","DOIUrl":"10.3892/or.2024.8846","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a malignant neoplasm that typically manifests with subtle clinical manifestations in its early stages and frequently eludes diagnosis until the advanced phases of the disease. The limited therapeutic options available for PDAC significantly contribute to its high mortality rate, highlighting the urgent need for novel biomarkers capable of effectively identifying early clinical manifestations and facilitating precise diagnosis. The pivotal role of cellular exosomes in both the pathogenesis and therapeutic interventions for PDAC has been underscored. Furthermore, researchers have acknowledged the potential of exosomes as targeted drug carriers against regulatory cells in treating PDAC. The present article aims to provide a comprehensive review encompassing recent advancements in utilizing exosomes for elucidating mechanisms underlying disease development, patterns of metastasis, diagnostic techniques and treatment strategies associated with PDAC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687743","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] Tripartite motif‑containing 11 regulates the proliferation and apoptosis of breast cancer cells.","authors":"Xianping Dai, Feng Geng, Mengshun Li, Ming Liu","doi":"10.3892/or.2024.8838","DOIUrl":"10.3892/or.2024.8838","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the flow cytometric plots shown in Fig. 5A and B on p. 2572, each figure part contained a pair of duplicated data panels; specifically, the panels depicting the 'NC/5‑FU' and the 'shTRIM11/Gemcitabine' experiments in Fig 5A (MCF‑7 cells), and the 'NC/Paclitaxel' and 'shTRIM11/Adriamycin' experi-ments in Fig. 5B (MDA‑MB‑231 cells), were apparently identical. The authors were able to re‑examine their original data files, and realize that this figure was inadverently assembled incorrectly. The revised version of Fig. 5, now showing the correct data for the 'shTRIM11/Gemcitabine' experiment in Fig 5A and the 'NC/Paclitaxel' experiment in Fig. 5B, is shown on the next page. Note that the revisions 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 Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 41: 2567‑2574, 2019; DOI: 10.3892/or.2019.7015].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11566101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605765","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":"METTL3‑mediated N6‑methyladenosine modification of MMP9 mRNA promotes colorectal cancer proliferation and migration.","authors":"Jie Chen, Henglan Wu, Ting Zuo, Jianming Wu, Zhiheng Chen","doi":"10.3892/or.2024.8842","DOIUrl":"10.3892/or.2024.8842","url":null,"abstract":"<p><p>N6‑methyladenosine (m⁶A) is the predominant chemical modification of eukaryotic mRNA, dynamically mediated by the RNA methyltransferase, methyltransferase-like 3 (METTL3). m⁶A modification plays a critical role in cancer progression through post‑transcriptional regulation in various types of cancer. However, the role of METTL3 and its associated m⁶A modification in colorectal tumorigenesis remains to be fully elucidated. In the present study, it was demonstrated that METTL3 expression and the m⁶A levels were both upregulated in colorectal cancer (CRC) and positively associated with clinical progression, based on the bioinformatics analysis of cancer databases. Furthermore, knockdown and overexpression of METTL3 notably affected CRC cell viability, apoptosis and migration <i>in vitro</i>. Similarly, xenograft animal models confirmed that METTL3 promoted CRC tumorigenicity <i>in vivo</i>. Mechanistically, it was revealed that the m⁶A modification of matrix metallopeptidase 9 (MMP9) mRNA mediated by METTL3 promoted its expression in CRC by decreasing its degradation. Collectively, the findings of the present study suggested that the METTL3/MMP9 axis could serve as a novel promising therapeutic candidate for CRC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624870","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] Dual inhibition of COX‑2/5‑LOX blocks colon cancer proliferation, migration and invasion <i>in vitro</i>.","authors":"Xiao-Hang Che, Chun-Lin Chen, Xiao-Lei Ye, Guo-Bin Weng, Xian-Zhi Guo, Wen-Ying Yu, Jin Tao, Yi-Chen Chen, Xiaodong Chen","doi":"10.3892/or.2024.8845","DOIUrl":"10.3892/or.2024.8845","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be a number of anomalies in the presentation of data, including both tabulated data and data in figures: First, a discrepancy was noted between the numbers of males and females reported in the Materials and methods section on p. 1681 (47 females and 47 males) and yet, in Table I, showing clinicopathological characteristics of the patients, different numbers of male and female patients were reported. Secondly, data in Fig. 1 on p. 1683 had been misassembled: Experiments with COX‑2 and 5‑LOX are shown, but the panels for the x40 and x100 magnified images are presented the wrong way around. Thirdly, regarding the western blotting data, there were a couple of instances where it appeared that different exposures of gels had been undertaken in an attempt to show the same data for different experimental conditions. Fourthly, western blotting data featured internally in Fig. 4C on p. 1686 appeared to be strikingly similar, such that the same data may have been used to show the results for differently performed experiments. Fifthly, the data shown in the left‑hand columns for the scratch‑wound assay experiments in Figs. 2A and 5A were the same, even though different experiments were intended to have been portrayed in these figures. Finally, after having conducted an independent investigation of this paper in the Editorial Office, the presence of overlapping sections was also noted comparing the Transwell cell invasion assay data in Figs. 3 and 5. Given the identification of these various issues in the paper, the Editor of <i>Oncology Reports</i> has decided that this article should be retracted from the Journal on account of the uncertainties, and an overall lack of 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 to the readership for any inconvenience caused. [Oncology Reports 35: 1680‑1688, 2016; DOI: 10.3892/or.2015.4506].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11603536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687740","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":"Compression force promotes glioblastoma progression through the Piezo1‑GDF15‑CTLA4 axis.","authors":"Ok-Hyeon Kim, Israt Jahan Tulip, Hana Kang, Eun Seo Chang, Hyun Jung Lee","doi":"10.3892/or.2024.8835","DOIUrl":"10.3892/or.2024.8835","url":null,"abstract":"<p><p>Glioma, a type of brain tumor, is influenced by mechanical forces in its microenvironment that affect cancer progression. However, our understanding of the contribution of compression and its associated mechanisms remains limited. The objective of the present study was to create an environment in which human brain glioma H4 cells experience pressure and thereby investigate the compressive mechanosensors and signaling pathways. Subsequent time‑lapse imaging and wound healing assays confirmed that 12 h of compression significantly increased cell migration, thereby linking compression with enhanced cell motility. Compression upregulated the expression of Piezo1, a mechanosensitive ion channel, and growth differentiation factor 15 (GDF15), a TGF‑β superfamily member. Knockdown experiments targeting <i>PIEZO1</i> or <i>GDF15</i> using small interfering RNA resulted in reduced cell motility, with Piezo1 regulating GDF15 expression. Compression also upregulated CTLA4, a critical immune checkpoint protein. The findings of the present study therefore suggest that compression enhances glioma progression by stimulating Piezo1, promoting GDF15 expression and increasing CTLA4 expression. Thus, these findings provide important insights into the influence of mechanical compression on glioma progression and highlight the involvement of the Piezo1‑GDF15 signaling pathway. Understanding tumor responses to mechanical forces in the brain microenvironment may guide the development of targeted therapeutic strategies to mitigate tumor progression and improve patient outcomes.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605781","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":"Huaier promotes sensitivity of colorectal cancer to oxaliplatin by inhibiting METTL3 to regulate the Wnt/β‑catenin signaling pathway.","authors":"Mingyi Huo, Zhixu Gao, Guizhen Wang, Zhiping Hou, Jining Zheng","doi":"10.3892/or.2024.8840","DOIUrl":"10.3892/or.2024.8840","url":null,"abstract":"<p><p>Colorectal cancer (CRC) ranks fifth in terms of incidence rate and mortality among malignant tumors in China. Oxaliplatin (OXA) is a first‑line drug for the clinical treatment of CRC, but its antitumor effect is limited because of the development of drug resistance. The present study aimed to investigate whether the traditional Chinese medicine Huaier can regulate the Wnt/β‑catenin signaling pathway by affecting the expression of METTL3, thereby promoting the sensitivity of HCT‑8/L cells to OXA. The expression of METTL3 was analyzed based on the UCSC Xena and Gene Expression Omnibus databases. Silent METTL3 and overexpression METTL3 models were constructed, and Cell Counting Kit‑8 and flow cytometry were used to detect the effects of Huaier on the viability and apoptosis of HCT‑8/L cells. Western blotting, reverse transcription‑quantitative PCR, nuclear cytoplasmic separation and immunofluorescence were used to detect the effects of Huaier on the expression of METTL3, Pgp, Wnt/β‑catenin signaling pathway‑related proteins, apoptosis‑related proteins and related mRNA. The results demonstrated that patients with high expression levels of METTL3 had a shorter overall survival period. The expression level of METTL3 significantly increased in drug‑resistant CRC cells. Silencing METTL3 promoted apoptosis of CRC cells and increased their sensitivity to OXA by inhibiting the Wnt/β‑catenin signaling pathway. Huaier downregulated the expression of METTL3, thereby promoting apoptosis of drug‑resistant CRC cells and increasing their sensitivity to OXA by inhibiting the Wnt/β‑catenin signaling pathway.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605800","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 long non‑coding RNA leucine‑rich repeat containing 75 A‑antisense RNA1 in the invasion and progression of renal cell carcinoma.","authors":"Takanori Tokunaga, Hiroshi Hirata, Yukihiro Hitaka, Nakanori Fujii, Keita Kobayashi, Takahide Hayano, Yoshiyuki Asai, Koji Shiraishi","doi":"10.3892/or.2024.8844","DOIUrl":"10.3892/or.2024.8844","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) serve pivotal roles in cancer biology. The present study investigated the oncogenic roles of lncRNAs in renal cell carcinoma (RCC) and their potential as prognostic biomarkers. The lncRNA leucine‑rich repeat containing 75 A‑antisense RNA1 (LRRC75A‑AS1) was identified through lncRNA microarray as a potential lncRNA that may predict the efficacy of immune checkpoint inhibitor therapy and cancer progression in RCC. The present study subsequently assessed the expression of LRRC75A‑AS1 in 212 patients with clear cell RCC (ccRCC) who underwent nephrectomy, and performed <i>in vitro</i> functional analysis of LRRC75A‑AS1 in RCC cell lines. Additionally, the interactions between LRRC75A‑AS1, microRNA (miR)‑370‑5p and ADAMTS5 were explored. LRRC75A‑AS1 was revealed to be significantly upregulated in ccRCC tissues compared with in adjacent normal tissues, and high LRRC75A‑AS1 expression was associated with poor prognosis, including lower progression‑free survival, in patients with RCC. The knockdown of LRRC75A‑AS1 in RCC cell lines resulted in reduced cell proliferation and invasion, highlighting its role in promoting tumorigenesis. Furthermore, the interaction among LRRC75A‑AS1, miR‑370‑5p and ADAMTS5 was suggested as a regulatory mechanism underlying RCC progression. These findings indicated that LRRC75A‑AS1 may function as an oncogene in RCC, promoting cell proliferation and invasion. Its significant upregulation in ccRCC tissues and association with poor prognosis underscore its potential as a prognostic biomarker for RCC. Understanding the regulatory interactions among LRRC75A‑AS1, miR‑370‑5p and ADAMTS5 may provide new insights into the molecular mechanisms underlying RCC and facilitate the identification of novel therapeutic targets.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11603548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687745","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}