Oncology reports最新文献

{"title":"cGAS/STING pathway and gastrointestinal cancer: Mechanisms and diagnostic and therapeutic targets (Review).","authors":"Chang Liu, Li Tang, Wenhui Yang, Yuning Gu, Wenrong Xu, Zhaofeng Liang, Jiajia Jiang","doi":"10.3892/or.2024.8848","DOIUrl":"10.3892/or.2024.8848","url":null,"abstract":"<p><p>The health of individuals is seriously threatened by intestinal cancer, which includes pancreatic, colorectal, esophageal, gastric and gallbladder cancer. Most gastrointestinal cancers do not have typical and specific early symptoms, and lack specific and effective diagnostic markers and treatment methods. It is critical to understand the etiology of gastrointestinal cancer and develop more efficient methods of diagnosis and treatment. The cyclic GMP‑AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway serves a crucial role in the occurrence, progression and treatment of gastrointestinal cancer. The present review focuses on the latest progress regarding the role and mechanism of the cGAS/STING pathway in gastrointestinal cancer, and discusses treatment approaches and related applications based on the cGAS/STING signaling pathway. In order to improve the knowledge of the connection between the cGAS/STING pathway and gastrointestinal cancer, aid the diagnosis and treatment of gastrointestinal cancer, and lessen the burden on patients and society, the present review also discusses future research directions and existing challenges regarding cGAS/STING in the study of gastrointestinal cancer.</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/PMC11632663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751365","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] Glutathione peroxidase 2 overexpression promotes malignant progression and cisplatin resistance of KRAS‑mutated lung cancer cells.","authors":"Mei Wang, Xu Chen, Guang Fu, Mingjian Ge","doi":"10.3892/or.2024.8834","DOIUrl":"10.3892/or.2024.8834","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 BrdU incorporation assay data shown in Fig. 7C were strikingly similar to data that had already appeared in another article written by different authors at different research institutes [Lu M, Qin X, Zhou Y, Li G, Liu Z, Geng X and Yue H: Long non‑coding RNA LINC00665 promotes gemcitabine resistance of Cholangiocarcinoma cells via regulating EMT and stemness properties through miR‑424‑5p/BCL9L axis. Cell Death Dis 12: 72, 2021]. Owing to the fact that the contentious data in the above article had already been published 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 48: 207, 2022; DOI: 10.3892/or.2022.8422].</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/PMC11541304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605770","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] Stimulation of peroxisome proliferator‑activated receptor γ inhibits estrogen receptor α transcriptional activity in endometrial carcinoma cells.","authors":"Guiyu Zhang, Xinxin Hou, Shuhong Gao","doi":"10.3892/or.2024.8836","DOIUrl":"10.3892/or.2024.8836","url":null,"abstract":"<p><p>Following the publication of this paper, after having performed an independent analysis of the data shown in the various of the figures in the Editorial Office, it was identified that, in Fig. 5A and B on p. 1232 showing the results of Transwell invasion and migration experiments, the majority of the data panels exhibited overlapping sections of data, such that the affected panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original sources. Owing to the large number of duplications of data that have been identified in this paper, the Editor of <i>Oncology Reports</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 33: 1227‑1234, 2015; DOI: 10.3892/or.2015.3729].</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/PMC11552468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605775","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":"Advances in research on the carcinogenic mechanisms and therapeutic potential of YAP1 in bladder cancer (Review).","authors":"Tianyu Huang, Longmei Fan, Jiajia Tang, Shicheng Chen, Guotu Du, Neng Zhang","doi":"10.3892/or.2024.8843","DOIUrl":"10.3892/or.2024.8843","url":null,"abstract":"<p><p>Bladder cancer is the most common malignant tumor of the urinary system with high morbidity and no clear pathogenesis. The Hippo signaling pathway is an evolutionarily conserved pathway that regulates organ size and maintains tissue homeostasis. Yes‑associated protein 1 (YAP1) is a key effector of this pathway and regulates downstream target genes by binding to transcriptional co‑activators with PDZ binding sequences (TAZ). Several studies have demonstrated that YAP1 is overexpressed in bladder cancer and is involved in adverse outcomes such as bladder cancer occurrence, progression, resistance to cisplatin and the recurrence of tumours. The present review summarized the involvement of YAP1 in bladder cancer disease onset and progression, and the mechanism of YAP1 involvement in bladder cancer treatment. In addition, this study further explored the potential of YAP1 in the diagnosis and treatment of bladder cancer. This study aimed to explore the potential mechanism of YAP1 in the treatment of bladder cancer.</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/PMC11599795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624867","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‑34a expression affects breast cancer invasion <i>in vitro</i> and patient survival via downregulation of <i>E2F1</i> and <i>E2F3</i> expression.","authors":"Rui Han, Jing Zhao, Lingeng Lu","doi":"10.3892/or.2024.8841","DOIUrl":"10.3892/or.2024.8841","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 overlapping sections of data in the three Transwell invasion assay images shown in Fig. 4A, and in the 3D sphere formation assay data shown in Fig. 5, on p. 2068; moreover, certain of the data featured in one of the data panels in Fig. 4A also appeared in a subsequent publication by the same research group in the journal <i>Scientific Reports</i>. The authors requested the publication of a corrigendum to acount for the errors made in assembling the data in Figs. 4 and 5; however, after careful consideration of the matter, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal on account of the number of issues that were identified, and a general lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 43: 2062‑2072, 2020; DOI: 10.3892/or.2020.7549].</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/PMC11576928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624865","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":"Potential of epithelial membrane protein 3 as a novel therapeutic target for human breast cancer.","authors":"Yi-Wen Wang, Yih-Lin Tuan, Jiu-Yao Wang, Hong-Yi Chang, Chien-An Chu, Yi-Lin Chen, Hui-Wen Chen, Chung-Liang Ho, Chung-Ta Lee, Nan-Haw Chow","doi":"10.3892/or.2024.8849","DOIUrl":"10.3892/or.2024.8849","url":null,"abstract":"<p><p>Amplification of human epidermal growth factor 2 receptor (HER2) and overexpression of estrogen receptor (ER) and/or progesterone receptor (PR) are key determinants in the treatment planning for human breast cancer (BC). Currently, targeted therapies for BC are focused mainly on these biomarkers. However, development of resistance to targeted drugs is almost unavoidable, emphasizing the importance of biochemical and pharmaceutical advances to improve treatment outcomes. To the best of our knowledge, the present study is the first to show functional crosstalk <i>in vitro</i> between HER2 and epithelial membrane protein 3 (EMP3), a tetraspan membrane protein, in human BC. EMP3 overexpression significantly promoted BC cell proliferation, invasion and migration by Transwell assays via epithelial-mesenchymal transition and transactivated the HER family, resulting in increased ER and PR expression <i>in vitro</i>. Knocking down EMP3 notably suppressed cell proliferation and migration and was accompanied by decreased expression of HER1‑HER3 and p‑SRC proteins. Suppression of EMP3 expression enhanced sensitivity of BC cells to trastuzumab <i>in vitro</i>. Xenograft experiments revealed decreased expression of HER1 and HER2 in stable EMP3‑knockdown cells, resulting in decreased tumor weight and size. In patients with BC, EMP3 overexpression was detected in 72 of 166 cases (43.4%), with 18 of 43 (41.9%) HER2‑amplified BC samples co‑expressing EMP3. Co‑expression of EMP3 and HER2 was positively associated with ER expression (P=0.028) and tended to be associated with nodal metastasis (P=0.085), however this was not significant. Taken together, the present results supported the potential of targeting EMP3 as a novel therapeutic strategy for human BC via co‑expression of HER2 and EMP3.</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/PMC11632653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751300","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 SIK1 in tumors: Emerging players and therapeutic potentials (Review).","authors":"Xinran Zhang, Jing Liu, Chenyang Zuo, Xiaochun Peng, Jinyuan Xie, Ya Shu, Dongxu Ao, Yang Zhang, Qingqing Ye, Jun Cai","doi":"10.3892/or.2024.8828","DOIUrl":"10.3892/or.2024.8828","url":null,"abstract":"<p><p>Salt‑induced kinase 1 (SIK1) is a serine/threonine protein kinase that is a member of the AMP‑activated protein kinase family. SIK is catalytically activated through its phosphorylation by the upstream kinase LKB1. SIK1 has been reported to be associated with numerous types of cancer. The present review summarizes the structure, regulatory factors and inhibitors of SIK1, and also describes how SIK1 is a signal regulatory factor that fulfills connecting roles in various signal regulatory pathways. Furthermore, the anti‑inflammatory effects of SIK1 during the early stage of tumor occurrence and its different regulatory effects following tumor occurrence, are summarized, and through collating the tumor signal regulatory mechanisms in which SIK1 participates, it has been demonstrated that SIK1 acts as a necessary node in cancer signal transduction. In conclusion, SIK1 is discussed independent of the SIKs family, its research results and recent progress in oncology are summarized in detail with a focus on SIK1, and its potential as a therapeutic target is highlighted, underscoring the need for SIK1‑targeted regulatory strategies in future cancer therapy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471614","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] Nucleosome‑binding protein HMGN2 exhibits antitumor activity in human SaO2 and U2‑OS osteosarcoma cell lines.","authors":"Guojun Liang, Enjie Xu, Chaoqun Yang, Chenglin Zhang, Xiaolong Sheng, Xuhui Zhou","doi":"10.3892/or.2024.8827","DOIUrl":"10.3892/or.2024.8827","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 5A on p. 1305, the same xenograft tumor image had been selected for a pair of the GFP/U2‑OS experiments, where the images from discretely performed experiments were intended to have been shown. Furthermore, upon performing an independent analysis of the data in the Editorial Office, it was noted that the data selected for the 'SaO2/GFP/24 h' and 'SaO2/HMGN2/48 h' experiments in Fig. 4A, also on p. 1305, were strikingly similar, such that the same data had apparently been chosen to show the results of differently performed experiments. After having inspected the figures, the authors realized that one of the n=3 experimental results had inadvertently been omitted from Fig. 5A, and the data shown to represent the 'SaO2/GFP/24 h' experiment had been chosen incorrectly. The revised and corrected versions of Figs. 4 and 5 are shown on the next page (also note that erroneously written labels have been corrected in Fig. 5C: \"Tumor volume\" has been replaced by \"Tumor weight\"). Note that the errors made in terms of the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for granting them this opportunity to publish a Corrigendum, and apologize to boh the Editor and the readership for any inconvenience caused. [Oncology Reports 33: 1300‑1306, 2015; DOI: 10.3892/or.2014.3689].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471608","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] lncRNA TTN‑AS1 upregulates RUNX1 to enhance glioma progression via sponging miR‑27b‑3p.","authors":"Keliang Chang, Genwei Wang, Jinfeng Lou, Sha Hao, Ranbo Lv, Desheng Duan, Wanhong Zhang, Yingchang Guo, Pengfei Wang","doi":"10.3892/or.2024.8830","DOIUrl":"10.3892/or.2024.8830","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 the immunohistochemical images shown in Fig. 7E were strikingly similar to data that had already been published in different form in a previous article in the journal PLoS One written by different authors at different research institutes. Owing to the fact that the abovementioned data had already apparently been published previously, the Editor of <i>Oncology Reports</i> 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 44: 1064‑1074, 2020; DOI: 10.3892/or.2020.7684].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505257","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":"Expression of EGFRvIII and its co‑expression with wild‑type EGFR, or putative cancer stem cell biomarkers CD44 or EpCAM are associated with poorer prognosis in patients with hepatocellular carcinoma.","authors":"Ozlem Sherif, Said A Khelwatty, Izhar Bagwan, Alan M Seddon, Angus Dalgleish, Satvinder Mudan, Helmout Modjtahedi","doi":"10.3892/or.2024.8831","DOIUrl":"10.3892/or.2024.8831","url":null,"abstract":"<p><p>The aberrant expression of HER family members and cancer stem cells (CSCs) have been associated with tumour progression and resistance to therapy. At present, several HER inhibitors have been approved for the treatment of patients with a range of cancers but not for the treatment of patients with hepatocellular carcinoma (HCC). The present study investigated the co‑expression and prognostic significance of HER family members, type‑III deletion mutant EGFR (EGFRvIII), and the putative CSC biomarkers CD44 and epithelial cell adhesion molecule (EpCAM) in 43 patients with HCC. The relative expression of these biomarkers was determined using immunohistochemistry. At a cut off value of >5% of tumour cells stained for these biomarkers, 35% [wild‑type (wt)EGFR], 58% (HER‑2), 0% (HER‑3), 19% (HER‑4), 26% (EGFRvIII), 40% (CD44) and 33% (EpCAM) of patients were positive. In 23, 14 and 9% of the patients, wtEGFR expression was accompanied by co‑expression with HER‑2, EGFRvIII and HER‑2/EGFRvIII, respectively. EGFRvIII expression, membranous expression of CD44 and co‑expression of wtEGFR/EGFRvIII were associated with poor overall survival (OS). By contrast, cytoplasmic CD44 expression was associated with a longer OS time. The present study also investigated the effect of several agents targeting one or more members of the HER family, other growth factor receptors and cell signalling proteins on the proliferation of HCC cell lines. Among agents targeting one or more members of the HER family, the pan‑HER family blocker afatinib was the most effective, inhibiting the proliferation of three out of seven human liver cancer cell lines (LCCLs), while the CDK inhibitor dinacicilib was the most effective agent, inhibiting the proliferation of all human LCCLs tested. Taken together, the present results suggested that EGFRvIII expression and its co‑expression with wtEGFR or CD44 was of prognostic significance. These results also support further investigations of the therapeutic potential of drugs targeting EGFRvIII and other members of the HER family in patients with HCC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11526438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505258","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}