Oncology reports最新文献

{"title":"The molecular mechanisms of chemotherapeutic resistance in tumors (Review).","authors":"Xin Weng, Wei-Hong Zeng, Li-Yuan Zhong, Li-Hua Xie, Wen-Jun Ge, Zhen Lai, Qin Qin, Peng Liu, De-Liang Cao, Xi Zeng","doi":"10.3892/or.2024.8816","DOIUrl":"10.3892/or.2024.8816","url":null,"abstract":"<p><p>Chemotherapy remains a prevalent treatment for a wide range of tumors; however, the majority of patients undergoing conventional chemotherapy experience varying levels of chemoresistance, ultimately leading to suboptimal outcomes. The present article provided an in‑depth review of chemotherapy resistance in tumors, emphasizing the underlying factors contributing to this resistance in tumor cells. It also explored recent advancements in the identification of key molecules and molecular mechanisms within the primary chemoresistant pathways.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372459","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":"Lung cancer and obesity: A contentious relationship (Review).","authors":"Vasiliki Epameinondas Georgakopoulou, Ioannis G Lempesis, Nikolaos Trakas, Pagona Sklapani, Yutong He, Demetrios A Spandidos","doi":"10.3892/or.2024.8817","DOIUrl":"10.3892/or.2024.8817","url":null,"abstract":"<p><p>The global obesity epidemic, attributed to sedentary lifestyles, unhealthy diets, genetics and environmental factors, has led to over 1.9 billion adults being classified as overweight and 650 million living with obesity. Despite advancements in early detection and treatment, lung cancer prognosis remains poor due to late diagnoses and limited therapies. The obesity paradox challenges conventional thinking by suggesting that individuals with obesity and certain diseases, including cancer, may have an improved prognosis compared with their counterparts of a normal weight. This observation has prompted investigations to understand protective mechanisms, including potentially favorable adipokine secretion and metabolic reserves that contribute to tolerating cancer treatments. However, understanding the association between obesity and lung cancer is complex. While smoking is the primary risk factor of lung cancer, obesity may independently impact lung cancer risk, particularly in non‑smokers. Adipose tissue dysfunction, including low‑grade chronic inflammation, and hormonal changes contribute to lung cancer development and progression. Obesity‑related factors may also influence treatment responses and survival outcomes in patients with lung cancer. The impact of obesity on treatment modalities such as chemotherapy, radiotherapy and surgery is still under investigation. Challenges in managing patients with obesity and cancer include increased surgical complexity, higher rates of postoperative complications and limited treatment options due to comorbidities. Targeted interventions aimed at reducing obesity prevalence and promoting healthy lifestyles are crucial for lung cancer prevention. The impact of obesity on lung cancer is multifaceted and requires further research to elucidate the underlying mechanisms and develop personalized interventions for prevention and treatment.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576727","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] miRNA‑490‑3p promotes the metastatic progression of invasive ductal carcinoma.","authors":"Ning Lu, Mei Zhang, Lu Lu, Yan-Zhao Liu, Hai-Hong Zhang, Xiao-Dong Liu","doi":"10.3892/or.2024.8802","DOIUrl":"10.3892/or.2024.8802","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 western blotting data shown in Fig. 2D, the cell migration and invasion assay data in Fig. 3C, the mouse imaging pictures in Fig. 4C and D, and the H&E‑stained images in Fig. 4E and F were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been submitted or published elsewhere prior to the submission of this paper to <i>Oncology Reports</i>. Given that the abovementioned data had already apparently been submitted or published prior to the receipt of this paper at <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. 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 45: 706‑716, 2021; DOI: 10.3892/or.2020.7880].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110421","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":"Antitumor activities of anti‑CD44 monoclonal antibodies in mouse xenograft models of esophageal cancer.","authors":"Kenichiro Ishikawa, Hiroyuki Suzuki, Tomokazu Ohishi, Takuro Nakamura, Miyuki Yanaka, Guanjie Li, Tomohiro Tanaka, Akira Ohkoshi, Manabu Kawada, Mika K Kaneko, Yukio Katori, Yukinari Kato","doi":"10.3892/or.2024.8806","DOIUrl":"10.3892/or.2024.8806","url":null,"abstract":"<p><p>CD44 is a type I transmembrane glycoprotein associated with poor prognosis in various solid tumors. Since CD44 plays a critical role in tumor development by regulating cell adhesion, survival, proliferation and stemness, it has been considered a target for tumor therapy. Anti‑CD44 monoclonal antibodies (mAbs) have been developed and applied to antibody‑drug conjugates and chimeric antigen receptor‑T cell therapy. Anti-pan‑CD44 mAbs, C₄₄Mab‑5 and C₄₄Mab‑46, which recognize both CD44 standard (CD44s) and variant isoforms were previously developed. The present study generated a mouse IgG_2a version of the anti‑pan‑CD44 mAbs (5‑mG_2a and C₄₄Mab‑46‑mG_2a) to evaluate the antitumor activities against CD44‑positive cells. Both 5‑mG_2a and C₄₄Mab‑46‑mG_2a recognized CD44s‑overexpressed CHO‑K1 (CHO/CD44s) cells and esophageal tumor cell line (KYSE770) in flow cytometry. Furthermore, both 5‑mG_2a and C₄₄Mab‑46‑mG_2a could activate effector cells in the presence of CHO/CD44s cells and exhibited complement-dependent cytotoxicity against both CHO/CD44s and KYSE770 cells. Furthermore, the administration of 5‑mG_2a and C₄₄Mab‑46‑mG_2a significantly suppressed CHO/CD44s and KYSE770 xenograft tumor development compared with the control mouse IgG_2a. These results indicate that 5‑mG_2a and C₄₄Mab‑46‑mG_2a could exert antitumor activities against CD44‑positive cancers and be a promising therapeutic regimen for tumors.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110422","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":"Routes and molecular mechanisms of central nervous system involvement in acute myeloid leukemia (Review).","authors":"Liucui Chen, Piaorong Zeng, Huifang Tang, Gang Chen, Juan Xie, Xiaoyan Yang, Xiaoyong Lei","doi":"10.3892/or.2024.8805","DOIUrl":"10.3892/or.2024.8805","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a predominant form of leukemia. Central nervous system (CNS) involvement complicates its diagnosis due to limited diagnostic tools, as well as its treatment due to inadequate therapeutic methodologies and poor prognosis. Furthermore, its incidence rate is unclear. The mechanisms of AML cell mobilization from the bone marrow (BM) to the CNS are not fully elucidated, and the molecular factors contributing to CNS infiltration are insufficiently recognized. The present review aimed to enhance the understanding of CNS involvement of AML and its impact on CNS. The latest research on the pathways and mechanisms facilitating AML cells to escape the BM and infiltrate the CNS was reviewed. Additionally, novel therapeutic strategies targeting specific molecules and genes for treating CNS involvement in AML were examined.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110424","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":"The role of lncRNA binding to RNA‑binding proteins to regulate mRNA stability in cancer progression and drug resistance mechanisms (Review).","authors":"Nianjie Zhang, Kunming Wen","doi":"10.3892/or.2024.8801","DOIUrl":"10.3892/or.2024.8801","url":null,"abstract":"<p><p>Cancer is a disease that poses a serious threat to human health, the occurrence and development of which involves complex molecular mechanisms. Long non‑coding RNAs (lncRNAs) and RNA‑binding proteins (RBPs) are important regulatory molecules within cells, which have garnered extensive attention in cancer research in recent years. The binding of lncRNAs and RBPs plays a crucial role in the post‑transcriptional regulation of mRNA, affecting the synthesis of proteins related to cancer by regulating the stability of mRNA. This, in turn, regulates the malignant biological behaviors of tumor cells, such as proliferation and metastasis, and serves an important role in therapeutic resistance. The present study reviewed the role of lncRNA‑RBP interactions in the regulation of mRNA stability in various malignant tumors, with a focus on the molecular mechanisms underlying this regulatory interaction. The aim of the present review was to gain a deeper understanding of these molecular mechanisms to provide new strategies and insights for the precise treatment of cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110425","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":"The combination of a PTP1B inhibitor, TNFR2 blocker, and PD‑1 antibody suppresses the progression of non‑small cell lung cancer tumors by enhancing immunocompetence.","authors":"Huan Gui, Yujie Nie, Haohua Yuan, Qianyu Jing, Linzhao Li, Lan Zhu, Shuanghui Chen, Mengjiao Wang, Quan Wan, Hang Lv, Yingjie Nie, Xiangyan Zhang","doi":"10.3892/or.2024.8808","DOIUrl":"https://doi.org/10.3892/or.2024.8808","url":null,"abstract":"<p><p>Lung cancer is increasingly recognized as a leading cause of cancer‑related mortality. Immunotherapy has emerged as a promising therapeutic approach for lung cancer, particularly non‑small cell lung cancer (NSCLC). Nonetheless, the response rate to programmed cell death 1 (PD‑1) inhibitors remains less than optimal. It has been suggested that protein tyrosine phosphatase 1B (PTP1B) plays a crucial role in the development and progression of cancer by facilitating T cell expansion and cytotoxicity. Our previous research demonstrated that the combination of tumor necrosis factor receptor 2 (TNFR2) with immune activity treatments synergistically suppresses tumor growth. This insight led to exploring the efficacy of a combined treatment strategy involving PD‑1 inhibitors, PTP1B inhibitors and TNFR2 antibodies (triple therapy) in NSCLC. In this context, the therapeutic effectiveness of these combination immunotherapies was validated in mouse models with NSCLC by analyzing the expansion and function of immune cells, thereby assessing their impact on tumor growth. The results indicated that inhibiting PTP1B decreases the expression of PD‑L1 and TNFR2 on LLC cells, along with an increase in the proportion of CD4⁺T and CD8⁺T cells. Compared with other treatment groups, the triple therapy significantly reduced tumor volume in mice with NSCLC and extended their survival. Moreover, this combination therapy altered the distribution of myeloid‑derived suppressor cells, dendritic cells, B cells and M1 macrophages, while increasing the proportion of CD8⁺T cells and reducing the proportion of Treg cells in the spleens, lymph nodes, and tumors of NSCLC models. The triple therapy also resulted in a decrease in PD‑L1, PTP1B and TNFR2 expression within NSCLC tumor tissues in mice. Overall, the triple therapy effectively suppressed tumor growth and improved outcomes in mice with NSCLC by modulating immune cell distribution and reducing levels of target immune proteins.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11411183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292695","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":"miR‑25‑3p serves as an oncogenic in colorectal cancer cells by regulating the ubiquitin ligase FBXW7 function.","authors":"Yanbin Chen, Bingchen Chen, Shiliang Tu, Hang Yuan","doi":"10.3892/or.2024.8812","DOIUrl":"10.3892/or.2024.8812","url":null,"abstract":"<p><p>Accumulating evidence indicates that the dysregulation of microRNAs (miRNAs or miRs), is associated with human malignancies and suggests a casual role of miRNAs in tumor initiation and progression. Even though it has been discovered that a number of miRNAs play significant parts in the development of colorectal cancer (CRC), it is crucial to comprehend the regulatory functions that other miRNAs play in CRC. Based on GSE183437 and GSE156719 microarray data that were obtained from Gene Expression Omnibus database, candidate miRNAs were researched. The oncogenic effects of miR‑25‑3p in different malignancies have led to its selection for additional investigation in the present study. The expression of miR‑25‑3p was verified by reverse transcription‑quantitative PCR, and its correlation with clinicopathological characteristics in patients with CRC was then investigated. <i>In vitro</i> assays were conducted to investigate the influence of miR‑25‑3p on the proliferative and apoptotic behaviors of HCT116 and Caco‑2 cells. The present data revealed that miR‑25‑3p exhibited one of the most significant upregulations in CRC tissues and cell lines. The expression levels of miR‑25‑3p were found to be intimately correlated with tumor size, distant metastasis, tumor‑node‑metastasis stage, and shorter overall survival rate. In terms of functionality, the downregulation of miR‑25‑3p led to the inhibition of cellular proliferation and the enhancement of apoptosis in both HCT116 and Caco‑2 cell lines. The critical tumor suppressor F‑box and WD repeat containing domain 7 (FBXW7) was identified as a direct molecular target for miR‑25‑3p, with an inverse relationship observed between the two in neoplastic tissues. Subsequent studies demonstrated that the tumor suppressive effects of miR‑25‑3p inhibitor were effectively negated by the silencing of FBXW7. Moreover, the ability of FBXW7 to inhibit the expression of several oncogenes was deemed essential for countering the anticancer effects mediated by miR‑25‑3p downregulation. These findings posit miR‑25‑3p as a promising therapeutic target and prognostic indicator for CRC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11450686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142351306","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":"Progress in antitumor mechanisms and applications of phenformin (Review).","authors":"Qi Zhong, Duo Li, Xiao-Ping Yang","doi":"10.3892/or.2024.8810","DOIUrl":"10.3892/or.2024.8810","url":null,"abstract":"<p><p>Phenformin, a biguanide compound, has attracted increased attention due to its prominent antitumor activity. As a multi‑target agent, the antitumor effects of phenformin involve a wide range of factors, including inhibition of mitochondrial complex I, activation of AMP‑activated protein kinase, impact on the tumor microenvironment, suppression of cancer stem cells and others. In addition, phenformin has been shown to markedly augment the effectiveness of various clinical treatment methods, including radiotherapy, chemotherapy, targeted therapy and immunotherapy. It is noteworthy that breakthrough progress has been made in the treatment of cancer with phenformin with application in clinical trials for the treatment of melanoma. Phenformin not only reduces the lesion area of patients, but also enhances the efficacy of dalafinib/trimetinib. In the present review, the novel breakthroughs in the antitumor effects and mechanisms of phenformin were discussed. In addition, the current review focuses on the clinical development value of phenformin, striving to provide new insights into the future research direction of phenformin in the field of tumor treatment.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11421015/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292694","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] Omi/HtrA2 pro-apoptotic marker differs in various hepatocellular carcinoma cell lines owing to ped/pea-15 expression level.","authors":"Zongquan Xu, Yu Chen, Guohui Xu, Cheng Peng, Enyu Liu, Yunguang Li, Jun Niu, Changhai Li","doi":"10.3892/or.2024.8804","DOIUrl":"10.3892/or.2024.8804","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the control western blots shown for Fig. 1A and B on p. 908 and Fig. 8A and C on p. 911 were apparently the same, where different experiments were intended to have been portrayed. After having re‑examined their original data files, the authors realized that these figures had been published with the control western blots shown incorrectly for Fig. 1A and 8C. The  corrected versions of this pair of figures are shown on the next page. Note that the corrections made to these figures 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 33: 905‑912, 2015; DOI: 10.3892/or.2014.3656].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110420","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}