Oncology reports最新文献

{"title":"[Retracted] Breast cancer cells are arrested at different phases of the cell cycle following the re‑expression of ARHI.","authors":"Xiaoxiao Zuo, Yan Qin, Xiaojin Zhang, Qian Ning, Shan Shao, Minna Luo, Na Yuan, Shangke Huang, Xinhan Zhao","doi":"10.3892/or.2025.8916","DOIUrl":"10.3892/or.2025.8916","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, a concerned reader drew the Editor's attention to the fact that, comparing the western blot data shown in Fig. 2 on p. 2360 and Figs. 5 and 6 on p. 2363, two of the β‑actin control protein bands appeared to be shared in common between Figs. 2 and 6, and one of the P21 protein bands in Fig. 6 was strikingly similar to a Cyclin D1 protein band shown in Fig. 5. Furthermore, based on the appearance of the gels, there appeared to be several breaks in the continuity of the gel slices between the second and third lanes in Fig. 6, such that these data were apparently not derived from the same set of experiments. Upon consulting the authors in relation to the unusual features in the abovementioned western blots in this paper, they were unable to offer a satisfactory explanation to account for the presentation of these figures (although offering to repeat the experiments in question). In view of the uncertainties in the affected data, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal on account of a 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 reply. The Editor apologizes for any inconvenience caused. [Oncology Reports 31: 2358‑2364, 2014; DOI: 10.3892/or.2014.3107].</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/PMC12117313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143222","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":"Tertiary lymphoid structures in head and neck squamous cell carcinoma (Review).","authors":"Shiqin Hong, Qiyue Wang, Dilong Yu, Juyan Zheng, Ping Huang, Jinping Gu, Yiwen Zhang","doi":"10.3892/or.2025.8909","DOIUrl":"https://doi.org/10.3892/or.2025.8909","url":null,"abstract":"<p><p>The tumor microenvironment in head and neck squamous cell carcinoma (HNSCC) has a critical role in tumor progression and prognosis. The organization of T cells, B cells and high‑endothelial venules into structures termed tertiary lymphoid structures (TLS), are associated with favorable outcomes in HNSCC. Despite their importance, the formation and function of TLS‑associated immune cells in HNSCC have remained elusive. The aim of the present review is to elucidate the mechanism underlying TLS formation, which may contribute to the development of novel and effective immunotherapies for HNSCC, and summarize recent advances in HNSCC treatment.</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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984810","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":"RNA‑binding protein MBNL1 regulates tumor growth, chemosensitivity and antitumor immunity in lung adenocarcinoma by controlling the expression of tumor suppressor RNF125.","authors":"Yubo Yan, Xianglong Kong, Xiangyuan Jin, Jianlong Bu, Boxiong Ni, Zuqin Rao, Junnan Guo, Shidong Xu","doi":"10.3892/or.2025.8907","DOIUrl":"10.3892/or.2025.8907","url":null,"abstract":"<p><p>Ring finger protein 125 (RNF125), a ubiquitin E3 ligase, has been reported to act as a tumor suppressor in several cancers, but its precise function in lung adenocarcinoma (LUAD) has not been elucidated. In the present study, through bioinformatics analysis and immunohistochemistry in LUAD and non‑cancerous samples, it was demonstrated that RNF125 was significantly downregulated in lung cancer. Low levels of RNF125 expression were associated with metastatic status, advanced tumor stage and poor overall survival in LUAD. The results of gain‑ and loss‑of‑function experiments demonstrated that RNF125 inhibited proliferation, colony formation, migration and invasion of LUAD cells. In addition, RNF125 increased the sensitivity of LUAD cells to cisplatin. Mechanistically, RNF125 interacted with programmed cell death ligand 1 (PD‑L1) and reduced PD‑L1 expression levels in LUAD cells. Furthermore, IL‑2 secretion by Jurkat T cells was significantly suppressed when co‑cultured with RNF125‑silenced LUAD cells. NK‑92 cell lysis of RNF125‑silenced LUAD cells was also weaker compared with that of control LUAD cells, suggesting that RNF125 knockdown enhanced the immune evasion ability of LUAD cells. Notably, the results of the present study identified that the RNA‑binding protein muscleblind‑like 1 (MBNL1) is the upstream regulator of RNF125 in LUAD. MBNL1 increased the stability of the RNF125 transcript in LUAD cells and knockdown of RNF125 reversed the antitumor effect of MBNL1 on LUAD cells. In conclusion, the present study demonstrated the tumor suppressor role of RNF125 in LUAD and implicated MBNL1 as an upstream regulator of RNF125 in LUAD. These findings contributed to an improved understanding of the molecular features of LUAD progression.</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/PMC12075997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039045","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] RNA interference against TRIM29 inhibits migration and invasion of colorectal cancer cells.","authors":"Weihong Xu, Bin Xu, Yiting Yao, Xiaoling Yu, Hua Cao, Jun Zhang, Jie Liu, Huiming Sheng","doi":"10.3892/or.2025.8908","DOIUrl":"10.3892/or.2025.8908","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 featured in Figs. 4C on p. 1415 and 5D on p. 1416 were strikingly similar to data that had already appeared in other articles written by different authors at different research institutes, one of which has been retracted. Owing to the fact that the abovementioned data had already been published prior to the receipt of this article at <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 36: 1411‑1418, 2016; DOI: 10.3892/or.2016.4941].</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/PMC12075994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007755","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":"SNX10 regulates the proliferation, apoptosis and cell cycle of acute B lymphoblastic leukemia cells via the PI3K/Akt signaling pathway.","authors":"Chenyu Wang, Xiulan Yang, Xue Shen, Shirong Yan, Jing Li, Yan Wang, Tian Tao, Tongqian Wu, Qian Kang, Fang Yu","doi":"10.3892/or.2025.8911","DOIUrl":"10.3892/or.2025.8911","url":null,"abstract":"<p><p>B‑cell acute lymphoblastic leukemia (B‑ALL) is a type of acute lymphoblastic leukemia that originates from B cells. It typically occurs in children and adolescents, but it can also appear in adults. Sorting nexin 10 (SNX10) has recently been identified as a significant regulatory factor in various tumors, although its specific roles remain contested. However, its function in B‑ALL has not been previously explored. The present study investigated the role of SNX10 in B‑ALL pathogenesis. Bioinformatics analysis identified SNX10 as a Core Hub gene in the B‑ALL signaling network, with significantly reduced expression in patients with B‑ALL. These findings were corroborated through analysis of clinical bone marrow samples and B‑ALL cell lines. Functional <i>in vitro</i> studies revealed that SNX10 knockdown markedly inhibited B‑ALL cell proliferation, increased apoptosis, and arrested cells in the G0/G1 phase. By contrast, SNX10 overexpression enhanced cell proliferation, suppressed apoptosis and promoted G2/M phase progression. Proteomic analysis further implicated the PI3K/Akt signaling pathway in mediating the effects of SNX10. Specifically, SNX10 overexpression increased the phosphorylation levels of PI3K and Akt, while SNX10 knockdown had the opposite effect. <i>In vivo</i> experiments demonstrated that elevated SNX10 expression accelerated leukemia progression in a mouse model. Collectively, these findings highlighted the pivotal role of SNX10 in promoting B‑ALL cell proliferation via the PI3K pathway, highlighting its potential as a therapeutic target for B‑ALL and providing a foundation for future investigations.</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/PMC12093086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984657","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] miR‑504 promotes tumour growth and metastasis in human osteosarcoma by targeting TP53INP1.","authors":"Qingchun Cai, Sixiang Zeng, Xing Dai, Junlong Wu, Wei Ma","doi":"10.3892/or.2025.8914","DOIUrl":"10.3892/or.2025.8914","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that, concerning the Transwell assay experiments shown in Fig. 2F on p. 2997, the 'Blank' and 'Normal control' data panels featured a strikingly similar overlapping area, such that these data had apparently been derived from the same original source where the results of differently performed experiments were meant to have been shown. After having re‑examined their original data, the authors realized that Fig. 2F had inadvertently been assembled incorrectly; however, the authors were able to repeat these experiments, and the revised version of Fig. 2, now including new data for the experiments shown in Fig. 2F, is shown on the next page. Note that the errors made in terms of assembling the data in Fig. 2 did not greatly affect either the results or the conclusions reported in this paper, and all the authors agree to the publication of this corrigendum. The authors regret that these errors went unnoticed prior to the publication of their article, and are grateful to the Editor of <i>Oncology Reports</i> for allowing them this opportunity to publish this corrigendum. They also apologize to the readership for any inconvenience caused. [Oncology Reports 38: 2993‑3000, 2017; DOI: 10.3892/or.2017.5983].</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/PMC12099282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079355","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":"Platelets and MMP‑9 contribute to esophageal cancer invasion via CD40‑CD154 interactions.","authors":"Kazufumi Umemoto, Toru Nakamura, Katsunori Sasaki, Osamu Sato, Tomohiro Suzuki, Satoshi Hirano","doi":"10.3892/or.2025.8912","DOIUrl":"10.3892/or.2025.8912","url":null,"abstract":"<p><p>CD40 expression in esophageal cancer (EC) is linked to poor prognosis, although its molecular role remains unclear. The present study explored the function of CD40 in EC progression and metastasis, focusing on its interaction with CD154 and the upregulation of MMP‑9. CD40 expression was confirmed in EC cell lines using quantitative PCR, western blotting, flow cytometry and immunocytochemistry. Functional assays showed that recombinant soluble CD154 stimulation enhanced the migration and invasion of CD40‑overexpressing EC cells without affecting viability. Co‑culture experiments with platelets demonstrated that platelet‑derived CD154 acted on CD40‑overexpressing esophageal cancer cells, leading to upregulation of MMP‑9 secretion, potentially driving tumor invasiveness. Serum analysis of patients who underwent esophagectomy revealed that low MMP‑9 levels were associated with longer survival in pathological Stage I, whereas the opposite trend was observed in stages II‑IV. These findings indicated that CD40 activation enhanced tumor cell invasiveness through MMP‑9 upregulation. This dual role of CD40, enhancing antitumor immunity via its expression on antigen‑presenting cells, while promoting tumor invasiveness through MMP‑9 secretion when expressed on esophageal cancer cells, may complicate immunotherapeutic strategies targeting CD40, as such interventions could inadvertently promote malignancy within the tumor microenvironment.</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/PMC12093935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079358","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":"Effect of <i>Polygonatum Sibiricum</i> polysaccharides on nude mice model of prostate cancer PC‑3 cells.","authors":"Chenxi Liu, Yuhong Tang, Jingjing Wang, Yan Zhou, Shuaibo Yang, Shaowen Dong, Guobin Zhao","doi":"10.3892/or.2025.8917","DOIUrl":"10.3892/or.2025.8917","url":null,"abstract":"<p><p>The present study aimed to explore the influence of <i>Polygonatum sibiricum</i> polysaccharides (PSP) on the progression of prostate cancer PC‑3 cell xenografts in nude mice, with a specific emphasis on analyzing the regulation of key proteins in the phosphatidylinositol 3‑kinase/protein kinase B (PI3K/Akt) and nuclear factor‑kappa B (NF‑κB) signaling pathways. An androgen‑independent PC‑3 prostate cancer cell line was subcutaneously injected into immunocompromised BALB/c nude mice to establish a xenograft model. The mice were randomly allocated into five groups, each comprising six animals. Drug dosages were determined according to the body surface area ratio between humans and nude mice. The control group was given normal saline, whereas the docetaxel (DTX) group received docetaxel at a dosage of 5 mg/(kg·d). The PSP treatment groups were administered PSP at low [100 mg/(kg x d)], medium [200 mg/(kg x d)], and high [400 mg/(kg x d)] doses. Each treatment was delivered via gavage at a volume of 0.2 ml every other day for a 30‑day period. Tumor volume and body weight were recorded every 3 days to evaluate the effect of PSP on xenograft growth, with tumor size and overall health status serving as the primary assessment criteria. A total of 4 h after drug administration, tumor volume was measured to calculate the tumor inhibition rate. Subsequently, apoptosis in tumor tissues was evaluated using the TUNEL assay. Immunohistochemistry was conducted to detect the expression levels of PI3K, Akt, NF‑κB p65, their phosphorylated forms (p‑PI3K, p‑Akt and p‑NF‑κB p65), and caspase‑3. At the initial stage of establishing the tumor‑bearing nude mouse model of prostate cancer, all groups of nude mice displayed stable mental states, high levels of activity, regular feeding habits and heightened responsiveness to external stimuli. However, as the tumors progressed, a decline in activity, food intake and responsiveness to stimuli was observed across all groups. PSP inhibited the proliferation of PC‑3 cells and induced apoptosis in tumor‑bearing nude mice, presumably by downregulating PI3K, Akt and NF‑κB p65, thereby suppressing the PI3K/Akt and NF‑κB signaling pathways. Simultaneously, PSP upregulated the expression of caspase‑3, which contributed to its antitumor effects in the PC‑3 prostate cancer model.</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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143237","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":"BCL2A1‑ and G0S2‑driven neutrophil extracellular traps: A protective mechanism linking preeclampsia to reduced breast cancer risk.","authors":"Lu Xiao, Jing Li, Jiahao Liao, Min Wu, Xiujing Lu, Jiehua Li, Yachang Zeng","doi":"10.3892/or.2025.8897","DOIUrl":"https://doi.org/10.3892/or.2025.8897","url":null,"abstract":"<p><p>Preeclampsia has been associated with a reduced risk of breast cancer (BC), but the mechanisms underlying this relationship remain unclear. It has been suggested that neutrophil extracellular traps (NETs), which are released upon neutrophil activation, play a key role in both preeclampsia and BC. To investigate this link, the single‑cell RNA sequencing dataset GSE173193 was analyzed and upregulated genes BCL2A1 and G0/G1 switch gene 2 (G0S2) were identified in neutrophils from preeclamptic placentas. These findings were validated using reverse transcription‑quantitative PCR and western blotting. Combined analyses of preeclampsia and BC tissues, from Gene Expression Omnibus (GSE24129) and The Cancer Genome Atlas databases respectively, identified 2,040 upregulated differentially expressed genes, including BCL2A1 and G0S2. Furthermore, these genes showed clinical relevance to BC, as demonstrated by Receiver Operating Characteristic curve, survival analyses and weighted gene co‑expression network analysis. Functional experiments revealed that overexpression of BCL2A1 and G0S2 increased NET release and inhibited BC cell proliferation, invasion and migration. The present study provides novel insights into the shared molecular pathways of preeclampsia and BC, emphasizing NETs as a potential protective mechanism as increased NET production in preeclampsia may contribute to a reduced BC risk by influencing tumor progression and offer avenues for further research into therapeutic interventions.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12030921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023572","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":"Multiple roles of S100P in pan carcinoma: Biological functions and mechanisms (Review).","authors":"Xinlong Wang, Dong Zhao, Ershu Zhao, Yanan Ge, Fei Cai, Yidan Xi, Jiatong Li, Xuefei Liu, Zhendong Zheng","doi":"10.3892/or.2025.8895","DOIUrl":"https://doi.org/10.3892/or.2025.8895","url":null,"abstract":"<p><p>This article examines the multifaceted roles of the S100P gene in pan‑cancer, with the aim of exploring its biological functions and related mechanisms in depth. S100P is a small calcium‑binding protein that recent studies have identified as playing a significant role in the occurrence and progression of various cancers. As research on cancer biomarkers advances, the relationship between S100P expression levels and cancer prognosis, metastasis and invasiveness has garnered increasing attention. However, the specific mechanisms underlying the role of S100P in different cancer types remain elusive and related research is still in the exploratory phase. Therefore, this review systematically summarizes the biological functions of S100P, clarifying its signaling pathways and regulatory mechanisms. This work provides new insights and strategies for targeted therapy and establishes a theoretical basis for subsequent clinical applications. Through this summary, the present review aims to enhance personalized treatment approaches for S100P‑related cancers and strengthen future explorations of S100P.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032771","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}