Oncol. Rep. [JOURNAL]
Sun
200 papers
[Retracted] Songorine suppresses cell growth and metastasis in epithelial ovarian cancer via the Bcl‑2/Bax and GSK3β/β‑catenin signaling pathways.
Zhang H, Dong R, Zhang P … +1 more , Wang Y
Oncol Rep · 2026 May · PMID 41789679 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in addition to the duplication of data within Fig. 3A (the 0 h wound‑healing assay experimental panels), ce...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in addition to the duplication of data within Fig. 3A (the 0 h wound‑healing assay experimental panels), certain of the immunohistochemical data featured in Fig. 6B were strikingly similar to data that have already appeared in an article in the journal that was written by different authors at different research institutes. A subsequent analysis of the data in this paper revealed that certain of the cell invasion assay data in Fig. 3B, western blot data in Figs. 4 and 6, and the histological data showing H&E staining in Fig. 6B had also appeared in articles published in other journals that were written by different authors at different research institutes, one of which has since been retracted. Owing to the fact that certain of the abovementioned data had already been published prior to the receipt of this article at , 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 41: 3069‑3079, 2019; DOI: 10.3892/or.2019.7070].
CXCL1 in triple‑negative breast cancer: Mechanisms, challenges, and therapeutic opportunities (Review).
Al Sayegh H, Assi Z, Kanaan A … +1 more , El Sibai M
Oncol Rep · 2026 May · PMID 41789677 · Full text
Triple negative breast cancer (TNBC) is an aggressive BC subtype with limited therapeutic options and poor clinical outcomes. This subtype accounts for 15‑20% of all BC cases and contributes to nearly 40% of BC mortaliti...
Triple negative breast cancer (TNBC) is an aggressive BC subtype with limited therapeutic options and poor clinical outcomes. This subtype accounts for 15‑20% of all BC cases and contributes to nearly 40% of BC mortalities. The chemokine C‑X‑C motif ligand 1 (CXCL1) is a key player in TNBC progression through several signaling pathways, including NF‑κB, MAPK and related cascades. CXCL1 contributes to tumor growth, metastasis, immune modulation and resistance to therapy, however its role and therapeutic potential in TNBC has not been comprehensively described. The present review aimed to summarize CXCL1 biology in TNBC, with a focus on its prognostic relevance, role in the tumor microenvironment and potential as a therapeutic target, as well as emerging strategies aimed at modulating CXCL1 signaling. However, challenges remain in translating these findings into clinical application, including incomplete understanding of certain molecular mechanisms underlying CXCL1 function, unclear prognostic value, the need for validation of potential inhibitors in large and diverse cohorts and the lack of well‑designed clinical trials testing CXCL1‑targeted approaches. Addressing these challenges through rigorous preclinical work and carefully designed clinical trials is key to define the true therapeutic potential of CXCL1 in TNBC to advance precision medicine strategies and enhance clinical outcomes in patients with TNBC.
Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest.
Bae M, Lee MK, Jeong MG … +7 more , Lee Y, Joo H, Lee YC, Lee JW, Kim SI, Ko SG, Eun YG
Oncol Rep · 2026 May · PMID 41789672 · Full text
Head and neck squamous cell carcinoma (HNSCC) is one of the most common malignancies worldwide. Cisplatin, a widely used chemotherapeutic agent, exerts its anticancer effect by inducing DNA damage, and inhibiting transcr...
Head and neck squamous cell carcinoma (HNSCC) is one of the most common malignancies worldwide. Cisplatin, a widely used chemotherapeutic agent, exerts its anticancer effect by inducing DNA damage, and inhibiting transcription and replication. However, its repeated administration can lead to severe side effects and the development of drug resistance, thereby limiting its clinical efficacy. Thus, novel combination strategies are urgently needed to enhance the anticancer effects of cisplatin. The present study aimed to investigate the potential of Platycodin D (PD), a natural saponin extracted from , to enhance cisplatin sensitivity in HNSCC cells. The results demonstrated that combination treatment with PD and cisplatin synergistically reduced cell viability and markedly suppressed colony formation compared with either agent alone. Furthermore, the combination treatment markedly increased intracellular reactive oxygen species (ROS) levels, and markedly downregulated the expression levels of antioxidant genes, including heme oxygenase‑1, NAD(P)H quinone dehydrogenase 1, superoxide dismutase 1 and sulfiredoxin 1. Additionally, the combination treatment excessively activated autophagy, whereas PD inhibited autophagic flux, as determined by LC3A/B and p62 accumulation following Bafilomycin A1 treatment, ultimately promoting apoptosis. These findings suggested that PD may serve as a potential cisplatin sensitizer by enhancing ROS accumulation and disrupting autophagy, thereby presenting a promising combination therapeutic strategy for the treatment of HNSCC.
[Expression of Concern] c‑Fos/ERK promotes the progression from pancreatic intraepithelial neoplasia to pancreatic ductal adenocarcinoma.
You L, Ren X, Du Y … +4 more , Zhao W, Cui M, Chen G, Zhao Y
Oncol Rep · 2026 May · PMID 41789670 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the histological images shown in Fig. 2B on p. 3416, the ῾Caerulein 7 days' and 'Caerulein 14 day...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the histological images shown in Fig. 2B on p. 3416, the ῾Caerulein 7 days' and 'Caerulein 14 days' panels showed an overlapping section, with the image also being magnified in the latter panel relative to the first. In addition, the immunohistochemical images shown for the 'c‑Fos/PK, caerulein+U0126' experiment in Fig. 3A and the 'c‑Fos/Control/Caerulein 7 days' experiment in Fig. 4A were identical, suggesting that at least one of these figures had been assembled incorrectly. The authors have been contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of these potential problems while the Editorial Office continues to investigate this matter further. [Oncology Reports 36: 3413‑3420, 2016; DOI: 10.3892/or.2016.5169].
Advances in the application of frailty scoring in the diagnosis and management of elderly patients with multiple myeloma (Review).
Liu J, Li D, Li C … +1 more , Chen Z
Oncol Rep · 2026 May · PMID 41789669 · Full text
Multiple myeloma (MM) is a hematological malignancy that disproportionately affects elderly populations, with age being a key risk factor for disease progression and adverse outcomes. Frailty, a multifaceted geriatric sy...
Multiple myeloma (MM) is a hematological malignancy that disproportionately affects elderly populations, with age being a key risk factor for disease progression and adverse outcomes. Frailty, a multifaceted geriatric syndrome characterized by reduced physiological reserve and increased vulnerability to stressors, is recognized as a pivotal factor influencing the diagnosis, prognosis and therapeutic management of elderly patients with MM. The present review explores the complex interplay between frailty and MM, discussing the underlying mechanisms, such as chronic inflammation, sarcopenia and immune dysfunction, that link these conditions. In addition, the clinical implications of frailty, including its association with higher treatment toxicity, prolonged hospitalization and diminished survival rates, are reviewed. The present study also aimed to evaluate commonly used frailty assessment tools, such as the International Myeloma Working Group frailty score and the Geriatric Assessment, and their use in guiding clinical decision‑making. Recent advancements in frailty scoring systems, which enable more precise risk stratification, are highlighted, emphasizing their role in tailoring individualized treatment strategies to balance efficacy and safety. Finally, the present review addresses current challenges in integrating dynamic frailty monitoring into routine clinical practice and outlines future directions, including the development of novel biomarkers and digital tools to enhance frailty assessment and improve long‑term patient outcomes.
Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation.
Li C, Yang L, Zhang Y … +2 more , Zhao B, Qu H
Oncol Rep · 2026 May · PMID 41789667 · Full text
Hepatocellular carcinoma (HCC) is an aggressive liver malignancy, the molecular mechanisms underlying the progression of which are not fully understood. As a component of the chaperonin‑containing tailless complex polype...
Hepatocellular carcinoma (HCC) is an aggressive liver malignancy, the molecular mechanisms underlying the progression of which are not fully understood. As a component of the chaperonin‑containing tailless complex polypeptide 1 (TCP1) ring complex, chaperonin‑containing TCP1 subunit 2 (CCT2) participates in the development of numerous types of liver disease. However, the potential role of CCT2 in regulating HCC malignant behaviors remains unclear. In the present study, bioinformatics analysis of patients with HCC from public datasets (The Cancer Genome Atlas‑Liver HCC, International Cancer Genome Consortium‑Liver Cancer‑Riken‑Japan and OEP00000321) demonstrated that CCT2 expression was upregulated in HCC tissue. High expression of CCT2 was also associated with an unfavorable overall survival prognosis. CCT2 knockdown was shown to inhibit the proliferation, migration, invasion and stemness and promote the apoptosis of HCC cells , as evidenced by EdU, colony formation, flow cytometry, caspase‑3/7 activity, gap closure, Transwell and tumor‑sphere formation assays. Consistently, knocking down CCT2 also suppressed the subcutaneous tumor proliferation and hematogenous lung metastasis of the human HCC HCCLM3 cells . Furthermore, downregulation of CCT2 decreased the phosphorylation of STAT3, as well as the expression of myeloid cell leukemia sequence 1, matrix metalloproteinase 2 and SRY‑box transcription factor 2 and . However, IL‑6 treatment rescued the levels of phosphorylated STAT3 and counteracted the inhibitory effects of CCT2 knockdown on proliferation and invasion. The findings suggest that CCT2 promotes HCC by activating the STAT3 signaling pathway. Therefore, CCT2 may serve as a survival biomarker and precision treatment target in HCC.
[Retracted] Growth and differentiation factor‑9 promotes adhesive and motile capacity of prostate cancer cells by up‑regulating FAK and Paxillin via Smad dependent pathway.
Bokobza SM, Ye L, Kynaston HG … +1 more , Jiang WG
Oncol Rep · 2026 May · PMID 41789666 · Full text
Subsequently to the publication of the above article, a concerned reader drew the Editor's attention to the fact that certain of the protein bands shown in lanes 1, 3 and 4 for the Smad3 experiments for the western blots...
Subsequently to the publication of the above article, a concerned reader drew the Editor's attention to the fact that certain of the protein bands shown in lanes 1, 3 and 4 for the Smad3 experiments for the western blots in Fig. 5A on p. 1657 were strikingly similar; furthermore, the protein bands shown in lanes 2 and 5 also appeared to be highly similar aside from a difference in the intensity of the shading (in conjunction with probable breaks in the continuity of the gel). In addition, the backgrounds of lanes 3 and 4 for the pSmad3 data shown in Fig. 5C were markedly similar in appearance. Having assessed these data independently in the Editorial Office, the concerns of the reader were judged to have been well founded, and the striking similarities in the appearance of the abovementioned protein bands/gel backgrounds could not easily be attributed to coincidence. Therefore, in view of the probable anomalies that were identified, the Editor of 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 24: 1653‑1659, 2010; DOI: 10.3892/or_00001030].
Role of iron and TfR1 in the application of high‑dose ascorbate against pancreatic cancer.
Piotrowsky A, Leischner C, Schmieder H … +8 more , Detert K, Schneider K, Schulte J, Hammerschmidt S, Marongiu L, Renner O, Burkard M, Venturelli S
Oncol Rep · 2026 Apr · PMID 41789665 · Full text
Pancreatic cancer remains one of the deadliest tumor diseases with an urgent need for new therapy options. At the same time, the use of high‑dose vitamin C in cancer treatment has been investigated for decades. Despite p...
Pancreatic cancer remains one of the deadliest tumor diseases with an urgent need for new therapy options. At the same time, the use of high‑dose vitamin C in cancer treatment has been investigated for decades. Despite promising and data and initial clinical studies, there is a need for optimization with regard to an ideal treatment regimen and suitable patient population for the use of high‑dose vitamin C. The aim of the present study was to evaluate for the first time the combination of high‑dose vitamin C with the administration of iron in three human pancreatic cancer cell lines and to determine the exact cell death mechanism. While the investigated cell lines showed a high susceptibility to ascorbate treatment, the combination treatment with FeCl generally led to a reduction in the ascorbate effect and in the formation of reactive oxygen species. The ascorbate‑induced cell death showed no signs of apoptosis but clear ferroptotic properties. Furthermore, treatment of the tumor cells with FeCl was accompanied by reduced expression of TfR1, preventing an increase in the intracellular labile iron pool. The present study provided valuable information on the mechanism of action of high‑dose vitamin C in pancreatic cancer, whereby a combination treatment with ferric iron in the context of tumor therapy is not recommended based on these data.
Cellular and inflammatory characteristics of patient‑derived glioblastoma organoids during cultivation.
Nojszewski J, Schröder NO, Clüver J … +4 more , Holler J, Ahmeti H, Synowitz M, Held-Feindt J
Oncol Rep · 2026 May · PMID 41789657 · Full text
Glioblastomas are characterized by extensive intra‑ and intertumoral heterogeneity, which drives their rapid invasive growth and frequent recurrence. As a result, prognosis remains poor, and developing effective treatmen...
Glioblastomas are characterized by extensive intra‑ and intertumoral heterogeneity, which drives their rapid invasive growth and frequent recurrence. As a result, prognosis remains poor, and developing effective treatments continues to be a major challenge. The survival and growth of glioblastomas are supported by a specific, protective tumor microenvironment (TME) that influences tumor morphology, growth rate, therapy resistance and recurrence. To better represent the complex TME with its immune cells and inflammatory mediators and the tumor heterogeneity, including glioma stem‑like cells (GSCs), realistic preclinical models are required. Patient‑derived glioblastoma organoids (GBOs), directly derived from tumor tissue obtained after surgical resection, were generated in the present study. Preserving the original tumor state in organoids, particularly regarding the TME and heterogeneity, is crucial. The present study evaluates the long‑term preservation of key tumor properties in cultivated GBOs, including glial structural proteins, GSCs, immune cells, endothelial cells, proliferation marker, and inflammatory mediators such as cytokines and chemokines. Expression levels of these components were measured at five defined time points in 10 independent GBO preparations, at both the mRNA and protein level, and statistical correlation analyses were performed. The findings of the present study indicate that the key components were generally maintained over a one‑month cultivation period. However, some markers showed reduced expression at later time points or recovered after an initial drop at early cultivation time points. Therefore, the optimal time window for employing patient‑derived organoids as an advanced preclinical model for glioblastoma research appears to be between 7‑14 days of cultivation.
ACSBG1‑driven lipid reprogramming unveiled: A fatty acid metabolism‑associated prognostic model for lung adenocarcinoma.
Hu P, Li A
Oncol Rep · 2026 May · PMID 41789655 · Full text
Lung adenocarcinoma (LUAD) remains a leading cause of cancer‑associated mortality with limited prognostic biomarkers. Fatty acid metabolism (FAM) reprogramming serves a pivotal role in tumor progression; however, the fun...
Lung adenocarcinoma (LUAD) remains a leading cause of cancer‑associated mortality with limited prognostic biomarkers. Fatty acid metabolism (FAM) reprogramming serves a pivotal role in tumor progression; however, the functional importance of specific FAM genes, such as ACSBG1, in LUAD remains elusive. In the present study, transcriptomics data from The Cancer Genome Atlas (n=517) and Gene Expression Omnibus‑GSE13213 (n=117) were analyzed to identify FAM‑related differentially expressed genes (DEGs). Least Absolute Shrinkage and Selection Operator regression and Shapley Additive Explanations (SHAP) interpretable analyses established a prognostic model, and experiments using A549 and H1299 cell lines with ACSBG1 overexpression (OE) and knockdown. Functional assays included Cell Counting Kit‑8, EdU, Transwell and apoptosis analyses. A total of 35 FAM‑related DEGs were identified, which were enriched in PPAR signaling and fatty acid degradation pathways (false discovery rate <0.05). Subsequently, a seven‑gene prognostic model was established, and demonstrated strong predictive power for 1‑, 3‑ and 5‑year survival (area under the curve values: 0.767, 0.769 and 0.700, respectively). SHAP analysis prioritized ACSBG1 as the dominant protective factor, and its low expression was associated with advanced Tumor‑Node‑Metastasis stages and poor survival. Mechanistically, ACSBG1 OE suppressed proliferation, migration and invasion, and promoted apoptosis. Immune profiling revealed ACSBG1 expression was positively correlated with the infiltration of CD4 T cells, CD8 T cells and B cells, suggesting its immunomodulatory potential. In conclusion, to the best of our knowledge, the present study established the first FAM‑based prognostic model for LUAD, and identified ACSBG1 as a novel tumor suppressor through dual mechanisms of metabolic regulation and immune microenvironment modulation. The risk score system established in the current study provides a clinically actionable tool for precision oncology, and ACSBG1‑targeted therapy represents a promising strategy against LUAD progression.
[Retracted] Overexpression of SHP2 tyrosine phosphatase promotes the tumorigenesis of breast carcinoma.
Hu Z, Fang H, Wang X … +3 more , Chen D, Chen Z, Wang S
Oncol Rep · 2026 Apr · PMID 41789646 · Full text
Following the publication of the above article and a corrigendum (doi: 10.3892/or.2017.5455) that was issued in 2017 to address issues of incorrect data assembly in Figs. 3 and 7, an interested reader drew to our attent...
Following the publication of the above article and a corrigendum (doi: 10.3892/or.2017.5455) that was issued in 2017 to address issues of incorrect data assembly in Figs. 3 and 7, an interested reader drew to our attention that data also appeared to be duplicated in Fig. 4C, and data featured in Figs. 2 and 5 subsequently appeared in an article published by the same research group in the journal Oncotarget. Additionally, following an independent re‑evaluation of the data in this paper made by the Editorial Office, duplicated data were also noted in Fig. 5A, and some of the data in question subsequently appeared in an article in in 2022 written by different authors at different institutes, which has since been retracted. In view of these additional findings, even though the possibility of a further corrigendum was originally considered, the Editor of has decided that the paper should be retracted on account of a 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 satisfactory reply. The Editor apologizes to the readrship for any inconvenience caused. [Oncology Reports 32: 205‑212, 2014; DOI: 10.3892/or.2014.3201].
Advances in immunotherapy and targeted therapy for nasopharyngeal carcinoma: Current progress and combined approaches (Review).
Yang Z, Liu H, Chen M … +3 more , Zhang L, Gong M, Yu R
Oncol Rep · 2026 Apr · PMID 41789645 · Full text
Nasopharyngeal carcinoma (NPC), a malignancy of the head and neck closely associated with Epstein‑Barr virus (EBV) infection, is highly prevalent in southern China and Southeast Asia. Traditional treatments such as radio...
Nasopharyngeal carcinoma (NPC), a malignancy of the head and neck closely associated with Epstein‑Barr virus (EBV) infection, is highly prevalent in southern China and Southeast Asia. Traditional treatments such as radiotherapy and chemotherapy have notable limitations in the management of locally advanced, recurrent or metastatic cases. Previously, immunotherapies, such as PD‑1/PD‑L1 inhibitors and targeted therapies, including EGFR and VEGF inhibitors, have emerged as breakthroughs in the treatment of NPC. The synergistic effects of combining these therapies have become a prominent area of research. While existing reviews have discussed the progress in immunotherapy and targeted therapy, most focus on single therapeutic modalities and lack a systematic integration of the latest clinical data and emerging treatment approaches. The present review discussed recent clinical trial results, focusing on the synergistic mechanisms of combined immunotherapy and targeted therapy, while also exploring the predictive value of EBV‑associated biomarkers. Additionally, it described cutting‑edge developments such as bispecific antibodies and antibody‑drug conjugates. The present article provides a comprehensive analysis of the mechanisms, clinical advancements, efficacy and safety of immunotherapy, targeted therapy and their combination in NPC, highlighting current challenges and future directions to offer precise guidance for personalized clinical treatment.
KDM5D expression is lost in cisplatin‑resistant neuroblastoma cells.
Podhorska N, Hrabeta J, Belhajova M … +1 more , Eckschlager T
Oncol Rep · 2026 Apr · PMID 41789643 · Full text
Chemoresistance is a major cause of cancer therapy failure. Increasing evidence points to the importance of histone lysine demethylase function, whose dysregulation has been described in several types of cancer. KDM5, a...
Chemoresistance is a major cause of cancer therapy failure. Increasing evidence points to the importance of histone lysine demethylase function, whose dysregulation has been described in several types of cancer. KDM5, a family of histone lysine demethylases, may carry out a key role in the downregulation of tumor‑suppressors or upregulation of oncogenes and in the development of drug tolerance. The present study examined the expression of KDM5D in cell lines derived from high‑risk neuroblastoma. The present study found that KDM5D expression was lost in all cisplatin‑chemoresistant neuroblastoma cell lines compared with sensitive parental cells. In addition, the cisplatin‑chemoresistant neuroblastoma cell line had increased expression of the ubiquitin ligase cullinaA 4A (CUL4A) compared with the sensitive parental cells. CUL4A carries out a role in cellular processes and its aberrant regulation has been observed in a number of types of cancer. The present study shows that silencing of KDM5D causes a more aggressive phenotype of neuroblastoma by promoting cell proliferation and migration, evading cell death, promoting S phase of the cell cycle and desensitizing sensitive cells to cisplatin via the gene . In addition, ectopic expression of KMD5D in a cisplatin‑resistant cell line reversed these phenomena. The results suggest that KDM5D and/or CUL4A may be a biomarkers of chemoresistance to cisplatin and a potential therapeutic target in neuroblastoma.
Hypoxia‑induced miR‑135b‑5p promotes neuroendocrine differentiation of prostate cancer cells through HIF1AN‑HIF1α axis.
Lakshmi PSV, Parashar J, Biswas B … +1 more , Ummanni R
Oncol Rep · 2026 Apr · PMID 41716025 · Full text
Neuroendocrine prostate cancer (NEPC) is a highly aggressive subtype of prostate cancer (PCa), associated with poor prognosis and resistance to androgen receptor (AR)‑targeted therapies. Hypoxia is a well‑established dri...
Neuroendocrine prostate cancer (NEPC) is a highly aggressive subtype of prostate cancer (PCa), associated with poor prognosis and resistance to androgen receptor (AR)‑targeted therapies. Hypoxia is a well‑established driver of lineage plasticity and has been implicated in promoting NE differentiation (NED) of tumors. However, the underlying molecular mechanisms linking hypoxia to NED remain unclear. In the present study, miR‑135b‑5p was identified as a critical regulator of hypoxia‑induced NED through modulation of the hypoxia‑inducible factor alpha‑1 subunit alpha inhibitor (HIF1AN)‑HIF1α axis. Exposure of androgen‑dependent PCa cell lines (LNCaP and VCaP) to hypoxia induced neurite outgrowth and increased expression of NE markers, concurrent with upregulation of miR‑135b‑5p. Target prediction followed by experimental validation in luciferase reporter assays confirmed that HIF1AN is a direct target of miR‑135b‑5p. Suppression of HIF1AN results in the stabilization of HIF1α, which in turn activates the AKT/mTOR signaling pathway, facilitating NE trans differentiation. Functional studies demonstrated that overexpression of miR‑135b‑5p by mimics promotes NED in LNCaP cells, while inhibition of miR‑135b‑5p reverses the NE features in NE‑LNCaP and NCI‑H660, NE cells. Furthermore, pharmacological inhibition of HIF1α using PX‑478 abrogated hypoxia‑induced NED and attenuated activation of AKT/mTOR signaling, further underscoring the significance of the miR‑135b‑5p‑HIF1AN‑HIF1α axis in NED of PCa cells. Collectively, the findings of the present study reveal a novel miR‑135b‑5p‑HIF1AN‑HIF1α signaling axis that is involved in hypoxia‑induced NED via AKT/mTOR activation and identify miR‑135b‑5p and HIF1α as potential therapeutic targets for NEPC.
NR4A1 mediates chemotherapy‑induced senescence via the PI3K/AKT pathway in gastric cancer cells.
Zhang T, Wang Y, Zhang J … +3 more , Ye X, Shen Y, Zhang Z
Oncol Rep · 2026 Apr · PMID 41716024 · Full text
Gastric cancer (GC) remains among the cancers with extremely high morbidity and mortality rates worldwide, and chemotherapy resistance limits its therapeutic efficacy. Therapy‑induced senescence (TIS) is vital for induci...
Gastric cancer (GC) remains among the cancers with extremely high morbidity and mortality rates worldwide, and chemotherapy resistance limits its therapeutic efficacy. Therapy‑induced senescence (TIS) is vital for inducing chemotherapy resistance and promoting tumor progression, highlighting the need to explore its regulatory mechanisms. To investigate oxaliplatin (OXA)‑induced senescence in GC cells, cellular senescence was assessed by senescence‑associated β‑galactosidase (SA‑β‑Gal) staining, western blotting, immunofluorescence, and reverse transcription‑quantitative polymerase chain reaction for the senescence‑associated secretory phenotype (SASP) factors. Moreover, multi‑omics integration including transcriptomic, proteomic and untargeted metabolomic, was used to identify key regulators and pathways. OXA induced a senescent phenotype characterized by p21 upregulation, SA‑β‑Gal staining, cell cycle arrest and SASP secretion. Integrative multi‑omics analysis revealed that NR4A1 is a central upstream regulator, and the PI3K/AKT pathway is suppressed in OXA‑induced senescence. Notably, survival analysis verified that NR4A1 expression was correlated with the prognosis of patients in GC. Functional studies demonstrated that NR4A1 knockdown attenuated OXA‑induced senescence, restored PI3K/AKT activity, and reduced SASP expression. Metabolomic profiling revealed that OXA‑induced senescence induced metabolic reprogramming, including glycolysis enhancement and oxidative phosphorylation suppression. Notably, NR4A1 knockdown reversed these metabolic alterations. The present study identified NR4A1 as a key regulated gene in chemotherapy‑induced senescence in GC and verified that the NR4A1/AKT‑metabolism axis is vital for the pivotal mechanism of TIS. These findings may provide a novel therapeutic strategy to optimize chemotherapy and develop 'one‑two punch' approaches targeting senescent tumor cells.
[Retracted] Knockdown of human antigen R reduces the growth and invasion of breast cancer cells and affects expression of cyclin D1 and MMP‑9.
Yuan Z, Sanders AJ, Ye L … +2 more , Wang Y, Jiang WG
Oncol Rep · 2026 Apr · PMID 41716014 · Full text
Following the publication of the above paper, a concerned reader drew to the Editor's attention that, for the RT‑qPCR experiments shown in Fig. 2A on p. 240, data which were intended to show the results of experiments pe...
Following the publication of the above paper, a concerned reader drew to the Editor's attention that, for the RT‑qPCR experiments shown in Fig. 2A on p. 240, data which were intended to show the results of experiments performed in two different cell lines (MCF7 and MDA‑MD‑231) appeared to have been duplicated, with some evidence of stretching of the bands. In addition, it was shown that, in Fig. 5A and C on p. 242, data which were also intended to show the results of RT‑qPCR and western blot analysis experiments performed in the same two cell lines appeared to have been duplicated; moreover, GAPDH data in Fig. 2C also appeared to have been included in Figs. 5C and 6C, but with the data bands shown in different orientations, and probable rearrangement of bands had occurred with the cyclin D1 / MMP‑9 data in Fig. 5C compared with Fig. 6C. Owing to the large number of duplications of data that have been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a 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 26: 237‑245, 2011; DOI: 10.3892/or.2011.1271].
Impact of the intratumoral resident microbiome on the immune microenvironment of malignant tumors (Review).
Oh HN, Hur H
Oncol Rep · 2026 Apr · PMID 41685611 · Full text
Advances in cancer research have highlighted the importance of tumor‑intrinsic factors, including tumor type, immune environment, immunogenicity, metabolic demands and the intratumoral microbiome. Together, these factors...
Advances in cancer research have highlighted the importance of tumor‑intrinsic factors, including tumor type, immune environment, immunogenicity, metabolic demands and the intratumoral microbiome. Together, these factors have reshaped the current understanding of cancer immunity and systemic therapies, particularly targeted treatments and immune checkpoint inhibitors that act on cancer cells, blood vessels and immune cells within the tumor microenvironment (TME). Among these, the presence of bacteria within tumors has emerged as a critical modulator of the TME, influencing tumor progression and antitumor responses across various cancer types. With the rapid expansion of cancer immunotherapies, advanced detection and sequencing technologies are increasingly applied to elucidate interactions between intratumoral microbiota and immune cells. The present review focuses on the mechanisms by which tumor bacteria modulate immune responses, supported by validations from and studies. The potential of intratumoral microbiota as biomarkers for prognosis and immunotherapy response is also discussed, alongside emerging biotechnological tools for microbiota profiling. By examining the dual roles of intratumoral microbiota in cancer biology, the current review provides a comprehensive overview of their implications and practical applications in cancer‑related research.
Suppressive role of SCN4B in the epithelial‑mesenchymal transition of lung adenocarcinoma.
Guo M, Li H, Zhao Z … +4 more , Wang Y, Tang J, Zhong B, Zhao Y
Oncol Rep · 2026 Apr · PMID 41685607 · Full text
The poor prognosis and high mortality rate of non‑small cell lung cancer are largely driven by its aggressive migratory and invasive behavior. Epithelial‑mesenchymal transition (EMT) is a central mechanism conferring the...
The poor prognosis and high mortality rate of non‑small cell lung cancer are largely driven by its aggressive migratory and invasive behavior. Epithelial‑mesenchymal transition (EMT) is a central mechanism conferring these malignant traits. The present study examined the expression profile of the sodium channel β4 subunit () in lung adenocarcinoma (LUAD) and explored its regulatory role in EMT. Transcriptomic data from The Cancer Genome Atlas were analyzed to compare expression between LUAD and normal tissues, and to assess its relationship with TNM clinical stage (I‑IV), overall survival and diagnostic performance using non‑parametric tests, Kaplan‑Meier analysis and receiver operating characteristic curves, respectively. Functional enrichment analysis, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and immune cell infiltration profiling were performed on ‑associated differentially expressed genes. , the A549 and H1299 LUAD cell lines were engineered to overexpress . Viability, migration, invasion and apoptosis were evaluated using Cell Counting Kit‑8 assays, wound healing assays, Transwell assays and flow cytometry. In addition, western blotting was conducted to assess EMT markers, including E‑cadherin, N‑cadherin, Vimentin and Snail. The results demonstrated that expression was markedly reduced in LUAD tissues and low SCN4B expression was associated with unfavorable clinical outcomes. KEGG analysis revealed enrichment of SCN4B‑related genes in the 'cell adhesion molecules' pathway, and SCN4B expression levels differed markedly between TNM tumor (T) pathologic stages T1 and T2. Furthermore, SCN4B overexpression suppressed viability, migration and invasion of A549 and H1299 cells, while promoting apoptosis. Western blotting demonstrated upregulation of E‑cadherin, and downregulation of N‑cadherin, Vimentin and Snail in the overexpression group compared with the empty vector group, indicating inhibition of EMT. In conclusion, low expression was associated with poor prognosis in LUAD. Notably, restoring levels suppressed LUAD cell viability, migration and invasion , accompanied by inhibition of EMT. These findings highlighted as a potential tumor suppressor and a promising therapeutic target for LUAD.
Regorafenib and Nifuroxazide exert enhanced suppression of hepatocellular carcinoma by inhibiting STAT3 and immune remodeling.
Li K, Chen J, Zheng Z … +10 more , Gao Y, Zhang J, Ding W, Yang T, Gu Y, Duan X, Zhao T, Jia H, Chen P, Ren J
Oncol Rep · 2026 Apr · PMID 41685604 · Full text
Regorafenib, a multi‑kinase inhibitor, has limited efficacy in hepatocellular carcinoma (HCC) due to dose‑-dependent toxicity. The present study explored whether low‑dose Regorafenib combined with Nifuroxazide exerts enh...
Regorafenib, a multi‑kinase inhibitor, has limited efficacy in hepatocellular carcinoma (HCC) due to dose‑-dependent toxicity. The present study explored whether low‑dose Regorafenib combined with Nifuroxazide exerts enhanced anti‑tumor effects in HCC models. experiments with HepG2 cells showed the combination inhibited cell viability, proliferation and migration, induced apoptosis and reduced expression of key proteins, including phosphorylated signal transducer and activator of transcription 3 (STAT3). , H22 tumor‑bearing mice treated with the combination exhibited suppressed tumor growth without systemic toxicity, along with changes in apoptotic proteins, enhanced tumor‑infiltrating immune cells and improved systemic immune responses. These findings indicated that the combination exerts enhanced suppression of HCC by inhibiting STAT3 and remodeling anti‑tumor immunity, providing preclinical evidence for a safe and effective strategy.
[Retracted] miR‑218 suppresses cardiac myxoma proliferation by targeting myocyte enhancer factor 2D.
Cao Q, Dong P, Wang Y … +3 more , Zhang J, Shi X, Wang Y
Oncol Rep · 2026 Apr · PMID 41685603 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the GAPDH and MEF21 protein bands shown in the western blots in Fig. 2C on p. 2608 were strikingly similar t...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the GAPDH and MEF21 protein bands shown in the western blots in Fig. 2C on p. 2608 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published, or were under consideration for publication at the same time, some of which have subsequently been retracted. Upon conducting an independent evaluation of the data in the Editorial Office, it emerged that the western blots shown in Fig. 1B in this paper had similarly appeared in a number of unrelated articles.In view of the fact that the abovementioned data in Figs. 1B and 2C had already apparently been published previously, the Editor of 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 33: 2606‑2612, 2015; DOI: 10.3892/or.2015.3861].
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