Oncol. Rep. [JOURNAL]
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200 papers
Cancer signaling networks in tumor progression and drug resistance: Crosstalk, adaptive reprogramming and therapeutic targeting (Review).
Li H, Song S, Wang L … +1 more , Liu Q
Oncol Rep · 2026 Jul · PMID 42138201 · Full text
Cancer signaling networks, highly dynamic with interconnected systems, regulate tumor initiation, its progression, therapeutic response and drug resistance. Rather than functioning as isolated pathways, these networks in...
Cancer signaling networks, highly dynamic with interconnected systems, regulate tumor initiation, its progression, therapeutic response and drug resistance. Rather than functioning as isolated pathways, these networks integrate extracellular and intracellular signals through coordinated interactions among membrane receptors, intracellular transducers and downstream effectors. Increasing evidence suggests that pathway crosstalk, feedback regulation and adaptive reprogramming are central to tumor phenotypic plasticity, microenvironmental adaptation and resistance to therapy. In this review, the core architecture of cancer signaling networks and the major oncogenic pathways embedded within them were summarized with a particular focus on PI3K/Akt/mTOR, MAPK/ERK and Wnt/β‑catenin signaling. The dynamic network properties that shape cancer behavior, including compensatory activation, context‑dependent signaling outputs and interactions with the tumor microenvironment, were further discussed. These features provide insights into why single‑pathway inhibition often produces only a limited and transient clinical benefit. Importantly, a network‑level understanding of cancer signaling has major translational implications. Therapeutic resistance frequently arises through pathway reactivation, bypass signaling and adaptive reprogramming, necessitating rational combination strategies and multi‑target interventions. Advances in multi‑omics, single‑cell and spatial technologies and computational modeling are crucial for characterizing signaling network dynamics and identifying clinically relevant vulnerabilities.
[Corrigendum] ENO2 affects the EMT process of renal cell carcinoma and participates in the regulation of the immune micro-environment.
Chen WJ, Yang W, Gong M … +10 more , He Y, Xu D, Chen JX, Chen WJ, Li WY, Wang YQ, Dong KQ, Song X, Pan XW, Cui XG
Oncol Rep · 2026 Jul · PMID 42138195 · Full text
Following the publication of this article, the authors have brought to the Editor's attention that they made an error in the compilation of the data in Fig. 4, as it appeared on p. 9. Specifically, some of the blots incl...
Following the publication of this article, the authors have brought to the Editor's attention that they made an error in the compilation of the data in Fig. 4, as it appeared on p. 9. Specifically, some of the blots included for the 769‑P cell line experiments in Fig. 4B had inadvertently been included in the figure incorrectly. The corrected version of Fig. 4, now showing all the correct western blot data in Fig. 4B, is shown on the next page. The authors sincerely apologize for the errors that were introduced during the preparation of this figure, and are grateful to the Editor of for granting them the opportunity to publish a Corrigendum. All the authors agree with the publication of this Corrigendum, and they also regret any inconvenience that this mistake may have caused. [Oncology Reports 49: 33, 2023; DOI: 10.3892/or.2022.8470].
SRRT promotes prostate cancer progression and serves as a prognostic biomarker through STAT3 pathway activation.
Lu L, Wu K, Wang Z … +5 more , Yang R, Li K, Guo S, Wang F, Ma Z
Oncol Rep · 2026 Jul · PMID 42138194 · Full text
Prostate cancer (PC) is a highly prevalent malignancy in men with substantial prognostic heterogeneity. The present study aimed to identify novel prognostic biomarkers and investigate their functional roles and underlyin...
Prostate cancer (PC) is a highly prevalent malignancy in men with substantial prognostic heterogeneity. The present study aimed to identify novel prognostic biomarkers and investigate their functional roles and underlying mechanisms in PC. To this end, integrated bioinformatics analyses were performed using The Cancer Genome Atlas‑prostate adenocarcinoma cohort and two Gene Expression Omnibus datasets. A total of 95 common differentially expressed genes were identified and were significantly enriched in the STAT3 signaling pathway. Lasso and Cox regression analyses screened nine independent prognostic genes, among which SRRT exhibited the highest risk coefficient. The constructed risk model showed strong predictive performance for disease‑free survival and favorable calibration in nomogram analysis. Experimental validation demonstrated that SRRT was markedly upregulated in PC tissues and cell lines, and functional assays revealed that SRRT knockdown inhibited, whereas overexpression promoted, proliferation and migration of DU145 and PC‑3 cells and tumor growth . Mechanistically, SRRT enhanced STAT3 phosphorylation, and activation of STAT3 by colivelin partially reversed the suppressive effects of SRRT silencing, indicating that SRRT promotes PC progression through activation of the STAT3 signaling pathway. Collectively, SRRT acts as an independent adverse prognostic biomarker that promotes PC progression, and the present findings provide integrated bioinformatic and experimental evidence linking SRRT to STAT3 pathway activation.
Effect of the miR‑26a/b‑5p‑STAT3‑YKL‑40 regulatory axis on proliferation, migration, and invasion of endometrial cancer cells.
Sun X, Lin S, Zhong X … +3 more , Luo Y, Yang J, Fan J
Oncol Rep · 2026 Jul · PMID 42138189 · Full text
The incidence of endometrial cancer (EC) is on the rise annually, emphasizing the importance of timely diagnosis and treatment. Signal transducer and activator of transcription 3 (STAT3) has been identified as a proto‑on...
The incidence of endometrial cancer (EC) is on the rise annually, emphasizing the importance of timely diagnosis and treatment. Signal transducer and activator of transcription 3 (STAT3) has been identified as a proto‑oncogene involved in multiple signaling pathways affecting various biological processes, especially in tumours. The aim of the present study was to validate the impact of STAT3 on EC phenotype and investigate its upstream and downstream regulatory mechanisms. Immunohistochemical analysis was conducted to assess STAT3 expression in EC tissues, followed by dual luciferase assays to confirm the regulatory relationship between STAT3 and microRNA (miR)‑26a/b‑5p. The effects of STAT3 and miR‑26a/b‑5p on HEC‑1A cell proliferation and metastasis were evaluated through Cell Counting Kit‑8 assays, cell scratch assays, and Transwell assays. Co‑immunoprecipitation assays verified the binding between STAT3 and chitinase‑3‑like protein 1 (CHI3L1, also known as YKL‑40). The results demonstrated high STAT3 expression in EC, associated with disease progression. miR‑26a/b‑5p directly targeted STAT3. Upregulated STAT3 enhanced HEC‑1A cell proliferation, migration, and invasion, counteracting the inhibitory effects of miR‑26a/b‑5p on cell migration and invasion. In addition, it was confirmed that STAT3 binds to and promotes the expression of YKL‑40. These findings contribute to clarifying the pathogenesis of EC.
Chronic stress and cancer progression through neuro‑endocrine‑immune networks (Review).
Zhu Z, Zhang X, Yan J … +5 more , Wang M, Lv Y, Zhang W, Guo H, Zheng A
Oncol Rep · 2026 Jul · PMID 42099244 · Full text
Chronic stress may influence cancer trajectories; however, the majority of current frameworks do not clearly define how organism‑level regulation interacts with tumor behavior. The present review summarizes mechanistic a...
Chronic stress may influence cancer trajectories; however, the majority of current frameworks do not clearly define how organism‑level regulation interacts with tumor behavior. The present review summarizes mechanistic and translational evidence to propose a testable model in which cancer progression can, in selected contexts, be understood as over‑adaptation to sustained stress within a hierarchical neuro‑endocrine‑immune network. Within this framework, stress‑related signals converge in brainstem‑hypothalamic control circuits, and engage sympathetic, hypothalamic‑pituitary‑adrenal and vagal effector pathways, which may influence cellular programs, microenvironmental remodeling and systemic dissemination. The evidence is organized into three sections: Cellular adaptation, microenvironmental remodeling and systemic progression. This multiscale perspective provides a host‑context framework for understanding how chronic stress‑related physiology may interact with tumor‑intrinsic processes. Therapeutic implications are also discussed, including psychosocial support, exercise, mindfulness‑based interventions, vagal modulation and perioperative β‑blocker/COX‑2 strategies. At present, the strongest clinical evidence for these approaches supports improvements in symptoms, patient‑reported outcomes and selected biomarkers, whereas durable effects on tumor control or survival remain uncertain. Overall, this framework is presented as a conceptual and testable model intended to guide future research on host‑tumor interactions in cancer.
[Retracted] SHIP1 is targeted by miR‑155 in acute myeloid leukemia.
Xue H, Hua LM, Guo M … +1 more , Luo JM
Oncol Rep · 2026 Jul · PMID 42099235 · Full text
Subsequently to the publication of the above article, a concerned reader drew the Editor's attention to the fact that the left‑hand, outer edges of the β‑actin protein blot of lane 1 and the SHIP‑1 protein blot for lane...
Subsequently to the publication of the above article, a concerned reader drew the Editor's attention to the fact that the left‑hand, outer edges of the β‑actin protein blot of lane 1 and the SHIP‑1 protein blot for lane 9 in Fig. 1B were hanging over the area representing the grey background of the gels, extending beyond the perceived boundary of these background regions and therefore raising possible concerns about post‑acquisition compositing or localized image processing during figure assembly. In addition, in the same figure, the control β‑actin western blots shown in Fig. 1B for the lanes 1‑8 and 9‑16 were apparently the same, albeit the bands in the lower set of blots (for lanes 9-16) were horizontally more compressed. In view of the potential anomalies described above for the data in Fig. 1B, the Editor of has decided that this paper 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 did not accept the decision to retract the paper. The Editor apologizes for any inconvenience caused. [Oncology Reports 32: 2253‑2259, 2014; DOI: 10.3892/or.2014.3435].
A novel regulatory role of microRNA‑5590‑3p in hepatocellular carcinoma via the HOXB2/MYC axis.
Li B, Zhou L
Oncol Rep · 2026 Jul · PMID 42099234 · Full text
The present study aimed to investigate the effects of microRNA (miR)‑5590‑3p on the biological functions of hepatocellular carcinoma (HCC) cells through the homeobox B2 (HOXB2)/MYC axis. The expression levels of miR‑5590...
The present study aimed to investigate the effects of microRNA (miR)‑5590‑3p on the biological functions of hepatocellular carcinoma (HCC) cells through the homeobox B2 (HOXB2)/MYC axis. The expression levels of miR‑5590‑3p, HOXB2 and MYC were measured in HCC tissues and cell lines, and the relationships between miR‑5590‑3p, HOXB2, and the clinicopathological characteristics and prognosis of patients with HCC were analyzed. The Cell Counting Kit‑8 assay assessed cell proliferation, flow cytometry measured apoptosis rate, and the Transwell and wound healing assays evaluated the invasive and migratory abilities of cells. The targeting interactions between miR‑5590‑3p and HOXB2, and between HOXB2 and MYC were assessed. In addition, a subcutaneous HCC xenograft model was established to assess the effects of miR‑5590‑3p on tumor growth. The results revealed that miR‑5590‑3p expression was downregulated in HCC tissues and cells, whereas HOXB2 and MYC expression were upregulated. Notably, low miR‑5590‑3p expression and high HOXB2 expression were both associated with a poor prognosis in patients with HCC. miR‑5590‑3p directly targeted and suppressed HOXB2, whereas HOXB2 promoted MYC transcription. Furthermore, downregulation of miR‑5590‑3p enhanced the invasion, migration and proliferation of Huh7 cells, and reduced their apoptotic rate. By contrast, miR‑5590‑3p overexpression or HOXB2 silencing decreased invasion, migration and proliferation, while increasing apoptosis. Moreover, HOXB2 overexpression reversed the inhibitory effect of miR‑5590‑3p upregulation on HCC cell proliferation. HOXB2 appeared to promote Huh7 cell proliferation and motility through MYC transcriptional activation, whereas miR‑5590‑3p overexpression suppressed tumor growth . In conclusion, miR‑5590‑3p may inhibit HCC cell proliferation and motility, and induce apoptosis by targeting HOXB2 and suppressing MYC transcription.
[Retracted] PTEN enhances G2/M arrest in etoposide‑treated MCF‑7 cells through activation of the ATM pathway.
Zhang R, Zhu L, Zhang L … +7 more , Xu A, Li Z, Xu Y, He P, Wu M, Wei F, Wang C
Oncol Rep · 2026 Jul · PMID 42059271 · Full text
Subsequently to the publication of the above article, a concerned reader drew to the Editor's attention that the β‑actin bands featured in Fig. 1A were also apparently included in the 'Ctrl' experiments for the phospho‑P...
Subsequently to the publication of the above article, a concerned reader drew to the Editor's attention that the β‑actin bands featured in Fig. 1A were also apparently included in the 'Ctrl' experiments for the phospho‑P53 protein bands in Fig. 1B. In addition, a specific pair of P53 bands in Fig. 1B had also apparently been re‑used as phospho‑CDC25C bands in Fig. 6A, suggesting that these figures may have potentially undergone inappropriate editing. After having evaluated these data independently in the Editorial Office, the concerns of the reader were shown to have been well‑founded. Therefore, in view of the uncertainties regarding the assembly of some of the western blot data in Figs. 1 and 6, the Editor of has decided that this paper should be retracted from the Journal on account of uncertainties with the presentation of the abovementioned data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply.The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 2707‑2714, 2016; DOI: 10.3892/or.2016.4674].
E3 ubiquitin ligase RNF40: Structure, function and its context‑dependent roles in tumorigenesis (Review).
Wu Z, Yang H, Chen G … +7 more , Zhao W, Bao B, Luv C, Zhu W, Liu F, Ai H, Li Z
Oncol Rep · 2026 Jun · PMID 42059264 · Full text
The ubiquitin‑proteasome system, a key protein degradation machinery in humans, mediates substrate recognition and proteolysis through ubiquitin‑tagged targeting of macromolecular proteins to the 26S proteasome. This evo...
The ubiquitin‑proteasome system, a key protein degradation machinery in humans, mediates substrate recognition and proteolysis through ubiquitin‑tagged targeting of macromolecular proteins to the 26S proteasome. This evolutionarily conserved system orchestrates fundamental cell processes, including cell cycle progression, DNA damage repair, immune regulation, signal transduction and clearance of misfolded proteins. Its functional integrity is involved in the pathogenesis of various malignancies (breast and small cell lung cancer and colorectal adenocarcinoma) and degenerative diseases (Parkinson's disease). As a really interesting new gene‑type E3 ubiquitin ligase, ring finger protein (RNF)40 has emerged as a key regulator of both physiological homeostasis and disease progression. The present review systematically examines RNF40 structural architecture and its multifaceted roles in ubiquitination‑dependent proteostasis, epigenetic modulation and DNA repair mechanisms, as well as its tumor‑specific regulatory networks across cancer subtypes and therapeutic potential as a novel drug target.
[Expression of Concern] Promoter methylation of death‑associated protein kinase and its role in irradiation response in cervical cancer.
Leung RC, Liu SS, Chan KY … +4 more , Tam KF, Chan KL, Wong LC, Ngan HY
Oncol Rep · 2026 Jun · PMID 42059254 · Full text
Following the publication of the above paper, and an Expression of concern statement (DOI: 10.3892/or.2025.9028), which notified the readers that the blots showing β‑actin mRNA expression in Fig. 1 on p. 1341 appeared to...
Following the publication of the above paper, and an Expression of concern statement (DOI: 10.3892/or.2025.9028), which notified the readers that the blots showing β‑actin mRNA expression in Fig. 1 on p. 1341 appeared to be similar to the β‑actin mRNA blots shown in Fig. 3 on p. 1342, albeit with some horizontal and vertical resizing, another reader has subsequently contacted the Editorial Office to explain that control western blot data featured in the same figures (Figs. 1 and 3) also appeared to be strikingly similar. We have again reached out to the authors, requesting an explanation for these apparent anomalies in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of additional potential issues surrounding the scientific integrity of this paper, we are issuing a second Expression of Concern to notify readers of these additional issues while the Editorial Office continues to investigate this matter. [Oncology Reports 19: 1339‑1345, 2008; DOI: 10.3892/or.19.5.1339].
Inhibitory role of angiopoietin‑like 4 for cancer progression in oropharyngeal squamous cell carcinoma.
Mikoshiba T, Sekimizu M, Nakahara N … +5 more , Saito S, Yoshihama K, Nagai R, Kono T, Ozawa H
Oncol Rep · 2026 Jun · PMID 42028751 · Full text
The mortality rate of head and neck squamous cell carcinoma (HNSCC), one of the most prevalent types of cancer, has remained unchanged despite advances in treatment strategies. Angiopoietin‑like 4 (ANGPTL4) exhibits both...
The mortality rate of head and neck squamous cell carcinoma (HNSCC), one of the most prevalent types of cancer, has remained unchanged despite advances in treatment strategies. Angiopoietin‑like 4 (ANGPTL4) exhibits both pro‑ and anti‑tumorigenic roles in various cancers depending on the tissue context. The present study investigated the role of ANGPTL4 expression in oropharyngeal squamous cell carcinoma (OPSCC). Data from 137 patients with OPSCC who underwent initial treatment were retrospectively analyzed. ANGPTL4 expression in tumor tissues was determined via immunohistochemistry. Survival outcomes [overall survival (OS) and disease‑free survival (DFS)] and clinicopathological correlations were evaluated. Tumor cell proliferation was assessed using an CellTiter‑Glo 2.0 luminescence‑based cell viability assay, immunofluorescence staining, and reverse transcription‑quantitative polymerase chain reaction following small interfering RNA‑mediated knockdown in a HNSCC cell line. Gene set enrichment analysis (GSEA) was performed using data from The Cancer Genome Atlas. ANGPTL4 expression (≥7.7%) in patients with OPSCC was significantly associated with improved OS and DFS. Multivariate analysis confirmed that low ANGPTL4 expression was an independent prognostic factor for OS [hazard ratio (HR)=3.676, 95% confidence interval (CI)=1.678‑8.056; P=0.001) and DFS (HR=2.959, 95% CI=1.533‑5.713; P=0.001)]. FaDu cells with knockdown demonstrated significantly increased proliferation compared with negative controls in the CellTiter‑Glo 2.0 assay (P=0.010), accompanied by a significant increase in Ki‑67 expression as revealed by immunofluorescence staining (P=0.021). The relative mRNA expression levels decreased to 38%, whereas those of increased significantly. GSEA revealed significant enrichment of cell cycle progression signatures in cases with low expression. ANGPTL4 expression was significantly associated with a favorable prognosis in OPSCC, and its knockdown increased proliferative activity in FaDu cells. Thus, ANGPTL4 may serve as a prognostic biomarker in OPSCC. Further studies are warranted to clarify causality and assess the therapeutic potential of targeting in OPSCC.
Hypermethylation‑induced silencing of ITGA4 promotes oral squamous cell carcinoma progression through SNX5 upregulation.
Tien NNT, Choe HC, Ahn SG
Oncol Rep · 2026 Jun · PMID 42028750 · Full text
Epigenetic modifications, especially DNA methylation, play an increasingly important role in oral cancer. However, their specific contributions to the progression of oral squamous cell carcinoma (OSCC) remain unclear. Th...
Epigenetic modifications, especially DNA methylation, play an increasingly important role in oral cancer. However, their specific contributions to the progression of oral squamous cell carcinoma (OSCC) remain unclear. The present study used the Shiny Methylation Analysis Resource Tool (SMART) database (https://smart.embl.de/smart/change_mode.cgi) to identify methylation‑driven genes associated with OSCC. Among the identified candidates, integrin subunit α4 (ITGA4) exhibited significantly elevated methylation levels in head and neck cancers. A methylation‑specific PCR assay showed that ITGA4 is highly methylated in OSCC cells compared with normal immortalized human normal oral keratinocyte (iNOK) cells. Additionally, the mRNA expression levels of ITGA4 were significantly lower in OSCC cell lines compared with normal iNOK cells. ITGA4 overexpression markedly inhibited the cell proliferation, migratory ability and capacity of colony formation and induced apoptosis in FaDu and YD‑15 cells. In proteomic analysis, ITGA4 suppressed the expression of Sorting Nexin 5 (SNX5), a protein linked to cancer progression. siRNA‑mediated knockdown of SNX5 importantly inhibited cell proliferation, migration, and colony formation in FaDu and YD‑15 cells. Moreover, in a chick chorioallantoic membrane xenograft model, overexpression of ITGA4 or small interfering SNX5 significantly inhibited OSCC tumor growth and angiogenesis . Collectively, these findings demonstrated that ITGA4 acts as a tumor suppressor in OSCC by downregulating SNX5 and suggested that ITGA4 may serve as a valuable prognostic biomarker and potential therapeutic target for OSCC.
[Expression of Concern] Pifithrin‑μ is efficacious against non‑small cell lung cancer via inhibition of heat shock protein 70.
Zhou Y, Ma J, Zhang J … +3 more , He L, Gong J, Long C
Oncol Rep · 2026 Jun · PMID 42028742 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that Fig. 6A on p. 320, showing the tumor volumes from the in vivo experiments, was lacking the units in the y‑ax...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that Fig. 6A on p. 320, showing the tumor volumes from the in vivo experiments, was lacking the units in the y‑axis, hence undermining the ability to usefully interpret the data in this figure part. In addition, after having performed an independent assessment of the data in this paper in the Editorial Office, it came to light that western blot data in Fig. 2D and flow cytometric plots in Fig. 3A appeared subsequently in different papers in different experimental contexts, one written by different authors in 2018 in the journal , and the other featuring an author named Cong Long in the journal . The authors have been contacted by the Editorial Office to offer an explanation for the concerns that have been identified in their paper, and we are awaiting their response. 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 37: 313‑322, 2017; DOI: 10.3892/or.2016.5286].
Mechanistic study of MUC3A in promoting progression of clear cell renal cell carcinoma via the JAK‑STAT pathway.
Yun Y, Ji X, Hu S … +7 more , Wu T, Liu Y, Li Z, Sun Z, Zhou P, Yang L, Yu W
Oncol Rep · 2026 Jun · PMID 41992986 · Full text
Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cancer and is associated with poor prognosis. The present study identified a membrane‑associated mucin, mucin 3A (MUC3A), a transmembrane glycop...
Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cancer and is associated with poor prognosis. The present study identified a membrane‑associated mucin, mucin 3A (MUC3A), a transmembrane glycoprotein, as a novel oncogenic factor in ccRCC. MUC3A was found to be highly expressed in ccRCC tissues and cell lines, with elevated levels associated with worse patient survival. Functional assays demonstrated that MUC3A knockdown significantly inhibited cell proliferation, migration, invasion, and promoted apoptosis. Mechanistically, MUC3A activated the Janus kinase‑signal transducer and activator of transcription (JAK‑STAT) signaling pathway, and activation of STAT3 reversed the effects of MUC3A knockdown. These findings suggest that MUC3A facilitates ccRCC progression via JAK/STAT signaling and may serve as a potential prognostic biomarker and therapeutic target.
[Expression of Concern] Adenovirus‑mediated truncated Bid overexpression induced by the Cre/LoxP system promotes the cell apoptosis of CD133 ovarian cancer stem cells.
Long Q, Yang R, Lu W … +6 more , Zhu W, Zhou J, Zheng C, Zhou D, Yu L, Wu J
Oncol Rep · 2026 Jun · PMID 41992980 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that a section of the western blot image for β‑actin in Fig. 1B on p. 157 had also been used for the control β‑ac...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that a section of the western blot image for β‑actin in Fig. 1B on p. 157 had also been used for the control β‑actin blots in Fig. 3C on p. 159, despite these data having come from different sources (Fig. 1: CD133 ovarian cancer cells compared with Fig. 3: CD133 ovarian cancer stem cells infected with recombinant adenovirus). In addition, upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that, regarding the TUNEL assay experiments shown in Figs. 2 and 4, the data shown for panel '1' in Fig. 2D was strikingly similar to that shown for the 'Blank' panel in Fig. 4C, even though the experimental conditions in these figures were reported to be different. The authors have been contacted by the Editorial Office to offer an explanation for this apparent duplication of data within these figures, and we are waiting their response. 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 37: 155‑162, 2017; DOI: 10.3892/or.2016.5263].
Perturbation of BRD4 and p300 activity suppresses super enhancer‑driven expression in renal carcinoma.
Zamberi NNM, Abuhamad AY, Yusuf SNHM … +3 more , Rahman NQAA, Mohtar MA, Syafruddin SE
Oncol Rep · 2026 Jun · PMID 41992978 · Full text
Super enhancers (SEs) are involved in regulating cell identity and lineage‑specific gene expression, and drive cancer‑associated gene expression. The transcription factor Kruppel‑like factor 6 (KLF6) promotes the growth...
Super enhancers (SEs) are involved in regulating cell identity and lineage‑specific gene expression, and drive cancer‑associated gene expression. The transcription factor Kruppel‑like factor 6 (KLF6) promotes the growth and progression of clear cell renal cell carcinoma (ccRCC), with its high expression driven by one of the strongest SEs in ccRCC. However, the mechanisms that establish and maintain SE activity, particularly the roles of epigenetic regulators bromodomain-containing 4 (BRD4) and p300, remain poorly understood. This study investigated the roles of BRD4 and p300 in modulating SE activity. The effects of JQ1‑mediated BRD4 and A‑485‑mediated p300 inhibition were assessed using cell viability and colony formation assays. Reverse transcription‑quantitative (q)PCR and ChIP‑qPCR were employed to evaluate the impact of BRD4 and p300 inhibition, as well as CRISPR‑mediated deacetylation of individual constituent enhancers, on expression and SE activity. Chemical inhibition of BRD4 and p300 significantly reduced ccRCC cell viability and colony formation, and decreased KLF6 expression and levels of acetylation at lysine 27 of histone H3 (H3K27ac) at enhancer regions SE_1, SE_2 and SE_3, suggesting decreased chromatin accessibility. On the other hand, deacetylation of SE_1 using dead Cas9 fused to histone deacetylase 3, led to downregulation, which was associated with decreased H3K27ac signals at this region. The present results demonstrated that BRD4 and p300 are key for maintaining SE activity and driving high expression in ccRCC. However, deacetylation of individual enhancer regions using CRISPR was insufficient to fully suppress transcription, emphasizing the robustness of the KLF6 SE and its modular role in sustaining high expression. Overall, the present study deepens the understanding of growth‑promoting KLF6 transcriptional networks in ccRCC and offers insights to support the development of diagnostic or therapeutic strategies.
Incorporating artificial intelligence into morphological diagnosis of acute leukemias: Current landscape, challenges and prospects (Review).
Cheng H, Zheng G, Yang Y … +3 more , Xu C, Tang G, Huang C
Oncol Rep · 2026 Jun · PMID 41992971 · Full text
Acute leukemias (ALs) are a diverse group of hematological malignancies characterized by the abnormal proliferation of immature cells. Microscopic observation of cell morphology based on the French‑American‑British class...
Acute leukemias (ALs) are a diverse group of hematological malignancies characterized by the abnormal proliferation of immature cells. Microscopic observation of cell morphology based on the French‑American‑British classification remains a fundamental diagnostic method for ALs. However, manual screening from bone marrow smear images is often inefficient, laborious and prone to subjective bias, leading to potential misdiagnosis or missed diagnosis. Artificial intelligence (AI), particularly machine learning (ML), has expanded human capabilities in analyzing complex datasets, leading to breakthroughs in multiple fields, including medical research and clinical practice. Increasingly, ML applications are being developed to diagnose hematological diseases by extracting and aggregating morphological characteristics from peripheral blood and bone marrow smears. However, applying ML methods to recognize cell morphology in hematological diseases presents unique challenges compared with other pathology subspecialties. The present review provided an overview of AI and ML applications in ALs diagnosis, focusing on cell segmentation and data mining methods from microscopy images, and highlights their advantages over manual microscopy.
PINK1‑mediated mitophagy enhances breast cancer proliferation through metabolic reprogramming.
Guo ZJ, Yu Q, Sha R … +2 more , Li W, Dai HJ
Oncol Rep · 2026 Jun · PMID 41992955 · Full text
Breast cancer is a predominant cause of cancer‑related mortality among women, particularly aggressive subtypes such as triple‑negative breast cancer (TNBC), which currently lack effective targeted therapies. While PTEN‑i...
Breast cancer is a predominant cause of cancer‑related mortality among women, particularly aggressive subtypes such as triple‑negative breast cancer (TNBC), which currently lack effective targeted therapies. While PTEN‑induced kinase 1 (PINK1) is known for its role in maintaining mitochondrial homeostasis via mitophagy, its specific contributions to breast cancer progression and metabolic regulation remain poorly defined. The present study aimed to investigate the oncogenic potential of PINK1 and its influence on metabolic reprogramming. To achieve this, the PINK1 expression levels in breast cancer tissues and cell lines were assessed. Gain‑ and loss‑of‑function methodologies were employed in luminal (MCF‑7) and TNBC (MDA‑MB‑231) cells. Then, mitophagy was evaluated by measuring LC3‑II levels, Parkin expression and utilizing transmission electron microscopy. Glucose uptake assays and metabolite quantification (including pyruvate and acetyl‑CoA) were conducted. Reverse transcription‑quantitative polymerase chain reaction identified phosphoglycerate kinase 2 (PGK2) as a downstream target of PINK1. Functional assays were then performed to examine the proliferation, migration and invasion of cells with PINK1 overexpression. The results demonstrated that PINK1 overexpression increased mitophagy and induced a glycolytic phenotype, characterized by enhanced glucose uptake and elevated PGK2 levels. Elevated concentrations of pyruvate and acetyl‑CoA indicated increased metabolic flux. Functionally, PINK1 promoted proliferation, migration and invasion in both cell types. Knockdown of PGK2 reversed these effects, underscoring its critical role in PINK1‑mediated metabolic reprogramming. Transcriptomic data obtained from online databases revealed a correlation between high PINK1 expression and immunosuppressive tumor microenvironments, as well as poor prognosis. The PINK1‑PGK2 axis constitutes a critical mechanism linking mitophagy to glycolytic reprogramming in breast cancer, representing a novel therapeutic target, particularly for TNBC. Targeting this axis may yield new strategies for addressing treatment‑resistant, metabolically adaptive breast cancer.
NF‑κB‑driven LUZP1 promotes metastasis and chemoresistance in head and neck squamous cell carcinoma.
Lin CY, Hsieh CY, Lan HC … +5 more , Lin CC, Chen TT, Tseng WC, Tsou YA, Chang WC
Oncol Rep · 2026 Jun · PMID 41952496 · Full text
Head and neck squamous cell carcinoma (HNSCC) remains a highly aggressive malignancy with poor prognosis driven by metastasis and therapeutic resistance. Through comparative proteomic profiling of tumor specimens from pa...
Head and neck squamous cell carcinoma (HNSCC) remains a highly aggressive malignancy with poor prognosis driven by metastasis and therapeutic resistance. Through comparative proteomic profiling of tumor specimens from patients with long‑ and short‑term survival, the present study identified leucine zipper protein 1 (LUZP1) as one of the most upregulated proteins in tumors from short‑term survivors. Functional assays revealed that LUZP1 knockdown impaired migration, invasion, invadopodia formation and epithelial‑mesenchymal transition, while enhancing sensitivity to docetaxel and cisplatin. Analysis of paired primary and metastatic tumors further confirmed elevated LUZP1 expression in metastatic sites. Mechanistically, NF‑κB inhibition markedly reduced LUZP1 expression, whereas stimulation with IL‑1β or TNF‑α induced its upregulation and rescued the migration defect caused by LUZP1 depletion, implicating NF‑κB as a key upstream regulator. Immunohistochemical analysis of clinical samples demonstrated that high LUZP1 expression was associated with shorter overall and progression‑free survival. Collectively, these findings identify LUZP1 as a novel NF‑κB‑regulated effector that promotes metastasis and chemoresistance and highlight its potential as a prognostic biomarker and therapeutic target in HNSCC.
[Expression of Concern] Metformin inhibits growth and sensitizes osteosarcoma cell lines to cisplatin through cell cycle modulation.
Quattrini I, Conti A, Pazzaglia L … +4 more , Novello C, Ferrari S, Picci P, Benassi MS
Oncol Rep · 2026 Jun · PMID 41952492 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Fig. 3 on p. 372, the C/U2OS and 48 h/U2OS, C/143B and 48 h/14...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Fig. 3 on p. 372, the C/U2OS and 48 h/U2OS, C/143B and 48 h/143B, and C/MG63 and 72 h/143B data panels, respectively, were strikingly similar, suggesting that this figure has been assembled incorrectly, and that these data were derived from a smaller number of original sources. The authors have been contacted by the Editorial Office to offer an explanation for the apparent duplication of these data panels within this figure, and we are waiting their response. 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 this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 31: 370‑375, 2014; DOI: 10.3892/or.2013.2862].
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