Oncol. Rep. [JOURNAL]
Sun
200 papers
GPR176 enhances the epithelial‑mesenchymal transition in gastric cancer cells by activating the PI3K/AKT/mTOR signaling pathway.
Mu G, Li K, Hu C … +4 more , Cai J, Ruan H, Zhu G, Liu D
Oncol Rep · 2026 Mar · PMID 41574720 · Full text
Gastric cancer is a malignancy with a high incidence and poor prognosis. The identification of novel molecular markers and elucidation of their underlying mechanisms may provide new avenues for improving therapeutic stra...
Gastric cancer is a malignancy with a high incidence and poor prognosis. The identification of novel molecular markers and elucidation of their underlying mechanisms may provide new avenues for improving therapeutic strategies. The present study analyzed the association between GPR176 expression and clinicopathological features using The Cancer Genome Atlas‑Stomach Adenocarcinoma and GSE66254 datasets, and further validated the findings in patients from The First Affiliated Hospital of Guangxi Medical University (Nanning, China). The migratory and invasive abilities of gastric cancer cells were assessed using Transwell and wound‑healing assays. Western blotting was carried out to evaluate the effects of GPR176 on the PI3K/AKT/mTOR signaling pathway. tumorigenesis assays in nude mice were carried out to confirm the role of GPR176 in tumor progression. Analysis revealed that GPR176 expression was significantly elevated in gastric cancer tissues and associated with unfavorable patient outcomes. Silencing GPR176 markedly suppressed the migration and invasion of gastric cancer cells, accompanied by inhibition of the PI3K/AKT/mTOR and EMT signaling pathways. These inhibitory effects were prevented by the overexpression of PIP5K1A. In line with the results, experiments with nude mice demonstrated that GPR176 knockdown impeded tumor growth, whereas its overexpression enhanced tumorigenicity. Furthermore, GPR176 suppression significantly attenuated EMT and PI3K/AKT/mTOR signaling , while GPR176 overexpression led to activation of these pathways. In summary, the present study identifies GPR176 as a novel prognostic biomarker in gastric cancer. Mechanistically, GPR176 promotes EMT and tumor progression, at least in part, through activation of the PI3K/AKT/mTOR signaling pathway.
Recapitulating lung cancer metastasis : Advances in organoid models and challenges in clinical translation (Review).
Jiang J, Dong G, Zhang Z … +8 more , Lei X, Huang F, Li S, Ma J, Bai J, Ge Q, Wei H, Zhao Z
Oncol Rep · 2026 Mar · PMID 41574717 · Full text
Lung cancer remains a significant global health challenge, with metastatic progression being the leading driver of mortality. Organoid technology provides a tractable, physiologically relevant platform to model key aspec...
Lung cancer remains a significant global health challenge, with metastatic progression being the leading driver of mortality. Organoid technology provides a tractable, physiologically relevant platform to model key aspects of lung cancer metastasis . The present review summarized methodologies for constructing and interrogating these models, covering tissue sources, culture modalities, gene editing and transplantation; applications in studying metastatic mechanisms, drug screening and capturing intra‑ and intertumoral heterogeneity are also highlighted. Persistent challenges include standardizing derivation and culture conditions, improving preservation of tumor‑microenvironmental interactions, expanding immune‑competent and vascularized models, and addressing scalability, cost, and regulatory and ethical considerations for clinical translation. Future directions include integrating multi‑omics approaches and spatial profiling, leveraging artificial intelligence for image and response analytics, advancing immune‑organoid models and establishing shared standards, reference materials and reporting guidelines to enhance reproducibility and clinical impact.
HMBOX1 inhibits hepatocellular carcinoma progression via PTPN1 mediated AKT1 phosphorylation.
Zhang C, Jiang Y, Liu J … +4 more , Zhang W, Qi J, Wen Q, Zhao H
Oncol Rep · 2026 Mar · PMID 41574716 · Full text
Hepatocellular carcinoma (HCC) represents the most common form of primary liver cancer and is characterized by a significant rate of recurrence. However, there is still a lack of effective therapeutic methods. Accumulati...
Hepatocellular carcinoma (HCC) represents the most common form of primary liver cancer and is characterized by a significant rate of recurrence. However, there is still a lack of effective therapeutic methods. Accumulating evidence has highlighted the importance of homeobox containing 1 (HMBOX1) in tumorigenesis. However, the relationship between HMBOX1 expression and HCC remains unclear. In the present study, through the analysis of public databases and staining analysis of tissue microarrays, it was found that compared with normal tissues, HMBOX1 was significantly downregulated in tumor tissues. Furthermore, through analyses such as Cell Counting Kit‑8 assay, wound healing assay and colony formation, it was found that overexpression of HMBOX1 could inhibit cell proliferation and migration, while silencing of HMBOX1 promoted tumor biological characteristics in HCC cell lines. The molecular biological mechanism was explored by using proteomics combined with bioinformatics analysis and western blotting. Mechanistically, AKT1 was identified as a downstream effector of HMBOX1, and protein tyrosine phosphatase non‑receptor type 1 (PTPN1) signaling might mediate the regulation of AKT1 by HMBOX1. tumor‑bearing experiments also verified the function of the HMBOX1/PTPN1/AKT1 pathway in HCC development. Taken together, the present findings revealed a new HMBOX1/PTPN1/AKT1 axis that inhibits tumor progression and provides new candidate therapy targets for HCC.
<p>CDK1 depletion suppresses glioma malignancy through cell cycle pathway regulation: Mechanistic insights from functional and molecular profiling</p>.
Wang Y, Zhou H, Han X … +6 more , Zhang D, Hou L, Li H, Fan T, Li S, Xue X
Oncol Rep · 2026 Mar · PMID 41543195 · Full text
<p>Glioblastoma remains a lethal malignancy with limited therapeutic advancements. Emerging evidence implicates cell cycle dysregulation in glioma pathogenesis, yet the mechanistic role of cyclin‑dependent kinase 1 (CDK1...
<p>Glioblastoma remains a lethal malignancy with limited therapeutic advancements. Emerging evidence implicates cell cycle dysregulation in glioma pathogenesis, yet the mechanistic role of cyclin‑dependent kinase 1 (CDK1) remains underexplored. The present study systematically evaluated the clinical relevance and functional impact of CDK1 in glioma progression through multi‑modal experimental approaches. CDK1 expression was analyzed using public datasets and then verified by western blotting using patient tissue samples (n=37) from the Second Hospital of Hebei Medical University (Shijiazhuang, China). Survival analysis was performed using Chinese Glioma Genome Atlas and The Cancer Genome Atlas datasets, alongside multivariate Cox regression to evaluate prognostic independence. Functional assays, including small interfering RNA‑mediated CDK1 knockdown, were conducted in glioma cell lines to assess proliferation (Cell Counting Kit‑8 and EdU), migration/invasion (Transwell), apoptosis (acridine orange/ethidium bromide staining and flow cytometry) and radiosensitivity (γ‑H2AX foci quantification post‑irradiation). The expression levels of downstream cell cycle regulators were quantified via quantitative PCR. The results indicated that CDK1 was significantly upregulated in glioma tissues compared with normal controls, with expression levels escalating with tumor grade. High CDK1 expression correlated with a reduced overall survival and served as an independent prognostic marker. CDK1 knockdown attenuated glioma cell proliferation, migration and invasion, while enhancing apoptosis and radiosensitivity. Mechanistically, CDK1 knockdown downregulated cell cycle regulators proliferating cell nuclear antigen, minichromosome maintenance complex component 2‑4 (MCM2‑4), MCM6, polo‑like kinase 1, TTK protein kinase and mitotic arrest deficient 2 like 1, implicating mitotic dysregulation as a central pathway. The present study established CDK1 as a master regulator of glioma progression through coordinated control of proliferation, DNA repair and metastatic potential. The robust association between CDK1 expression, tumor grade and survival, coupled with functional validation across complementary assays, positions CDK1 inhibition as a promising therapeutic strategy. The mechanistic elucidation of its cell cycle network provides a novel framework for targeting glioma‑specific therapeutic targets.</p>.
<p>Tumor microenvironment in bone sarcomas: Implications for immunotherapy and emerging therapeutic vulnerabilities (Review)</p>.
Li W, Lv L, Jin Y … +1 more , Yuan X
Oncol Rep · 2026 Mar · PMID 41543186 · Full text
<p>Bone sarcomas remain lethal despite multimodal therapy, primarily because the mineralized, immunosuppressive tumor microenvironment (TME) promotes chemo‑ and immune‑resistance. Integrating single‑cell and spatial omic...
<p>Bone sarcomas remain lethal despite multimodal therapy, primarily because the mineralized, immunosuppressive tumor microenvironment (TME) promotes chemo‑ and immune‑resistance. Integrating single‑cell and spatial omics across osteosarcoma, Ewing sarcoma and chondrosarcoma delineates subtype‑specific TME archetypes dominated by M2 macrophages, exhausted T cells and a stiff extracellular matrix. Mechanistic dissection reveals tractable vulnerabilities, myeloid reprogramming, extracellular matrix modulation and metabolic and epigenetic checkpoints, that can be targeted with bone‑selective delivery systems and biomarker‑driven combination trials to convert therapeutic failure into durable remission. Therefore, the aim of the present review is to synthesize the latest single‑cell, spatial and functional data to map bone‑sarcoma TME heterogeneity, dissect resistance mechanisms and propose integrated, biomarker‑guided therapeutic strategies that can be translated into treatments.</p>.
[Corrigendum] Triptolide inhibits JAK2/STAT3 signaling and induces lethal autophagy through ROS generation in cisplatin‑resistant SKOV3/DDP ovarian cancer cells.
Zhong Y, Le F, Cheng J … +6 more , Luo C, Zhang X, Wu X, Xu F, Zuo Q, Tan B
Oncol Rep · 2026 Mar · PMID 41543179 · Full text
<p>Following the publication of the above article, the authors contacted the Editorial Office to explain that they had made inadvertent errors in compiling a couple of the figures in the above paper; first, regarding the...
<p>Following the publication of the above article, the authors contacted the Editorial Office to explain that they had made inadvertent errors in compiling a couple of the figures in the above paper; first, regarding the immunohistochemical images shown in Fig. 2D on p. 5, the data panel shown correctly for the 'LC3/TPL+DDP' experiment contained an overlapping section with the 'LC3/TPL' data panel in the same figure part (the latter of which had been incorporated into this figure incorrectly). Secondly, the β‑actin bands correctly shown in Fig. 3D on p. 6 had incorrectly been included to represent the JAK2 western blot data in Fig. 4F on p. 7. However, the authors were able to re‑examine their original data, and realized how these errors had occurred. The revised and corrected versions of Figs. 2 and 4, now showing the correct data for the 'LC3/TPL' experiment in Fig. 2D and the JAK2 western blot data in Fig. 4F, are shown on the next two pages. Note that the errors made with the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors apologize to the Editor of and to the readership for any inconvenience caused. [Oncology Reports 45: 69, 2021; DOI: 10.3892/or.2021.8020]</p>.
<p>Immunotherapy after EGFR‑TKI treatment in advanced non‑small cell lung cancer: Current status and future perspectives (Review)</p>.
Ma H, Li L, Jiao C … +6 more , Cheng Y, He J, Jiang C, Tong Q, Yi D, Zhang Y
Oncol Rep · 2026 Mar · PMID 41543165 · Full text
<p>The tumor microenvironment (TME) of epidermal growth factor receptor (EGFR)‑mutant non‑small cell lung cancer (NSCLC) exhibits notable immunosuppressive properties. EGFR tyrosine kinase inhibitors (EGFR‑TKIs) induce d...
<p>The tumor microenvironment (TME) of epidermal growth factor receptor (EGFR)‑mutant non‑small cell lung cancer (NSCLC) exhibits notable immunosuppressive properties. EGFR tyrosine kinase inhibitors (EGFR‑TKIs) induce dynamic remodeling of the TME. By boosting the infiltration of immune cells such as T cells and dendritic cells and decreasing immunosuppressive elements such as tumor‑associated macrophages and regulatory T cells, short‑term TKI treatment can effectively enhance antitumor immunity. However, the TME changes to an immunosuppressive state marked by PD‑L1 upregulation and immune escape with continued therapy and the emergence of resistance. This creates a transient immunotherapy window period during EGFR‑TKI treatment, when immune checkpoint inhibitors may achieve optimal efficacy. It is essential to identify and take advantage of this window in order to enhance treatment results. The present review highlights the importance of understanding TME dynamics in EGFR‑mutant NSCLC to optimize combination strategies and guide future therapeutic development.</p>.
[Retracted] Downregulated microRNA‑200a promotes EMT and tumor growth through the Wnt/β‑catenin pathway by targeting the E‑cadherin repressors ZEB1/ZEB2 in gastric adenocarcinoma.
Cong N, Du P, Zhang A … +7 more , Shen F, Su J, Pu P, Wang T, Zjang J, Kang C, Zhang Q
Oncol Rep · 2026 Mar · PMID 41543153 · Full text
<p>Subsequently to the publication of the above paper, a concerned reader has drawn to the Editor's attention that, for the immunohistochemical data shown in Fig. 2E, the same data panel had apparently been included for...
<p>Subsequently to the publication of the above paper, a concerned reader has drawn to the Editor's attention that, for the immunohistochemical data shown in Fig. 2E, the same data panel had apparently been included for the 'ZEB1/Con' and 'SEB2/Min' experiments. In addition, for the Snail2 experiments shown in Fig. 3A, the Snail Con(trol) and Snail Mimi panels looked strikingly similar, even though the intensity of the antibody (red) channel appeared to have been decreased in the Mimi panel. Finally, for the immunohistochemical images shown in Fig. 3C, the E‑cadherin Con(trol) and Scr panels appeared to show a region of overlap, suggesting that these data were derived from the same original source, where the results of differently performed experiments were intended to have been portrayed. Given that it has come to light that this trio of figures had apparently been assembled incorrectly, which might have had an adverse effect on the interpretation of the results and conclusions in the article, 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. 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 29: 1579‑1587, 2013; DOI: 10.3892/or.2013.2267]</p>.
Role of tumor‑infiltrating lymphocytes and miR‑155 in breast cancer: Insights into carcinogenesis and their potential as prognostic biomarkers (Review).
Alvares-Vilela MM, Schlemmer F, Ferrari SSAR … +2 more , Xavier ME, Titze-De-Almeida R
Oncol Rep · 2026 Mar · PMID 41543151 · Full text
<p>Breast cancer is the most common cancer in the female population worldwide. The present review examines the biology of breast cancer, with a focus on the interplay between tumor‑infiltrating lymphocytes (TILs) and mic...
<p>Breast cancer is the most common cancer in the female population worldwide. The present review examines the biology of breast cancer, with a focus on the interplay between tumor‑infiltrating lymphocytes (TILs) and microRNAs (miRNAs or miRs). TILs, which reflect the immune system activity in combating tumors, are associated with more favorable prognoses and positive response to therapies. Elevated levels of TILs characterize lymphocyte‑predominant breast cancers (LPBCs), which are associated with higher therapeutic response rates in triple‑negative breast cancer, a type of LPBC. Defining the threshold for LPBCs presents a challenge: TIL levels ≥50% are associated with short‑term pathological complete response as well as long‑term overall and disease‑free survival; however, this percentage is not often achieved in clinical practice. Conversely, a lower threshold of 30% lymphocyte infiltration can predict favorable prognosis for anticancer therapy and allows for the identification of a broader range of patients. The tumor inflammatory landscape is regulated by miRNAs, particularly miR‑155. Elevated levels of miR‑155 are associated with the presence of TILs and a favorable inflammatory profile, leading to a tumor‑inflamed microenvironment. Moreover, miR‑155 is associated with various antitumoral immune cells, including CD8 T cells and M1 macrophages, but negatively associated with pro‑tumoral regulatory T cells and M2 macrophages. Overexpression of miR‑155 results in an increase in the levels of the C‑X‑C chemokine ligands, constituted by two conserved cysteines separated by a different amino acid which bind to the same chemokine receptor CXC chemokine receptor 3. These results in activation of T cells a process that involves the inhibition of suppressor of cytokine signaling 1 and an elevated ratio of phosphorylated STAT1/STAT3. Additionally, miR‑155 affects key signaling pathways, including the PI3K/AKT and IL‑6/STAT3 pathways, and increases sensitivity to immune checkpoint blockade therapy. In clinical samples from patients with BC, serum levels of miR‑155 align with both tumor miR‑155 levels and the immune status of the tumor. The present review emphasizes the importance of understanding the dynamics between TILs and miRNAs to identify new prognostic and predictive biomarkers, proposing a more integrated and personalized approach in the management of BC.</p>.
Advances in targeting KRAS mutations: A promising approach for the treatment of non‑small cell lung cancer (Review).
Sharma U, Song J, Kandu H … +2 more , Zhu Y, Dai Z
Oncol Rep · 2026 Mar · PMID 41508946 · Full text
Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are among the most frequent oncogenic drivers in cancer, particularly in non‑small cell lung cancer (NSCLC). KRAS was previously considered an 'undruggable' tar...
Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are among the most frequent oncogenic drivers in cancer, particularly in non‑small cell lung cancer (NSCLC). KRAS was previously considered an 'undruggable' target due to the protein's smooth molecular surface and the absence of obvious drug binding sites. However, the development of selective KRAS G12C inhibitors, such as sotorasib and adagrasib, together with progress in immunotherapy, have demonstrated potential clinical activity. Further understanding of the complex signaling networks driven by KRAS has revealed new opportunities to target this pathway directly or through rational combination strategies. The present review explored KRAS‑targeted therapies and immunotherapies, including limitations, resistance mechanisms and the efficacy of combination regimens. Although there has been notable progress, concerns regarding optimal therapy combinations, resistance management and early treatment strategies remain. The present review demonstrated the need for continued research to address these challenges and improve outcomes for patients with KRAS‑mutated NSCLC.
[Corrigendum] CXCR6 predicts poor prognosis in gastric cancer and promotes tumor metastasis through epithelial-mesenchymal transition.
Jin JJ, Dai FX, Long ZW … +7 more , Cai H, Liu XW, Zhou Y, Hong Q, Dong QZ, Wang YN, Huang H
Oncol Rep · 2026 Mar · PMID 41508934 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the cell migration and invasion assay experiments shown in Figs. 3 and 4, the 'WT/Migration' and 'C...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the cell migration and invasion assay experiments shown in Figs. 3 and 4, the 'WT/Migration' and 'Ctrl/Invasion' panels in Fig. 3C contained an overlapping section of data, and the 'WT/Invasion' and 'CXCR-sh/Migration' panels in Fig. 4A were duplicates, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. Upon examining the data independently in the Editorial Office, it also came to light that the E-cadherin western blot in Fig. 3E was strikingly similar to the N-cadherin western blot shown in Fig. 4A. However, the authors were able to consult their original data, and recognized that these data had inadvertently been included in these two figures incorrectly. Revised and corrected versions of Figs. 3 and 4, now showing the correct data for the E-cadherin blot in Fig. 3E and the 'Ctrl/Invasion' experiment in Fig. 3C, and the 'CXCR-sh/Migration' panel in Fig. 4A, are shown on the next page. The authors regret the errors that were made during the compilation of the original figures, and are grateful to the editor of for allowing them the opportunity to publish this Corrigendum. Note that these errors did not have a significant impact on the conclusions reached in this study. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 37: 3279-3286, 2017; DOI: 10.3892/or.2017.5598].
Exploring the role of disulfidptosis‑related signatures in immune microenvironment, prognosis and therapeutic strategies of cholangiocarcinoma.
Chen Y, Wu J, Zhu D … +4 more , Jiang L, Wang J, Zhang D, He W
Oncol Rep · 2026 Feb · PMID 41480714 · Full text
Cholangiocarcinoma (CCA) is an aggressive malignancy with poor prognosis and a limited number of treatments is available. Disulfidptosis, a newly identified form of cell death triggered by disulfide bond accumulation dur...
Cholangiocarcinoma (CCA) is an aggressive malignancy with poor prognosis and a limited number of treatments is available. Disulfidptosis, a newly identified form of cell death triggered by disulfide bond accumulation during glucose deprivation, may influence cancer progression but its role in CCA is poorly understood. The present study investigated disulfidptosis‑related genes (DRGs) and their impact on CCA prognosis and immune modulation. Differential expression analysis of 100 DRGs using RNA sequencing data from The Cancer Genome Atlas and EMBL‑EBI identified 74 dysregulated genes in CCA. Unsupervised clustering stratified patients with CCA into two distinct subtypes (Subs): i) SubA; and ii) SubB. A four‑gene prognostic signature was developed using least absolute shrinkage and selection operator regression and validated via Kaplan‑Meier survival analysis and receiver operating characteristic curves. Immune infiltration and tumor microenvironment were evaluated using Cell‑type Identification by Estimating Relative Subsets of RNA Transcripts, Estimation of Stromal and Immune cells in Malignant Tumor tissues using Expression data and single‑sample Gene Set Enrichment Analysis. Functional assays, including small interfering RNA knockdown of and in CCA cell lines were used to investigate proliferation, migration, invasion and F‑actin staining. Results showed SubB, associated with higher disulfidptosis activity, had worse prognosis, increased immune cell infiltration and elevated immune checkpoint gene expression. The four‑gene signature effectively stratified patients into risk groups. Knockdown of and significantly suppressed CCA cell proliferation, migration and invasion while it promoted disulfidptosis under glucose deprivation. The present study established an association between DRGs and CCA prognosis/immune dynamics, provided a robust four‑gene prognostic signature, and identified and as potential therapeutic targets, positioning disulfidptosis as a promising focus for precision medicine in CCA.
[Corrigendum] Isolinderalactone enhances the inhibition of SOCS3 on STAT3 activity by decreasing miR‑30c in breast cancer.
Yen MC, Shih YC, Hsu YL … +6 more , Lin ES, Lin YS, Tsai EM, Ho YW, Hou MF, Kuo PL
Oncol Rep · 2026 Feb · PMID 41456436 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, regarding the western blot data shown in Fig. 4 on p. 1361, the lower of the control GAPDH blots in Fig. 4A an...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, regarding the western blot data shown in Fig. 4 on p. 1361, the lower of the control GAPDH blots in Fig. 4A and B appeared to be essentially the same (albeit the blots were more exposed in Fig. 4B), even though the experimental conditions in the two figure parts were reported to be different. The authors were able to re‑examine their original data files, and realized that the western blot image for Fig. 4B had inadverently been selected incorrectly. The revised version of Fig. 4, now containing the correct data for the lower GAPDH blots in Fig. 4B, is shown below. Note that the correction made to this figure does not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 35: 1356‑1364, 2016; DOI: 10.3892/or.2015.4503].
[Retracted] β‑elemene decreases cell invasion by upregulating E‑cadherin expression in MCF‑7 human breast cancer cells.
Zhang X, Zhang Y, Li Y
Oncol Rep · 2026 Feb · PMID 41416443 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the '50 g/ml ELE' and '100 g/ml ELE' data panels shown in Fig. 6A were apparently identical, suggesting that...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the '50 g/ml ELE' and '100 g/ml ELE' data panels shown in Fig. 6A were apparently identical, suggesting that the same data panel had been inserted twice into this figure to show the results from differently performed experiments. Moreover, data featured in the microscopic images in Fig. 2 overlapped with images in a paper that had been published by the same research group in 2013 in the journal , where the treatment represented was different (treatment with TGF‑β1). Upon performing an independent analysis of the data in the Editorial Office, it also came to light that one of the same microscopic images was strikingly similar to a data panel featured in Fig. 4 in another article written by different authors at different research institutes that was published subsequently in the journal , albeit the image was featured in colour in that publication, whereas it had appeared in greyscale in the above paper. Given the nature of the contentious issues repported above, 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. 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 30: 745‑750, 2013; DOI: 10.3892/or.2013.2519].
Research progress on the regulation of ferroptosis in NPC (Review).
Bai S, Guo Y, Qiang J … +2 more , Dai Q, Yang Y
Oncol Rep · 2026 Feb · PMID 41416424 · Full text
Ferroptosis is a novel form of iron‑dependent programmed apoptosis, characterized by dysregulated iron metabolism, impaired antioxidant defense systems and accumulation of lipid peroxidation products. Nasopharyngeal carc...
Ferroptosis is a novel form of iron‑dependent programmed apoptosis, characterized by dysregulated iron metabolism, impaired antioxidant defense systems and accumulation of lipid peroxidation products. Nasopharyngeal carcinoma (NPC) cells exhibit marked susceptibility to ferroptosis, and its induction can effectively suppress tumor progression, offering a potential therapeutic strategy for NPC. At the molecular level, ferroptosis‑related genes [such as Solute Carrier Family 7 Member 11 (SLC7A11), Glutamate‑Cysteine Ligase Modifier Subunit (GCLM) and Glutamate‑Cysteine Ligase Catalytic Subunit (GCLC)] are notably upregulated in NPC tissues compared with normal tissues, and their overexpression associates with poor patient prognosis, suggesting their utility as diagnostic or prognostic biomarkers. The present review systematically summarizes the molecular mechanisms of ferroptosis, elucidates its role in NPC pathogenesis and discusses ferroptosis‑targeted therapeutic approaches for NPC.
Hypoxia‑mediated Krebs von den Lungen‑6 expression in breast cancer: Implications for tumor invasion and metastasis.
Ichihara T, Hayashi Y, Sato T … +4 more , Iguchi M, Toi M, Satake H, Murakami I
Oncol Rep · 2026 Feb · PMID 41416421 · Full text
Krebs von den Lungen‑6 (KL‑6), a high‑molecular‑weight glycoprotein, is frequently elevated in patients with cancer; however, its precise role in the clinical progression of breast cancer (BC) remains unclear. Tumor hypo...
Krebs von den Lungen‑6 (KL‑6), a high‑molecular‑weight glycoprotein, is frequently elevated in patients with cancer; however, its precise role in the clinical progression of breast cancer (BC) remains unclear. Tumor hypoxia has been recognized as a critical driver of cancer progression. The present study aimed to investigate the effects of hypoxia on KL‑6 expression and its contribution to the invasive behavior of BC cells. Immunohistochemical analysis of KL‑6 and hypoxia‑inducible factor‑1α (HIF‑1α) was performed in 30 clinical BC tissue samples, and their expression levels were correlated with patient outcomes. BC cell lines (MCF‑7 and MDA‑MB‑231) were used for analyses, including immunofluorescence, western blotting, wound healing assays, and three‑dimensional spheroid cultures under normoxic and hypoxic conditions, as well as chemically induced hypoxia using cobalt chloride (CoCl). The subcellular localization of KL‑6 was further examined through immunoelectron microscopy. In clinical specimens, high KL‑6 expression was significantly associated with increased recurrence or metastasis, as was elevated HIF‑1α expression. Although MCF‑7 cells exhibited higher basal KL‑6 expression, marked upregulation was observed in MDA‑MB‑231 cells under hypoxic spheroid conditions, where KL‑6 co‑localized with HIF‑1α, particularly within invasive cellular protrusions. Functional inhibition of KL‑6 suppressed the migration of MCF‑7 cells. Treatment with CoCl significantly induced KL‑6 and HIF‑1α expression in MCF‑7 cells. Ultrastructural analysis confirmed the localization of KL‑6 on cell membranes and within protrusive structures. Collectively, these findings demonstrated that hypoxia enhances KL‑6 expression in BC cells, partly mediated by HIF‑1α, and that KL‑6 contributes to tumor cell invasion.
[Retracted] Platelet‑derived growth factor BB mediates the glioma‑induced migration of bone marrow‑derived mesenchymal stem cells by promoting the expression of vascular cell adhesion molecule‑1 through the PI3K, P38 MAPK and NF‑κB pathways.
Hu Y, Cheng P, Ma JC … +2 more , Xue YX, Liu YH
Oncol Rep · 2026 Feb · PMID 41384304 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that areas of the cellular images shown in Fig. 3A and B appeared to be identical to data shown in Fig. 1 of an a...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that areas of the cellular images shown in Fig. 3A and B appeared to be identical to data shown in Fig. 1 of an article published in a year earlier (in 2012) by the same research group, although in that case, these data were used to represent different experiments. Moreover, comparing the two publications, for the same data, the bar charts showing the 'number of migrating BMSCs' reported very different average measurements (~38 in the paper, and ~220 in the paper above). Owing to the fact that the abovementioned data had been re‑used in the above paper in an unrelated experimental context, 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. 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 30: 2755‑2764, 2013; DOI: 10.3892/or.2013.2780].
[Retracted] Downregulation of Bmi‑1 is associated with suppressed tumorigenesis and induced apoptosis in CD44 nasopharyngeal carcinoma cancer stem‑like cells.
Xu X, Liu Y, Su J … +8 more , Li D, Hu J, Huang Q, Lu M, Liu X, Ren J, Chen W, Sun L
Oncol Rep · 2026 Feb · PMID 41347836 · Full text
Following the publication of the above article, a concerned reader drew to the Editor's attention that one set of the tumor data comparing between the 'CD44' experiments in Fig. 4A and the 'CON' experiments in Fig. 4B on...
Following the publication of the above article, a concerned reader drew to the Editor's attention that one set of the tumor data comparing between the 'CD44' experiments in Fig. 4A and the 'CON' experiments in Fig. 4B on p. 428 had apparently been duplicated; moreover, several of the images of various of the mice shown in this figure looked more similar in appearance than might have been expected. Furthermore, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that the data panel showing the results of the migratory assay experiment relating to the 'KD' group in Fig. 2B on p. 926 contained an internally duplicated area that would have been difficult to attribute to coincidence. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. Therefore, 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. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 923‑931, 2016; DOI: 10.3892/or.2015.4414].
Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).
Zhu W, Wu Z, Luv C … +7 more , Bao B, Zhao W, Chen G, Yang H, Ai H, Liu F, Li Z
Oncol Rep · 2026 Feb · PMID 41347834 · Full text
Alternative splicing (AS) is one of the principal mechanisms of post‑transcriptional regulation that confers transcriptomic plasticity and proteomic diversity in cancer, thereby enabling tumor adaptation to therapeutic p...
Alternative splicing (AS) is one of the principal mechanisms of post‑transcriptional regulation that confers transcriptomic plasticity and proteomic diversity in cancer, thereby enabling tumor adaptation to therapeutic pressure. However, two obstacles impede the translation of these findings into clinical benefit: The absence of systematic functional annotation of the numerous splice variants associated with drug resistance and the paucity of biomarkers capable of distinguishing from acquired splice‑mediated resistance. In the present review, the current mechanistic understanding of AS‑driven drug resistance was briefly synthesized, and it was evaluated how existing strategies address these challenges. It was also described how knowledge of dysregulated splicing networks, due to mutations in cis‑regulatory elements such as ESS, overexpression of trans‑acting factors such as , as well as mechanisms such as alternative trans‑splicing, in which the spliceosome interacts with splice sites on two distinct RNA molecules and which can be driven by complementary sequences or other trans‑acting factors, could be used to more accurately identify tumors dependent on aberrant splicing for survival. In addition, it was outlined how targeting aberrant splice variants to overcome therapeutic resistance can be achieved, such as through spliceosome inhibition (for example, H3B‑8800) or antisense oligonucleotides directed to a specific exon or splice junction (for example, targeting exon 2 of , which is implicated in cis‑regulated AS isoforms, or alternatively spliced isoforms of , and ). However, therapeutic strategies to target adaptive resistance mechanisms such as AS remain limited, as intratumoral heterogeneity may facilitate the emergence of resistant subpopulations, and as most spliceosome inhibitors are not spliceosome‑specific, they exhibit off‑target effects. Importantly, it was also discussed how pan‑cancer splicing databases and single‑cell isoform expression profiling can be integrated with deep‑learning models, thereby informing the design of therapeutic strategies to overcome splicing‑mediated adaptive drug resistance. Notably, such integration will enable the rational design of isoform‑specific combination regimens to dismantle drug‑resistance circuits. It is anticipated that the present review will assist the scientific community, including both basic and translational researchers, in translating these findings into interventions that mitigate therapeutic failure in recalcitrant cancers.
Prognostic significance of fibroblast senescence and senescence-associated secretory phenotype factor expression in the tumor microenvironment of pancreatic ductal adenocarcinoma.
Kitano Y, Miyashita T, Shimasaki T … +5 more , Makino I, Endo Y, Yamamoto Y, Inaki N, Yagi S
Oncol Rep · 2026 Feb · PMID 41347831 · Full text
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense fibrous stroma, within which a subset of fibroblasts function as cancer‑associated fibroblasts (CAFs) and contribute to tumor progression. Some of these...
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense fibrous stroma, within which a subset of fibroblasts function as cancer‑associated fibroblasts (CAFs) and contribute to tumor progression. Some of these fibroblasts undergo senescence and promote malignancy through the senescence‑associated secretory phenotype (SASP). The present study investigated SASP factor expression in senescent fibroblasts within the PDAC microenvironment and evaluated their impact on tumor progression. The expression levels of the senescence marker p16 and the SASP factor interleukin‑6 (IL‑6) were assessed using fluorescence immunostaining in resected specimens from 90 patients with PDAC who underwent pancreaticoduodenectomy. Senescence was induced in primary human pancreatic fibroblasts via X‑ray irradiation , followed by evaluation of SASP factor expression. These senescent fibroblasts were then co‑cultured with human pancreatic cancer Panc‑1 cells to assess their effects on cancer cell invasion, migration and proliferation. Immunostaining demonstrated the presence of p16‑ and IL‑6‑expressing fibroblasts in the PDAC stroma of patient samples. A positive correlation was observed between p16 and IL‑6 expression levels in fibroblasts. Notably, increased expression levels of IL‑6‑positive fibroblasts were associated with reduced postoperative survival. Multivariate analysis identified high IL‑6 expression and lymph node metastasis as independent prognostic indicators of poor outcome. In co‑culture experiments, senescent fibroblasts enhanced Panc‑1 cell invasion, migration and proliferation. These findings suggested that senescent fibroblasts within the PDAC stroma, with high SASP factor expression, contribute to tumor aggressiveness and are associated with poor prognosis. The present study demonstrated that IL‑6‑expressing senescent fibroblasts are potential prognostic markers and therapeutic targets in PDAC, therefore the targeted elimination of senescent cells may represent a promising therapeutic strategy.
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