Oncol. Rep. [JOURNAL]
Sun
200 papers
Induction of immunogenic necroptosis by shikonin in drug‑resistant head and neck squamous cell carcinoma cells.
Kishita S, Umemura N, Miyazaki H … +3 more , Adachi M, Yagi H, Ohkoshi E
Oncol Rep · 2025 Dec · PMID 40999957 · Full text
In recent years, immune checkpoint inhibitors such as nivolumab have been used to treat recurrent or metastatic head and neck cancer. However, some patients do not respond to nivolumab, and the treatment options for thes...
In recent years, immune checkpoint inhibitors such as nivolumab have been used to treat recurrent or metastatic head and neck cancer. However, some patients do not respond to nivolumab, and the treatment options for these patients are limited. Therefore, identifying compounds for developing new therapeutic strategies for intractable cancer is important. The acquired multidrug‑resistant metastatic head and neck squamous cell carcinoma cell line, R HSC‑3, expresses refractory cancer‑specific proteins such as the drug excretion transporter, ATP binding cassette subfamily G member 2, the cancer stem cell markers, CD44, SRY‑box transcription factor 9 and Notch, and the poor prognosis factor, fibroblast growth factor 9, and is a useful model for acquired multidrug resistance. In the present study, compounds that may be more effective than conventional chemotherapeutic drugs in R HSC‑3 cells were searched and the cell death mechanism was investigated. The results showed that naphthoquinones inhibited the viability of R HSC‑3 cells at low concentrations and induced necroptotic cell death. Naphthoquinone‑induced necroptotic cell death in R HSC‑3 cells induced the expression of calreticulin, an immunogenic marker. It was further found that mitochondrial‑derived reactive oxygen species mediated the oxidative stress damage by naphthoquinone‑induced necroptotic cell death in these cells. Moreover, necroptotic cell death by shikonin, a naphthoquinone, may generate immunogenic signals from multidrug‑resistant cancer cells. The present study revealed that naphthoquinones may not only induce necroptosis in refractory head and neck cancer cells but also induce tumor immunity. Therefore, naphthoquinones may represent a new avenue for the development of new therapeutic agents targeting multidrug‑resistant head and neck cancer.
REV1‑targeting inhibitor JH‑RE‑06 induces ferroptosis via NCOA4‑mediated ferritinophagy in colorectal cancer cells.
Cheng J, Yang X, Zhao W … +3 more , Xu J, Hao Y, Xu F
Oncol Rep · 2025 Dec · PMID 40999956 · Full text
Oncogenes accelerate DNA replication, leading to the activation of excessive replication origins. This process triggers replication stress (RS) and genomic instability in cancer cells, positioning RS as a promising thera...
Oncogenes accelerate DNA replication, leading to the activation of excessive replication origins. This process triggers replication stress (RS) and genomic instability in cancer cells, positioning RS as a promising therapeutic target. Translesion synthesis (TLS) functions as a DNA damage repair bypass mechanism, compensating for RS and conferring a proliferation advantage to cancer cells. Despite its therapeutic potential, the application of the TLS polymerase REV1 (REV1 DNA directed polymerase (REV1) inhibitor JH‑RE‑06 in colorectal cancer (CRC) remains unexplored. Bioinformatics analysis of clinical samples from The Cancer Genome Atlas (TCGA) database demonstrated marked REV1 upregulation in colorectal tumors compared with normal tissues, which was associated with a poorer prognosis. JH‑RE‑06 effectively suppressed CRC tumorigenesis both and . Mechanistically, drug rescue experiments and proteomics revealed that cell death triggered by JH‑RE‑06 was associated with elevated oxidative stress and induction of ferroptosis‑associated signaling. Transmission electron microscopy revealed characteristic morphological changes associated with ferroptosis, including a significant reduction in mitochondrial abundance and the presence of autophagic vacuoles containing engulfed mitochondria. Biochemical assays confirmed that JH‑RE‑06 significantly increased intracellular Fe and malondialdehyde (MDA) levels while reducing glutathione levels, indicative of ferroptosis. Western blot analysis revealed decreased levels of antioxidant proteins, including superoxide dismutase 2 (SOD2) and glutamate‑cysteine ligase catalytic subunit (GCLC), as well as ferritin. Furthermore, western blot and FerroOrange assays, combined with Autophagy‑related Gene 7 (ATG7) and Nuclear Receptor Coactivator 4 (NCOA4) knockdown experiments, demonstrated that JH‑RE‑06 activated ferroptosis in CRC via NCOA4‑mediated ferritinophagy. Safety evaluation via hematoxylin and eosin staining of major organs in mice showed no notable pathological damage induced by JH‑RE‑06. Taken together, these findings establish REV1 as a potential diagnostic biomarker and therapeutic target in CRC. REV1 inhibitor JH‑RE‑06 promoted NCOA4‑mediated ferritinophagy and induced programmed cell death, thereby highlighting its potential as a safe and effective therapeutic strategy for CRC.
Hydroxypropyl‑β‑cyclodextrin/thymoquinone inclusion complex inhibits non‑small cell lung cancer progression through NF‑κB‑mediated ferroptosis.
Zheng WW, Ding JX, Liang YX … +1 more , Ye L
Oncol Rep · 2025 Dec · PMID 40970359 · Full text
Thymoquinone (TQ) is a quinone isolated from the black seed and has been extensively investigated in the pharmaceutical field due to its promising therapeutic value. There have been reports on the potential anti‑cancer...
Thymoquinone (TQ) is a quinone isolated from the black seed and has been extensively investigated in the pharmaceutical field due to its promising therapeutic value. There have been reports on the potential anti‑cancer properties of TQ, whereas the clinical application of TQ is greatly restricted by its low water solubility and poor delivery. In the present study, TQ was encapsulated into hydroxypropyl‑β‑cyclodextrin (HP‑β‑CD) using the freeze‑drying method to form a TQ/HP‑β‑CD inclusion complex. Then, the TQ/HP‑β‑CD inclusion complex was characterized by Fourier transform infrared, differential scanning calorimetry, X‑ray diffraction and scanning electron microscopy. HP‑β‑CD as an excipient significantly enhances the water solubility of TQ, and TQ/HP‑β‑CD demonstrated excellent biocompatibility on normal cells both and . Moreover, the complexation with HP‑β‑CD enhanced the anticancer activity of TQ against non‑small cell lung cancer cells and its mechanism of action is related to ferroptosis mediated by NF‑κB. Such an enhanced cytotoxic effect may be attributed to the effective complexation of TQ in HP‑β‑CD, which enhances its water solubility and bioavailability.
Senescence‑associated IL‑33 secretion undermines sorafenib efficacy in hepatocellular carcinoma via immune evasion.
Lin YX, Liu H, Liao WC … +5 more , Wang YC, Zhang BC, Wan SW, Chen CC, Chang CP
Oncol Rep · 2025 Nov · PMID 40970356 · Full text
Hepatocellular carcinoma (HCC) is a highly lethal cancer with increasing incidence rates worldwide. The recommended treatments for advanced‑stage HCC are sorafenib and regorafenib; however, developing resistance to these...
Hepatocellular carcinoma (HCC) is a highly lethal cancer with increasing incidence rates worldwide. The recommended treatments for advanced‑stage HCC are sorafenib and regorafenib; however, developing resistance to these medications significantly limits their effectiveness, and the underlying mechanisms are poorly understood. The present study demonstrated that interleukin‑33 (IL‑33) promotes sorafenib resistance via immune regulation. , western blotting and reverse transcription‑quantitative PCR showed that both sorafenib and regorafenib treatments led to an increase in the upregulation and secretion of IL‑33 through a positive feedback loop involving the IL‑33/transmembrane suppression of tumorigenicity 2 (ST2L) pathway. Senescence‑associated β‑galactosidase staining and western blotting revealed that sorafenib and regorafenib treatments induce cell senescence in HCC cells. Flow cytometric analysis indicated that he secreted IL‑33 enhanced programmed cell death ligand 1 (PD‑L1) expression in HCC cells by activating NF‑κB pathways in response to the treatments. , a HCC‑bearing subcutaneous mouse model revealed that blocking the IL‑33 signaling pathway with anti‑IL‑33 or anti‑ST2L neutralizing antibodies, combined with sorafenib, significantly reduced tumor size, growth rate, and weight. Additionally, there was a notable decrease in tumor PD‑L1 expression and an increase in intra‑tumor CD8 T cells infiltration. Importantly, the enhanced therapeutic efficacy of the anti‑IL‑33 treatment in sorafenib‑treated HCC‑bearing mice was lost in immunocompromised mice. This indicates that the anti‑IL‑33 neutralizing antibody enhances the antitumor activity of sorafenib by modulating the immune response rather than directly affecting HCC cell proliferation. The findings of the present study suggested that IL‑33 plays a role in decreasing the therapeutic effectiveness of sorafenib and regorafenib in HCC cells. The present study highlights the potential of targeting the IL‑33/ST2L axis in combination with targeted therapies as a novel strategy to improve the limited efficacy of sorafenib and regorafenib.
[Expression of Concern] Hypoxia and macrophages promote glioblastoma invasion by the CCL4‑CCR5 axis.
Wang Y, Liu T, Yang N … +3 more , Xu S, Li X, Wang D
Oncol Rep · 2025 Dec · PMID 40970355 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the 'Normoxia / U87' panel in Fig. 1A appeared to overlap with the 'CCR5 siRNA' panel in Fig. 2B; in addition, th...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the 'Normoxia / U87' panel in Fig. 1A appeared to overlap with the 'CCR5 siRNA' panel in Fig. 2B; in addition, the 'Hypoxia / U87‑Mφ' panel in Fig. 1A appeared to overlap with the 'Control siRNA' panel in Fig. 2B. The authors were contacted by the Editorial Office to offer 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 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 36: 3522‑3528, 2016; DOI: 10.3892/or.2016.5171].
Novel tetravalent bispecific antibody, PSMA/TRAIL‑R2 REGULGENT™, induces selective tumor cell apoptosis without hepatotoxicity.
Nakayama M, Takagi-Maeda S, Machino Y … +4 more , Nihira K, Inoue M, Takahashi N, Usami K
Oncol Rep · 2025 Nov · PMID 40970352 · Full text
Tumor necrosis factor‑related apoptosis‑inducing ligand‑receptor 2 (TRAIL‑R2) can induce apoptosis in various tumors through the oligomerization of TRAIL. Several TRAIL‑R2 agonistic monoclonal antibodies have been tested...
Tumor necrosis factor‑related apoptosis‑inducing ligand‑receptor 2 (TRAIL‑R2) can induce apoptosis in various tumors through the oligomerization of TRAIL. Several TRAIL‑R2 agonistic monoclonal antibodies have been tested in clinical trials but have failed owing to a lack of efficacy or severe hepatotoxicity. Although bispecific constructs have been developed to improve TRAIL‑R2 targeting and enhance efficacy against tumors while reducing adverse effects on hepatocytes, the risk of hepatotoxicity still persists. The present study used a TRAIL‑R2 antibody, E11, that does not trigger apoptosis in the absence of crosslinking and constructed a novel tetravalent bispecific IgG4‑based antibody, REGULGENT™, comprised of E11 and a clone that binds to prostate‑specific membrane antigen (PSMA), a specific marker for prostate tumors. PSMA/TRAIL‑R2 REGULGENT™ selectively induced death in PSMA/TRAIL‑R2 double‑positive cells but not in TRAIL‑R2 single‑positive cells and . By contrast, a bivalent bispecific antibody did not result in tumor cell death, indicating that tetravalent bispecific antibodies have an important role in inducing tumor cell apoptosis by binding to TRAIL‑R2 in a bivalent manner. Moreover, the present study demonstrated, for the first time to the best of the authors' knowledge, that PSMA/TRAIL‑R2 REGULGENT™ is not hepatotoxic (primary human hepatocytes) or (chimeric human hepatocyte‑transplanted PXB mouse model). This finding suggests that tetravalent bispecific therapeutics such as REGULGENT™ can be promising therapeutic agents for TRAIL‑R2‑positive tumors by exerting tumor‑specific activity while avoiding toxicity.
[Expression of Concern] Downregulation of miR‑145 contributes to lung adenocarcinoma cell growth to form brain metastases.
Zhao C, Xu Y, Zhang Y … +6 more , Tan W, Xue J, Yang Z, Zhang Y, Lu Y, Hu X
Oncol Rep · 2025 Dec · PMID 40970346 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the cell migration and invasion assay experiments shown in Fig. 4, the 'Mock' data panel in Fig....
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the cell migration and invasion assay experiments shown in Fig. 4, the 'Mock' data panel in Fig. 4A‑a (A549 cell line, migration assay) was apparently identical to the 'Mock' data panel in Fig. 4B‑b (SPC‑A1 cell line, invasion assay), even though the reported experimental conditions were different. The authors were contacted by the Editorial Office to offer an explanation for this apparent data duplication; 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 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 30: 2027‑2034, 2013; DOI: 10.3892/or.2013.2728].
Irradiation‑induced cellular senescence is linked to pro‑survival signaling and checkpoint regulation in a 2D and 3D model for head and neck cancer.
Bugia L, Affolter A, Kern J … +6 more , Sohn E, Jungbauer F, Fleckenstein J, Lammert A, Rotter N, Scherl C
Oncol Rep · 2025 Nov · PMID 40937576 · Full text
Fractionated irradiation causes premature senescence of tumor cells. Interactions between senescence, the immune system and survival signaling are poorly understood to date. As MAP kinases are implicated in immune resist...
Fractionated irradiation causes premature senescence of tumor cells. Interactions between senescence, the immune system and survival signaling are poorly understood to date. As MAP kinases are implicated in immune resistance, the present study addressed the detection of senescence‑associated modulation of postradiogenic programmed death‑ligand 1 (PD‑L1) and MAP kinase ERK1/2 expression in an and model for head and neck squamous cell carcinoma (HNSCC). Established HNSCC cell lines (UM-SCC-11B, UM-SCC-14C and UM-SCC-22B) were employed to study the expression levels of p21, histone H2AX (γH2AX), PD-L1 and phosphorylated (p)ERK1/2 via immunohistochemistry following application of 4x2 Gy. Using senescence‑associated β‑galactosidase (SA‑ß‑Gal) staining, postradiogenic induction of senescence was additionally assessed. Results were validated in a 3D HNSCC model with vital explants. Upon ionizing radiation (IR), senescence‑like subpopulations were observed in all cell lines, showing upregulation of PD‑L1 and pERK1/2 as well as of established senescence markers p21 and γH2AX. SA‑β‑Gal‑positive cells were found in all lines. These results were supported in a 3D tumor model. Fractionated IR can generate a subpopulation of HNSCC cells characterized by senescence‑typical cellular changes and marked expression of PD‑L1 and pERK1/2. Postradiogenic senescence in both 2D and 3D cancer models was possibly related to survival signaling and immune checkpoint regulation, crucial elements in tumor development and progress.
ISG20: The multifaceted 'molecular star' in cancer research (Review).
Zhu X, Jiang S, Zhang L … +6 more , Zou S, Zhang H, Zhang J, Chen L, Li H, Zong Z
Oncol Rep · 2025 Nov · PMID 40937574 · Full text
IFN‑stimulated gene (ISG)20 is a key member of the ISG family, serving a central role in antiviral defense, immune regulation and cell metabolism through its exonuclease activity. ISG20 is markedly dysregulated in variou...
IFN‑stimulated gene (ISG)20 is a key member of the ISG family, serving a central role in antiviral defense, immune regulation and cell metabolism through its exonuclease activity. ISG20 is markedly dysregulated in various malignancies, including clear cell renal cell carcinoma, glioma, breast cancer and hepatocellular carcinoma, and it is associated with tumor proliferation, metastasis, angiogenesis and immune evasion. Its dual regulatory roles, such as promoting tumor progression via the MMP9/CCND1 signaling axis or enhancing antitumor immunity by activating the IFN‑β pathway, highlight its complex involvement in tumor biology. The present review aimed to summarize the discovery, structural characteristics and physiological functions of ISG20, and its multifaceted roles in tumor development. Moreover, the potential of ISG20 as a novel biomarker, immunoadjuvant and therapeutic target is discussed, offering theoretical insight and translational directions for precision oncology.
Ursolic acid: A natural pentacyclic triterpenoid with clinical promise in gynecological and breast cancers (Review).
Chen T, Sun S, Zhou Z … +1 more , Zhang X
Oncol Rep · 2025 Nov · PMID 40937560 · Full text
Gynecological and breast cancers pose significant challenges to women's health worldwide. Despite notable advancements in diagnosis and treatment, they remain leading causes of cancer‑related mortality. Ursolic acid (UA)...
Gynecological and breast cancers pose significant challenges to women's health worldwide. Despite notable advancements in diagnosis and treatment, they remain leading causes of cancer‑related mortality. Ursolic acid (UA), a naturally occurring pentacyclic triterpenoid widely found in plants, has garnered considerable attention due to its diverse pharmacological activities. It has been demonstrated that UA exhibits a range of biological effects, including antitumor, anti‑inflammatory, and antioxidant properties, with particularly promising therapeutic potential in breast and gynecological cancers. UA exerts its anticancer effects by modulating multiple signaling pathways, such as PI3K/AKT, NF‑κB, and Wnt/β‑catenin, thereby effectively inhibiting tumor cell proliferation, inducing apoptosis, reversing chemoresistance, and suppressing cancer stem cell characteristics. When combined with chemotherapeutic agents such as cisplatin and doxorubicin, UA not only enhances antitumor efficacy but also mitigates the adverse effects associated with chemotherapy. The present review summarizes the recent research progress and underlying mechanisms of UA in the treatment of gynecological and breast cancers, aiming to provide valuable insights for researchers and clinicians in the field.
Lactylation modification in lung cancer: A review of current research and future directions (Review).
Lv Q, Xu J, Hu N … +4 more , Zhao Y, Wang X, Wang T, Tian L
Oncol Rep · 2025 Nov · PMID 40910276 · Full text
Lung cancer is a common malignancy that poses risks to human health and quality of life. The primary treatment options currently available include surgery, chemotherapy and radiotherapy. However, the aggressive metastati...
Lung cancer is a common malignancy that poses risks to human health and quality of life. The primary treatment options currently available include surgery, chemotherapy and radiotherapy. However, the aggressive metastatic nature of the disease combined with the development of drug and radiation resistance results in suboptimal survival outcomes. Consequently, there is a need to explore novel therapeutic approaches and develop more effective drugs. Lactylation, an epigenetic modification induced by lactate, alters histone proteins to modify the chromatin structure, as well as non‑histone proteins. This post‑translational modification is associated with the initiation and progression of lung cancer. Lactylation carries out a considerable role in the onset, progression and resistance of the disease by influencing tumor metabolism and the surrounding microenvironment. Targeting lactylation could provide innovative strategies for the targeted therapy of lung cancer.
DBN1‑mediated upregulation of GAB2 facilitates the migration and invasion of T‑cell acute lymphoblastic leukemia cells.
Sun J, Huang X, Zeng X … +8 more , Lei Y, He H, Wei Z, Xiao D, Zhang Q, Li X, Zhou F, Shao L
Oncol Rep · 2025 Nov · PMID 40910271 · Full text
T-cell acute lymphoblastic leukemia (T‑ALL) is an aggressive hematological malignancy. The poor prognosis of T‑ALL is closely associated with extensive leukemic infiltration into critical organs. Therefore, the mechanism...
T-cell acute lymphoblastic leukemia (T‑ALL) is an aggressive hematological malignancy. The poor prognosis of T‑ALL is closely associated with extensive leukemic infiltration into critical organs. Therefore, the mechanism underlying T‑ALL infiltration is worth investigating. Databases and clinical samples were utilized to examine drebrin 1 (DBN1) expression in T‑ALL. DBN1 knockdown cell lines were established by lentivirus transfection, and cell migration and invasion were examined using Transwell and Matrigel‑Transwell assays. The molecular mechanism was investigated by RNA sequencing and further validated at the molecular level. Reverse transcription‑quantitative PCR and western blotting were employed to examine the expression of downstream molecules following DBN1 knockdown, with subsequent rescue experiments. DBN1‑targeting microRNA (miR) predicted using bioinformatics websites was confirmed using dual‑luciferase assays. In T‑ALL cells, miRNA mimics transfection enabled functional validation, and investigations into the underlying molecular mechanisms encompassing rescue experiments. Clinical samples and publicly available databases revealed that DBN1 was upregulated in patients with T‑ALL patients. DBN1 knockdown significantly decreased the migration and invasion of T‑ALL cells . RNA sequencing revealed that downregulation of DBN1 could reduce Grb2‑associated binding protein 2 (GAB2) expression. Western blotting revealed that GAB2 expression, and PI3K/AKT and MAPK/ERK signaling were decreased in DBN1‑knockdown cells. GAB2 overexpression restored the phosphorylation of downstream effectors (AKT and ERK1/2). Bioinformatics and dual‑luciferase reporter experiments identified miR‑218‑5p binding to the 3'-untranslated region of DBN1, which suppressed DBN1 expression. In addition, the experiments demonstrated that miR‑218‑5p acted as an upstream regulator of DBN1, and was involved in cell migration and invasion. Overall, DBN1 was upregulated in T‑ALL, and its depletion inhibited cell migration and invasion through downregulation of GAB2 and consequent inhibition of AKT and ERK signaling cascades. The present data suggested that DBN1 could be a novel biomarker of T‑ALL infiltration, which is a novel perspective in the field of leukemia research.
BUB1B promotes homologous recombination‑mediated DNA damage repair in breast cancer cells through the PI3K/AKT signaling pathway.
Luo X, Wei Y, Lin H … +2 more , Xiao N, Zhao W
Oncol Rep · 2025 Nov · PMID 40910254 · Full text
Radioresistance is a major obstacle to effective radiotherapy in breast cancer. BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) is involved in numerous biological processes associated with cancer; however, its...
Radioresistance is a major obstacle to effective radiotherapy in breast cancer. BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) is involved in numerous biological processes associated with cancer; however, its specific role in mediating radioresistance in breast cancer remains poorly characterized. The present study first evaluated its expression profile and association with patient prognosis through bioinformatics analysis. Subsequently, BUB1B expression in various breast cancer cell lines was validated by reverse transcription‑quantitative PCR. Following short hairpin RNA‑mediated knockdown of BUB1B in MDA‑MB‑231 cells, the impact of BUB1B on the biological functions and radiosensitivity of breast cancer cells was investigated using Cell Counting Kit‑8, colony formation, EdU staining, gap closure, Transwell, immunofluorescence and comet assays, flow cytometric cell cycle analysis, and xenograft tumor experiments. Downstream signaling pathways regulated by BUB1B were identified via RNA sequencing and western blotting. The results revealed that BUB1B expression was elevated in breast cancer tissues and cell lines, and higher BUB1B expression was associated with poorer prognosis in patients with breast cancer. Functional investigations demonstrated that BUB1B may facilitate the proliferation, invasion and migration of breast cancer cells. Furthermore, BUB1B had a significant influence on the radioresistance of breast cancer, and promoted homologous recombination‑mediated DNA damage repair and cell cycle arrest. At the molecular level, BUB1B may exert its effects through regulation of the PI3K/AKT signaling cascade. In conclusion, these findings indicated that BUB1B may be a potential therapeutic target to overcome radioresistance in breast cancer.
[Expression of Concern] miR‑30a inhibits glioma progression and stem cell‑like properties by repression of Wnt5a.
Zhang Y, Wu Z, Li L … +1 more , Xie M
Oncol Rep · 2025 Nov · PMID 40910220 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control GADPH western blots shown in Fig. 5D were strikingly simillar to three lanes in the GAPDH panel shown...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control GADPH western blots shown in Fig. 5D were strikingly simillar to three lanes in the GAPDH panel shown in Fig. 4D, even though the experimental conditions reported in these figure parts were different, suggesting that one of these figures may have been assembled incorrectly. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly 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 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 38: 1156‑1162, 2017; DOI: 10.3892/or.2017.5728].
[Retracted] Expression of α‑fetoprotein in gastric cancer AGS cells contributes to invasion and metastasis by influencing anoikis sensitivity.
Lu S, Ma Y, Sun T … +3 more , Ren R, Zhang X, Ma W
Oncol Rep · 2025 Sep · PMID 40908679 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that several instances of duplicated data existed within several of the figures in this article; specifically: i) two...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that several instances of duplicated data existed within several of the figures in this article; specifically: i) two pairs of data panels in the four‑panel Fig. 2B (so affecting all the panels in this figure part, which showed the results from migration and invasion assay experiments) were overlapping; ii) a pair of data panels for the fluorescence experiments shown in Fig. 4 were also found to be overlapping; and iii) one set of protein bands in the western blots featured in Fig. 5 (for the caspase‑3 data) had also been included in a paper submitted to and published in a few months earlier, with the author Tao Sun held in common between these papers. Owing to the number of cases of data duplication that were 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. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 2984‑2990, 2016; DOI: 10.3892/or.2016.4678].
Serum from patients with oral squamous cell carcinoma remodels the tumor immune escape ecological niche by promoting regulatory T‑cell differentiation and T‑cell exhaustion.
Chen H, Chen J, Cui B … +4 more , Lv D, Han W, Feng Y, Zhang P
Oncol Rep · 2025 Nov · PMID 40878964 · Full text
Oral squamous cell carcinoma (OSCC) ranks as the sixth most prevalent malignancy worldwide, and is characterized by high morbidity and mortality rates. Elucidating the molecular and cellular mechanisms of tumor‑directed...
Oral squamous cell carcinoma (OSCC) ranks as the sixth most prevalent malignancy worldwide, and is characterized by high morbidity and mortality rates. Elucidating the molecular and cellular mechanisms of tumor‑directed immune escape through ecological niche remodeling is crucial for advancing tumor biotherapy. The serum of patients with cancer contains not only tumor biomarkers but also immune regulators secreted by immune cells and/or cancer cells. Notably, the interstitial fluid within the cancer ecological niche is derived from serum. The cross‑talk between serum and cancer cells determines the future of cancer cells, either cell survival or death. The present study revealed that serum from patients with OSCC could remodel the cancer immune escape ecological niche by promoting antigen‑induced regulatory T‑cell (Treg) differentiation and T‑cell exhaustion. When serum from patients with OSCC was added to a phytohemagglutinin‑stimulated peripheral blood mononuclear cell (PBMC) culture system, the Treg subset was significantly increased compared with that in the culture system treated with fetal bovine serum. Moreover, when the serum of patients with OSCC was added to a PBMC culture system stimulated with tumor antigens, the activation of the CD3 subset was significantly inhibited, and high levels of IL‑4, IL‑10 and TGF‑β were detected in the supernatant; moreover, CD3 T cells expressed high levels of T‑cell immunoglobulin and mucin‑domain containing‑3 and programmed death ligand 1, which is known to induce T‑cell apoptosis and exhaustion. Finally, the antitumor effect of T cells were significantly decreased. These results indicated that the serum of patients with cancer can promote the inhibition and exhaustion of antitumor T cells, thereby remodeling the tumor immune escape ecological niche.
[Expression of Concern] Src homology phosphotyrosyl phosphatase 2 mediates cisplatin‑related drug resistance by inhibiting apoptosis and activating the Ras/PI3K/Akt1/survivin pathway in lung cancer cells.
Tang C, Hahm E, Bae S … +2 more , Kang JS, Lee WJ
Oncol Rep · 2025 Nov · PMID 40878959 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the immunohistochemical images shown in Figs. 1E and 5E appeared to show an overlapping section, even though Figs...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the immunohistochemical images shown in Figs. 1E and 5E appeared to show an overlapping section, even though Figs. 1 and 5 were intended to show the results of SHP2 and Ras expression experiments, respectively. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly 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 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 39: 611‑618, 2018; DOI: 10.3892/or.2017.6109].
T cell exhaustion‑related gene CD79B predicts prognosis, inhibits malignant progression and promotes tumor‑associated macrophage M1‑like polarization in lung adenocarcinoma.
Wu X, Qu C, Ouyang Y … +2 more , Yang L, Jiang W
Oncol Rep · 2025 Nov · PMID 40878933 · Full text
Lung adenocarcinoma (LUAD) is one of the most common malignancies in the lung. T cell exhaustion (TEX) is an important immune escape mechanism that may be targeted to improve tumor immunotherapy. The present study invest...
Lung adenocarcinoma (LUAD) is one of the most common malignancies in the lung. T cell exhaustion (TEX) is an important immune escape mechanism that may be targeted to improve tumor immunotherapy. The present study investigated TEX‑related genes in the tumor microenvironment to predict the prognosis of patients with LUAD. Data from 516 patients with LUAD were collected from The Cancer Genome Atlas database and classified them into TEX‑C1 and TEX‑C2 by unsupervised clustering based on the TEX‑related genes. Compared with TEX‑C1, TEX‑C2 cluster had worse prognosis, with shorter overall and progression‑free survival. Functional analysis revealed that upregulated genes in the TEX‑C2 cluster were significantly enriched in tumor immune‑ and metabolism‑related pathways. TEX‑C2 cluster had a poor immune checkpoint blockade (ICB) response and a shorter survival after ICB treatment by Tumor Immune Dysfunction and Exclusion algorithm. A prognostic TEX‑related gene signature was constructed for patients with LUAD by Least Absolute Shrinkage and Selection Operator regression analysis. B cell antigen receptor complex‑associated protein β chain (CD79B) was considered an independent prognostic indicator; in the clinical correlation analysis, the effect of CD79B on prognosis was associated with advanced lung cancer, advanced age, female sex and patients with history of smoking. The overexpression of CD79B was associated with more infiltration of CD8 T cells, M1 macrophages (the classically activated type 1, pro‑inflammatory type), and less infiltration of M0 (undifferentiated) and M2 macrophages (the alternatively activated type 2, anti‑inflammatory type) by CIBERSORT algorithm, which was also significantly correlated with gene markers of innate and adaptive immune cells, and higher levels of immune checkpoint genes. Upregulation of CD79B could inhibit the proliferation, migration and invasion capabilities and promote the apoptosis of LUAD cells, and induce M1‑like tumor‑associated macrophage (TAM) polarization. In conclusion, patients with LUAD in the TEX‑C2 cluster had worse prognosis and adverse immune microenvironment. CD79B may be a potential prognostic indicator, which could inhibit malignant progression of LUAD cells and induce M1‑like TAM polarization.
[Corrigendum] Overexpression of SET oncoprotein is associated with tumor progression and poor prognosis in human gastric cancer.
Yuan X, Zhang T, Zheng X … +9 more , Zhang Y, Feng T, Liu P, Sun Z, Qin S, Liu X, Zhang L, Song J, Liu Y
Oncol Rep · 2025 Nov · PMID 40849826 · Full text
Subsequently to the publication of the above paper, the authors contacted the Editor to explain that, concerning the cell invasion assay experiments shown in Fig. 4, and due to an error made in filing the data, the image...
Subsequently to the publication of the above paper, the authors contacted the Editor to explain that, concerning the cell invasion assay experiments shown in Fig. 4, and due to an error made in filing the data, the image featured for the OA group / MGC803 cellular experiment in Fig. 4C had been inadvertently duplicated from the invasion image showing the shSET group / SGC7901 cellullar experiment in Fig. 1A. Additionally, a partial overlap was noted between the migration image of the MGC803 cells for the NC siRNA group in Fig. 4D (scratch‑wound assay experiments) and the corresponding image in Fig. 3B. Although both images represent the same cell line with the NC siRNA group, the authors wished to provide a revised version of this data panel in Fig. 4D (in addition to the correction needed for Fig. 4C) for the sake of clarity. The corrected version of Fig. 4 is shown on the next page. Note that the revisions made to this figure do not affect the overall conclusions reported in the paper, and all the authors agree with the publication of this corrigendum. The authors are grateful to the Editor of for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 38: 1733‑1741, 2017; DOI: 10.3892/or.2017.5788].
Role of autophagy‑modulating long non‑coding RNAs in tumor radioresistance (Review).
Li H, He Z
Oncol Rep · 2025 Nov · PMID 40849822 · Full text
Radiotherapy improves survival rates in patients with cancer; however, the development of radioresistance hinders its effectiveness, resulting in unfavorable outcomes. A key factor in cancer progression is the dysregulat...
Radiotherapy improves survival rates in patients with cancer; however, the development of radioresistance hinders its effectiveness, resulting in unfavorable outcomes. A key factor in cancer progression is the dysregulation of autophagy, a lysosomal degradation process governed by various evolutionarily conserved autophagy‑related genes (ATGs). Long non‑coding RNAs (lncRNAs) serve a crucial role in the regulation of autophagy. lncRNAs modulate ATGs and their signaling pathways, contributing to the emergence of radioresistance. The present review offers a comprehensive examination of the critical roles of autophagy and lncRNAs in mediating radioresistance. By enhancing the understanding of these mechanisms, novel therapeutic strategies aimed at increasing tumor radiosensitivity through the modulation of autophagy may be revealed.
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