Oncol. Rep. [JOURNAL]
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200 papers
Identification of RRM2 as a key regulator of malignant epithelial cells in gastric cancer through single‑cell transcriptomics.
Cai X, He Y, Kang L … +3 more , Zhou D, Wang M, Ma T
Oncol Rep · 2026 Sep · PMID 42396657 · Full text
Gastric cancer (GC) is one of the most prevalent and life‑threatening malignancies of the digestive tract worldwide. Ribonucleotide reductase regulatory subunit M2 (RRM2), a rate‑limiting subunit in deoxyribonucleotide s...
Gastric cancer (GC) is one of the most prevalent and life‑threatening malignancies of the digestive tract worldwide. Ribonucleotide reductase regulatory subunit M2 (RRM2), a rate‑limiting subunit in deoxyribonucleotide synthesis, is overexpressed and is associated with a poor prognosis in various solid tumors. However, its functional role and mechanisms in GC‑specific malignant epithelial cell populations remain unclear. Single‑cell transcriptomic data from GC and adjacent normal tissues were analyzed. Key malignant epithelial cell populations were identified using inferCNV, pseudotime trajectory analysis, and weighted gene co‑expression network analysis. RRM2 was identified as a core gene by integrating data from TCGA‑STAD, GSE66229, and GSE84433 datasets and analyzing its clinical relevance. To evaluate the biological effects of RRM2, functional assays, including colony formation, apoptosis, Transwell migration, and wound healing assays, were performed using AGS and HGC‑27 GC cells with RRM2 knockdown. DNA damage was assessed using the alkaline comet assay and phosphorylated histone H2AX (γH2AX) immunofluorescence, and the expression of DNA damage repair‑related proteins [including γH2AX, phosphorylated tumor protein p53 (p‑p53), RAD51 recombinase (RAD51), poly(ADP‑ribose) polymerase 1 (PARP‑1), and X‑ray repair cross‑complementing protein 1 (XRCC1)] was examined using western blotting. Through analysis of gastric epithelial cell populations, a major malignant epithelial effector population in GC was identified, enriched in cells with active DNA replication and repair. Differentially expressed genes specific to this population were intersected with prognostic genes from GEO GC datasets, resulting in the identification of RRM2 as a key effector gene. Transcriptomic analysis revealed that high RRM2 expression was associated with an active immune microenvironment. Functional assays showed that RRM2 knockdown significantly inhibited GC cell proliferation and migration while promoting apoptosis. In addition, RRM2 knockdown exacerbated DNA damage, upregulated p‑p53, and downregulated RAD51, with no significant effects on PARP‑1 or XRCC1 expression. Collectively, RRM2 was shown to be a crucial regulator of the malignant phenotype of gastric epithelial cells. It promoted GC cell proliferation, invasion, and migration and modulated DNA damage and homologous recombination repair. In addition, RRM2 influenced the tumor immune microenvironment, highlighting its potential as a driver of malignant progression and a promising target for immunotherapy in GC.
Impact of WFDC2 on the biological functions of cervical cancer cells and the regulation of the ERK/NF‑κB signaling pathway.
Zhang Y, Zou H, Deng S … +3 more , Zou L, Xia M, Tao L
Oncol Rep · 2026 Sep · PMID 42396650 · Full text
WAP four‑disulfide core domain 2 (WFDC2) may serve a notable regulatory role in cervical cancer, which is the most prevalent tumor of the female reproductive system. The present study aimed to investigate the function of...
WAP four‑disulfide core domain 2 (WFDC2) may serve a notable regulatory role in cervical cancer, which is the most prevalent tumor of the female reproductive system. The present study aimed to investigate the function of WFDC2 in cervical cancer through both and experiments. Specifically, the present study examined the influence of WFDC2 on the biological functions and the ERK/NF‑κB signaling in cervical cancer cells by creating WFDC2 knockdown and overexpression plasmids, which were transfected into HeLa cells. The expression levels of genes such as WFDC2, E‑cadherin, p38, ERK, p65 and IκBα were assessed using reverse transcription‑quantitative (RT‑q)PCR, while the protein levels of WFDC2, E‑cadherin, p38, ERK, p65, IκBα, phosphorylated (p)‑p38, p‑ERK, p‑NFκB p65 and p‑IκBα were analyzed via western blotting. To evaluate the impact of WFDC2 on the growth of cervical cancer tumors , BALB/c nude mice (age, 6‑8 weeks) were injected with HeLa cells that had a stable WFDC2 knockout. Immunohistochemistry was performed to assess the expression of Ki67 and epithelial‑mesenchymal transition (EMT) markers, including E‑cadherin, vimentin and N‑cadherin. Following WFDC2 knockdown, the expression of the epithelial marker E‑cadherin increased, while the levels of mesenchymal markers (N‑cadherin and vimentin) decreased, indicating a decrease in EMT, as well as diminished cell mobility and migration. When cells with overexpressed WFDC2 were treated with ERK inhibitor PD98059 and NF‑κB inhibitor PDTC, cell activity decreased, along with decreased invasion and migration. The animal experiments further showed that WFDC2 promoted the proliferation and invasion of cervical carcinoma cells. WFDC2 enhanced the migration, invasion and proliferation of cervical cancer cells via the ERK/NF‑κB signaling pathway.
Schisandrin B exhibits anti‑proliferative effects by inducing ferroptosis in pancreatic cancer.
Li F, Fu J, Lin X … +5 more , Liu Y, Yang L, Li Y, Peng T, Qi L
Oncol Rep · 2026 Aug · PMID 42318966 · Full text
Pancreatic cancer (PC) is a lethal malignant tumor of the digestive system with a low survival rate. Current therapies provide only modest benefits for patients and new therapeutic options are urgently needed. Schisandri...
Pancreatic cancer (PC) is a lethal malignant tumor of the digestive system with a low survival rate. Current therapies provide only modest benefits for patients and new therapeutic options are urgently needed. Schisandrin B (Sch B) has demonstrated novel antitumor activity in several preclinical models; however, its effects on PC remain unclear. In the present study, the anti‑proliferative effects of Sch B were evaluated in PC cell lines. The underlying molecular mechanisms were explored using RNA sequencing, drug affinity responsive target stability (DARTS), molecular docking and small interfering RNA transfection. The antitumor effects of Sch B were evaluated using both a subcutaneous xenograft mouse model and an orthotopic genetically engineered mouse model. The studies showed that Sch B significantly inhibited the proliferation of PC cells and induced cell death in a dose‑dependent manner. Mechanistically, transcriptome Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that differentially expressed genes were significantly enriched in the 'ferroptosis' signaling pathway. Sch B triggered ferroptosis by promoting iron overload, lipid peroxidation and glutathione (GSH) depletion, as well as regulating the expression of ferroptosis‑related proteins [including GSH peroxidase 4, solute carrier family 3 member 2, acyl‑CoA synthetase long‑chain family member 4 (ACSL4), γ‑glutamyl‑cysteine ligase catalytic subunit and GSH synthetase]. Furthermore, pre‑treatment with the ferroptosis inhibitor ferrostatin‑1 partially reversed the anti‑proliferative effects and ferroptosis‑related events induced by Sch B. DARTS assays and molecular docking analyses confirmed the direct interaction between Sch B and ACSL4. Notably, silencing ACSL4 expression also partially reversed the anti‑proliferative effects and ferroptosis‑related events induced by Sch B. The studies demonstrated that Sch B suppressed tumor growth in subcutaneous xenograft models with good biosafety, and inhibited metastasis in orthotopic genetically engineered mice. In conclusion, Sch B may exert anti‑proliferative effects at least partially by inducing ACSL4‑dependent ferroptosis in PC.
Research advances on DKK1 in head and neck squamous cell carcinoma: Linking molecular mechanisms to clinical applications (Review).
Zhu X, Hong L, Chen W … +6 more , Tan J, Zhou J, Yang L, Liu Y, Zhai T, Chen K
Oncol Rep · 2026 Aug · PMID 42318960 · Full text
Head and neck squamous cell carcinoma (HNSCC) is one of the most common malignancies worldwide, characterized by persistently high and increasing rates of incidence, recurrence and mortality, thereby posing a considerabl...
Head and neck squamous cell carcinoma (HNSCC) is one of the most common malignancies worldwide, characterized by persistently high and increasing rates of incidence, recurrence and mortality, thereby posing a considerable global public health challenge. Within the complex molecular network driving the malignant progression of HNSCC, Dickkopf‑1 (DKK1), a classical secreted antagonist of the Wnt signaling pathway, has garnered considerable attention due to its pleiotropic roles in tumor initiation, progression and therapeutic resistance. The expression of DKK1 is regulated by a sophisticated network involving both canonical and non‑canonical Wnt pathways, and it exhibits high spatiotemporal specificity and context dependency. The present narrative review discusses the regulatory mechanisms underlying DKK1 expression, its prognostic significance in HNSCC, pro‑tumorigenic molecular mechanisms, immunomodulatory functions and its clinical translational potential as a biomarker and therapeutic target. The present review aims to provide novel insights into the pathogenesis of HNSCC and establish a theoretical foundation for advancing DKK1‑based precision diagnostics and therapeutic strategies.
PI3Kδ inhibitor YY‑20394 is effective alone or in combination with Bcl‑2 inhibitor ABT199 in acute myeloid leukemia cells.
Geng Y, Zhou L, Lou Y … +5 more , Chen J, Liu Q, Shen J, Yang Y, Wu W
Oncol Rep · 2026 Aug · PMID 42318952 · Full text
YY‑20394 (linperlisib), a highly specific PI3Kδ inhibitor, has demonstrated promising efficacy in a variety of hematological malignancies in clinical trials. ABT199 (venetoclax) as a monotherapy shows limited effects in...
YY‑20394 (linperlisib), a highly specific PI3Kδ inhibitor, has demonstrated promising efficacy in a variety of hematological malignancies in clinical trials. ABT199 (venetoclax) as a monotherapy shows limited effects in acute myeloid leukemia (AML), underscoring the need for novel combinatorial therapeutic strategies. The drug sensitivity and potential synergistic effects of YY‑20394 and ABT199 were evaluated in three AML cell lines, MV‑4‑11, U937 and THP‑1, using a Cell Counting Kit‑8 assay. Apoptosis and cell cycle distribution were assessed using dual acridine orange/ethidium bromide staining and flow cytometry. Reverse transcription‑quantitative PCR and western blot analyses were employed to quantify the levels of Bcl‑2 apoptotic family members, c‑Myc, Akt and ERK. YY‑20394 inhibited the viability of MV‑4‑11, U937 and THP‑1 cells in a concentration‑dependent manner. In U937 cells, the highest IC50 value was observed, and YY‑20394 effectively suppressed their proliferation, induced apoptosis and caused cell cycle arrest. Furthermore, the combination of YY‑20394 and ABT199 demonstrated a synergistic effect in MV‑4‑11 cells, significantly enhancing apoptosis compared with either agent alone. Compared with the negative control group, the levels of c‑Myc and Akt phosphorylation were significantly reduced in the YY‑20394 group, and their inhibitory effects were retained in the combination group. ERK phosphorylation was significantly increased in the combination group. However, alterations in the Bcl‑2 pathways did not show a pattern consistent with the observed apoptotic phenotype. In summary, YY‑20394 is effective for inhibiting proliferation of AML cells, and its combination with ABT199 has synergistic pro‑apoptotic effects in MV‑4‑11 cells, which provides new insights and potential avenues for the treatment of AML and its subtypes. Further studies are warranted to explore the therapeutic efficacy and underlying molecular mechanisms of this combination in additional AML subtypes.
A fibroblast activation protein degrader enhances cisplatin sensitivity in non‑small cell lung cancer.
Zhou Y, Li R, Chen X … +8 more , Zhang C, Bao Y, Cui Y, Tong X, Xia T, Yang X, Yang J, Yin X
Oncol Rep · 2026 Aug · PMID 42272260 · Full text
The therapeutic effect of cisplatin against non‑small cell lung cancer (NSCLC), the most common lung cancer, is limited by resistance. In the present study, a fibroblast activation protein (FAP) degrader (Pomalidomide‑PE...
The therapeutic effect of cisplatin against non‑small cell lung cancer (NSCLC), the most common lung cancer, is limited by resistance. In the present study, a fibroblast activation protein (FAP) degrader (Pomalidomide‑PEG2‑FAP2286: FAP‑D) was utilized to enhance cisplatin sensitivity in NSCLC. The study specifically assessed the viabilities of NCI‑H1299 and NCI‑H460 cells (human NSCLC cell lines) and the growth of heterogeneous tumors in mice. The binding between FAP‑D and FAP was studied by molecular docking. The ability of FAP‑D to induce FAP and CD26 degradation was examined by western blotting, as was caspase‑3 and cleaved caspase‑3 expression. The viabilities of H1299 and H460 cells were analyzed using a Cell Counting Kit‑8 assay (CCK‑8). Cell migration rates were studied via wound‑healing assays. Apoptotic features were confirmed in tumors by hematoxylin‑eosin staining assay. FAP was degraded by FAP‑D in a time‑ and concentration‑dependent manner, whereas CD26 protein expression was not altered by FAP‑D. FAP‑D exhibited favorable biocompatibility. The half‑maximal inhibitory concentration (IC) of cisplatin was reduced by co‑treatment with FAP‑D, which could be attributable to the inhibition of cell migration by FAP‑D. Heterogeneous tumor growth was also strongly suppressed by cisplatin + FAP‑D. The apoptotic features of H1299/H460 cells and tumors were enhanced by cisplatin + FAP‑D treatment. In conclusion, the study demonstrated that FAP‑D can enhance the cisplatin sensitivity of H1299 cells and NSCLC tumors. The present findings shed new light into promising treatment strategies and demonstrated the potential clinical utility of cisplatin + FAP‑D for NSCLC treatment.
Sterol regulatory element‑binding proteins: Master regulators of lipid metabolic reprogramming in cancer and emerging therapeutic targets (Review).
Liu Q, Wang R, Li Z … +4 more , Liu Y, Wu L, Zhao Y, Yang J
Oncol Rep · 2026 Aug · PMID 42246192 · Full text
Sterol regulatory element‑binding proteins (SREBPs) are key regulatory factors of lipid synthesis. Tumor cells are highly dependent on SREBP‑driven lipid synthesis for the biogenesis of their cell membranes and signaling...
Sterol regulatory element‑binding proteins (SREBPs) are key regulatory factors of lipid synthesis. Tumor cells are highly dependent on SREBP‑driven lipid synthesis for the biogenesis of their cell membranes and signaling molecules. The aberrant activation of SREBPs is a critical event that drives tumorigenesis and progression. SREBPs are a subset of membrane‑bound proteins that function as basic helix‑loop‑helix leucine zipper (bHLH‑Zip) transcription factors. They mainly maintain the homeostasis of lipid metabolism in the body by activating the genes related to the synthesis and uptake of cholesterol, fatty acids and triglycerides. In addition to their involvement in tumor lipid metabolic reprogramming, SREBPs play critical roles in obesity, atherosclerosis, diabetes mellitus and neurodegenerative diseases. The present review summarizes the regulatory mechanisms of SREBPs, their aberrant activation in tumors, their role in promoting the malignant progression of tumors, as well as the relevant targeted therapeutic strategies from different aspects. In conclusion, targeting SREBPs is a promising anticancer strategy, and future studies are needed to further elucidate their intricate regulatory networks to advance precision medicine.
Dual targeting of mitochondrial metabolism and Rho GTPase signaling to suppress cancer metastasis (Review).
Daher A, Assi Z, Kanaan A … +2 more , Al Khatib A, El Sibai M
Oncol Rep · 2026 Aug · PMID 42246188 · Full text
Despite the numerous advances in cancer therapy, disseminated neoplastic disease remains largely incurable and the primary cause of cancer‑related deaths. This process demands substantial bioenergetic and mechanical adap...
Despite the numerous advances in cancer therapy, disseminated neoplastic disease remains largely incurable and the primary cause of cancer‑related deaths. This process demands substantial bioenergetic and mechanical adaptability, orchestrated by two core cellular systems: Mitochondrial metabolism and Rho GTPase‑driven cytoskeletal dynamics. Traditionally studied independently, these systems form a tightly integrated, bidirectional network. Mitochondria supply ATP and reactive oxygen species (ROS) that fuel and signal through Rho GTPases to drive invasion, while cytoskeletal remodeling and cell polarity direct mitochondrial positioning to meet local energy demands. The present review synthesizes the molecular mechanisms underlying this metabolic‑mechanical crosstalk and highlights a feedforward loop in which mitochondrial oxidative phosphorylation‑derived ATP and ROS activate Rho GTPase signaling, while Rho‑driven cytoskeletal remodeling increases energy demand and promotes mitochondrial redistribution, thereby reinforcing metastatic progression. Critically, this interdependence represents a therapeutic vulnerability. A dual‑targeting strategy was discussed, combining Rho GTPase silencing (via small interfering RNA) with mitochondrial inhibition (via repurposed antibiotics) to simultaneously disrupt the cytoskeletal 'engine' and its metabolic 'fuel'. Such approaches may overcome compensatory adaptive resistance that limits single‑target therapies. By framing mitochondrial and Rho GTPase signaling as an integrated functional axis, the present review provides a mechanistic and translational framework for the development of next‑generation, combination‑based anti‑metastatic therapies.
[Expression of Concern] Antitumor activity of Notch‑1 inhibition in human colorectal carcinoma cells.
Liao W, Li G, You Y … +4 more , Wan H, Wu Q, Wang C, Lv N
Oncol Rep · 2026 Aug · PMID 42246178 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the cell morphology experiments shown in Fig. 4C and 9B on p. 1066 and p. 1069 respectively, the 'NC'...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the cell morphology experiments shown in Fig. 4C and 9B on p. 1066 and p. 1069 respectively, the 'NC' data panel in Fig. 4C appeared to match with the data shown to represent the 'Control' data panel in Fig. 9B, albeit the images appeared in these figures at different sizes. The authors have been contacted by the Editorial Office to offer an explanation for the apparent re‑use of the same data in this 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 this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 39: 1063‑1071, 2018; DOI: 10.3892/or.2017.6176].
Targeting colorectal cancer and T‑cell metabolism for the treatment of colorectal cancer (Review).
Yu Q, Luan P, Liang J … +1 more , Wang L
Oncol Rep · 2026 Aug · PMID 42246177 · Full text
Colorectal cancer (CRC) is a malignant tumor of the digestive tract that is highly prevalent worldwide, which is associated with a poor prognosis in advanced stages and for which current treatment plans have limited effi...
Colorectal cancer (CRC) is a malignant tumor of the digestive tract that is highly prevalent worldwide, which is associated with a poor prognosis in advanced stages and for which current treatment plans have limited efficacy. T cells serve a crucial role in immune clearance and immune evasion within the tumor microenvironment. However, tumor cells directly impair the function of T cells through nutrient competition and the release of inhibitory metabolites. Notably, targeting 'metabolic checkpoints' has emerged as a crucial strategy to enhance T‑cell efficacy. The present literature review summarizes the role of reprogramming glycolysis, glutaminolysis and lipid metabolism in driving immune evasion in CRC, and discusses potential intervention strategies from two perspectives: Modulating tumor metabolism and optimizing the intrinsic metabolic functions of T cells. Finally, it is proposed that stratified precision therapy based on individual metabolic profiles represents a future direction for overcoming immune heterogeneity and drug resistance in CRC.
Ferroptosis in colorectal cancer: Molecular mechanisms and regulatory crosstalk with therapeutic prospects (Review).
Wu M, Zhang M
Oncol Rep · 2026 Jul · PMID 42212391 · Full text
Colorectal cancer (CRC) is a common malignancy of the colonic and rectal epithelia. Numerous patients with CRC derive only limited and unsustained benefit from conventional chemotherapy or immunotherapy, underscoring the...
Colorectal cancer (CRC) is a common malignancy of the colonic and rectal epithelia. Numerous patients with CRC derive only limited and unsustained benefit from conventional chemotherapy or immunotherapy, underscoring the need for novel treatments. Ferroptosis is an iron‑dependent, lipid peroxidation‑driven form of regulated cell death, controlled by iron and lipid metabolism, as well as antioxidant defense pathways, which represent attractive therapeutic targets. Ferroptosis‑related genes are closely linked to immune status, and metabolic reprogramming within the tumor microenvironment can modulate immune cell activation and antitumor immunity. Induction of ferroptosis suppresses CRC proliferation and overcomes resistance to cytotoxic drugs, whereas inhibition of ferroptosis may alleviate inflammatory bowel disease and limit CRC initiation in specific settings. This review summarizes the molecular basis and immunological relevance of ferroptosis in CRC, and discusses recent advances in combination strategies involving chemotherapy, immunotherapy, gut microbiota‑based therapy and nanotherapy, as well as current clinical progress, potential biomarkers and translational challenges.
[Corrigendum] 17‑AAG synergizes with Belinostat to exhibit a negative effect on the proliferation and invasion of MDA‑MB‑231 breast cancer cells.
Zuo Y, Xu H, Chen Z … +6 more , Xiong F, Zhang B, Chen K, Jiang H, Luo C, Zhang H
Oncol Rep · 2026 Jul · PMID 42212389 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the Transwell migration assay experiments shown in Fig. 6F on p. 1940, the 'NC' and 'siTEAD3' exper...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the Transwell migration assay experiments shown in Fig. 6F on p. 1940, the 'NC' and 'siTEAD3' experiments showed an overlapping section of data, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. The authors proposed removing Fig. 6F from the figure, as they considered that the conclusions of these experiments were sufficiently well supported by the data shown in Fig. 6D and E, although the Editor expressed to them our preference that the authors should repeat these experiments, if necessary, to rectify the original errors made during the inaccurate assembly of data in Fig. 6F. The authors were willing to perform the requested experiments, and the revised version of Fig. 6, showing the replacement data for the migration assay experiments in Fig. 6F, is shown on the next page. The authors wish to draw the readers' attention to the fact that the statistical significance of the experiments featured in the new Fig. 6F was not exactly the same as that in the original figure (note the change to the wording of the figure legend opposite, which is highlighted in bold); however, the conclusion that knocking out TEAD family proteins significantly inhibits the migration of MDA-MB-231 cells is completely consistent with the conclusion of the original article. This difference in the statistical significance of the results is reflected in a proposed change of the wording to describe the results of Fig. 6F in the manuscript; therefore, the final sentence of the Results section, left-hand column on p. 1941, should now read as follows: 'As shown in the results of the cell migration assay (Fig. 6F), '. The authors regret the errors that were made during the preparation of the Fig. 6. They are grateful to the editor of for allowing them the opportunity to publish this Corrigendum, and all the authors agree to this publication. Furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 43: 1928-1944, 2020; DOI: 10.3892/or.2020.7563].
Immune network remodeling driven by ferroptosis: Bidirectional interaction mechanisms among multiple immune cells in the lung cancer immune microenvironment (Review).
Qu F, Tong J, Qian W … +1 more , He Q
Oncol Rep · 2026 Jul · PMID 42212386 · Full text
The efficacy of immunotherapy for lung cancer is largely constrained by the highly complex and dynamically evolving tumor immune microenvironment (TIME). Previous studies have mainly focused on single immune checkpoints...
The efficacy of immunotherapy for lung cancer is largely constrained by the highly complex and dynamically evolving tumor immune microenvironment (TIME). Previous studies have mainly focused on single immune checkpoints or individual immune cell types, thus hindering the comprehensive elucidation of variations in immune responses and the emergence of resistance. Ferroptosis, a form of programmed cell death characterized by iron‑dependent lipid peroxidation imbalance, has emerged as a pivotal hub linking tumor metabolism, cellular fate and immune regulation due to high dependence on metabolic states and its capacity to release multiple immunomodulatory signals. The unique environment of lung tissue, characterized by high oxygen levels, active lipid metabolism and easily disrupted iron homeostasis, provides a distinct biological foundation for the initiation and amplification of ferroptosis within the lung cancer TIME. Increasing evidence indicates that ferroptosis affects not only tumor cell survival, but also immune regulation. Through lipid peroxidation products, iron‑related metabolites and damage‑associated molecular patterns, it forms bidirectional regulatory networks with multiple immune cell subsets, including CD8 T‑cells, dendritic cells, macrophages, natural killer cells and neutrophils, thereby shaping the functional state of the immune microenvironment. Distinct from previous reviews that broadly discuss ferroptosis in cancer immunity or the tumor microenvironment, the present review specifically focuses on the lung cancer‑specific immune microenvironment and integrates ferroptosis‑mediated bidirectional interactions across multiple immune cell subsets. The present review emphasizes that ferroptosis should not be viewed merely as a tumoricidal form of cell death, but as a context‑dependent immunometabolic hub that drives immune network remodeling in lung cancer. By this conceptual perspective, the present review aimed to provide a novel framework for understanding heterogeneous immunotherapy responses and for designing rational ferroptosis‑based combination strategies.
Acylglycerol kinase contributes to cell proliferation by activating NF‑κB signaling pathway in pancreatic cancer.
Han K, Zhang Q, Gao S … +6 more , Zhang J, Mei X, Li F, Xu X, Li S, Chen G
Oncol Rep · 2026 Aug · PMID 42212382 · Full text
Pancreatic cancer mortality remains high due to late diagnosis and therapeutic resistance. The present study investigated acylglycerol kinase (AGK), which has been implicated in other tumors, in pancreatic cancer. Quanti...
Pancreatic cancer mortality remains high due to late diagnosis and therapeutic resistance. The present study investigated acylglycerol kinase (AGK), which has been implicated in other tumors, in pancreatic cancer. Quantitative PCR, western blotting and immunohistochemistry analyses showed that AGK was markedly upregulated in pancreatic cancer tissues and cell lines and its expression associated with poor prognosis. Furthermore, functional studies using AGK knockdown and overexpression models demonstrated that AGK promoted cancer cell proliferation by upregulating proliferation‑associated genes, such as and . Mechanistically, AGK activates NF‑κB signaling pathway by facilitating p65 nuclear translocation and enhancing its phosphorylation. Additionally, CCK‑8 and colony formation assays further indicated that elevated AGK levels reduced sensitivity to therapeutic drugs and irradiation in pancreatic cancer cells. These findings revealed the critical role of AGK in pancreatic cancer progression and treatment resistance, identifying it as a potential novel therapeutic target and diagnostic marker.
Targeting lung cancer with tanshinones: Current mechanistic evidence and emerging opportunities (Review).
Guo Z, Li X, Suo P … +3 more , Lin Z, Liu R, Chi C
Oncol Rep · 2026 Jul · PMID 42212375 · Full text
Lung cancer (LC) remains a leading cause of cancer‑related morbidity and mortality worldwide, with non‑small cell lung cancer (NSCLC) comprising ~85% of cases. Although therapeutic options have expanded in recent years,...
Lung cancer (LC) remains a leading cause of cancer‑related morbidity and mortality worldwide, with non‑small cell lung cancer (NSCLC) comprising ~85% of cases. Although therapeutic options have expanded in recent years, drug resistance and tumor relapse continue to limit durable responses, highlighting the need for novel treatment strategies and effective adjuvant agents. Tanshinones are major bioactive diterpenoid quinones derived from (Danshen) and exhibit diverse pharmacological activities, including anti‑inflammatory, anti‑angiogenic, and antitumor effects. Growing evidence indicates that tanshinones suppress LC progression through multi‑level regulation of cancer hallmarks, including inhibition of proliferation, induction of apoptosis, attenuation of invasion and metastasis, and modulation of antitumor immunity. Notably, tanshinones have also shown promise as sensitizers in combination regimens, where they enhance the efficacy of standard anticancer agents and may help overcome acquired resistance in LC models. In the present review, current mechanistic evidence on tanshinone‑mediated anticancer actions in LC was synthesized and opportunities and challenges for clinical translation are examined, with the aim of informing the development of tanshinone‑based therapeutic strategies and next‑generation derivatives.
Advances in Kruppel‑like factor 5 as a transcription factor and its role in gynecological tumors (Review).
Zhang S, Li P, Zhu L
Oncol Rep · 2026 Jul · PMID 42212364 · Full text
Krüppel‑like factor (KLF) 5 has garnered increasing interest in cancer research, as a zinc finger transcription factor integral to the regulation of cellular growth and division through gene transcription control. Initia...
Krüppel‑like factor (KLF) 5 has garnered increasing interest in cancer research, as a zinc finger transcription factor integral to the regulation of cellular growth and division through gene transcription control. Initially investigated for its role in transcriptional regulation during normal tissue development, KLF5 was subsequently identified as a driver of cancer progression upon aberrant activation of its transcriptional activity. This functional dichotomy in transcriptional regulation has considerably enhanced the current understanding of the significance of KLF5 in human cancer. The dysregulation of such critical transcription factors has been shown to be closely linked with gynecological tumors, including cervical, ovarian and endometrial cancer. However, the specific regulatory mechanisms by which KLF5 influences the initiation and progression of gynecological tumors remains to be elucidated. The present review highlights the role of the KLF5 transcriptional regulatory network in the pathogenesis of gynecological tumors and its potential as a therapeutic target.
Dual roles of lactylation modification in gastric cancer: Crosstalk between metabolic reprogramming and epigenetic regulation (Review).
Xu Y, Wang W, Zhang Y … +3 more , Fan Y, Dong W, Yang J
Oncol Rep · 2026 Jul · PMID 42169652 · Full text
Gastric cancer (GC) is among the most prevalent malignant tumors worldwide, and its occurrence and progression are closely associated with metabolic abnormalities and remodeling of the tumor microenvironment. As an emerg...
Gastric cancer (GC) is among the most prevalent malignant tumors worldwide, and its occurrence and progression are closely associated with metabolic abnormalities and remodeling of the tumor microenvironment. As an emerging metabolism‑related post‑translational modification, lactylation acts as a central hub connecting metabolic reprogramming and epigenetic regulation in tumor cells. The present review systematically describes the reprogramming features of lactate metabolism in the GC microenvironment; dissects the enzymatic system and molecular characteristics of lactylation; and reveals a bidirectional positive feedback loop in which histone H3 lysine 18 lactylation (H3K18la) promotes lactate production by upregulating glycolytic genes, and lactate accumulation, in turn, enhances H3K18la levels. A three‑dimensional regulatory network of 'metabolic reprogramming‑epigenetic regulation‑immune microenvironment remodeling' is thereby established in GC. The present review also reveals the clinical value of lactylation as a prognostic biomarker for GC, proposes combination therapeutic strategies targeting lactylation, and provides a theoretical basis and translational direction for the precise diagnosis and treatment of GC.
[Corrigendum] Rapamycin enhances the sensitivity of ER‑positive breast cancer cells to tamoxifen by upregulating p73 expression.
Zhu L, Li XX, Shi L … +8 more , Wu J, Qian JY, Xia TS, Zhou WB, Sun X, Zhou XJ, Wei JF, Ding Q
Oncol Rep · 2026 Jul · PMID 42169645 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the western blots shown in Fig. 1 on p. 457, the p73 data shown for the ZR75‑1 and MCF‑7 cell lines...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the western blots shown in Fig. 1 on p. 457, the p73 data shown for the ZR75‑1 and MCF‑7 cell lines in Fig. 1A and B respectively were very similar if the latter blot were to be flipped vertically. The authors were able to re‑examine their original data, and realized that the p73 data for the ZR75‑1 cell line in Fig. 1A had inadvertently been copied across to show the results for the MCF‑7 cell line experiments in Fig. 1B. The revised version of Fig. 1, now showing the correct data for the p73 blot in Fig. 1B, is shown on the next page. 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 41: 455‑464, 2019; DOI: 10.3892/or.2018.6842].
[Retracted] Hsp90 inhibitor 17‑AAG inhibits stem cell‑like properties and chemoresistance in osteosarcoma cells via the Hedgehog signaling pathway.
Shu X, Liu H, Zhen R … +7 more , Jie Y, Chen L, Qi H, Wang C, Wang R, Chen D, Ran Y
Oncol Rep · 2026 Jul · PMID 42169640 · Full text
Following the publication of the above article and a corrigendum (doi: 10.3892/or.2023.8593) that was published 3 years ago to resolve the issue of duplicated data that had been noted comparing Figs. 1B and C, and 3B and...
Following the publication of the above article and a corrigendum (doi: 10.3892/or.2023.8593) that was published 3 years ago to resolve the issue of duplicated data that had been noted comparing Figs. 1B and C, and 3B and C, respectively, a concerned reader has contacted the Editorial Office to draw our attention to the fact that a series of potential duplications of western blot data had also been noted comparing Fig. 4 with Fig. 5B. Given the discovery of these additional errors that were made in terms of the assembly of two other figures in the above paper, the Editor of has decided that this article should now be retracted from the Journal on account of a lack of confidence in the originally 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 44: 313‑324, 2020; DOI: 10.3892/or.2020.7597].
Combination of ivermectin and metformin promotes autophagy in MCF‑7 cells by inhibiting phosphorylation of the PI3K/AKT/mTOR pathway.
Feng H, He L, Umar T … +9 more , Wang H, Gao Y, Chen G, Sun P, Yin L, Zhao W, Lu H, Deng G, Qiu C
Oncol Rep · 2026 Jul · PMID 42138203 · Full text
Breast cancer remains one of the leading causes of cancer‑related mortality among women globally, necessitating the exploration of novel therapeutic strategies. The present study investigated the combined effects of Iver...
Breast cancer remains one of the leading causes of cancer‑related mortality among women globally, necessitating the exploration of novel therapeutic strategies. The present study investigated the combined effects of Ivermectin (IVM) and metformin (MET) on the human mammary tumor cell line MCF‑7, with a focus on their mechanisms of action. Cell Counting Kit‑8 assays were employed to evaluate proliferative activity, while Transwell migration and scratch assays assessed invasive and migratory capabilities. Transcriptomic analysis identified differentially expressed genes and key signalling pathways, while flow cytometry quantified reactive oxygen species (ROS) levels. Autophagosome formation was visualized using transmission electron microscopy. Western blotting and immunofluorescence staining were employed to detect changes in the expression of key proteins. Results demonstrated that combined IVM and MET intervention significantly inhibited MCF‑7 cell viability after 24 h, showing concentration‑dependent reductions in proliferation, migration and invasiveness. Transcriptomic analysis revealed a significant enrichment of the PI3K/AKT/mTOR signaling pathway, accompanied by decreased expression of thrombospondin‑1 (THBS1). Western blotting revealed that the combination therapy reduced phosphorylation levels of phosphorylated (p‑)PI3K, p‑AKT and p‑mTOR. Through the use of THBS1 overexpression plasmids, the present study validated its positive regulatory role in the PI3K/AKT/mTOR pathway, demonstrating that THBS1 mediates phosphorylation within this signaling cascade. Flow cytometry analysis demonstrated that the IVM combined with MET treatment group exhibited significantly elevated intracellular ROS levels compared with the single‑drug therapy group, triggering oxidative stress responses. After clearing ROS using N‑acetyl‑L‑cysteine, the PI3K/AKT/mTOR signaling pathway was reactivated. Additionally, transmission electron microscopy revealed extensive autophagosome formation within tumor cells of the IVM‑MET combination group. The results indicate that IVM‑MET inhibits PI3K/AKT/mTOR pathway phosphorylation through the accumulation of ROS and the downregulation of THBS1 expression, thereby activating autophagy programs and ultimately leading to tumor cell death.
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