International Journal Of Oncology[JOURNAL]
Sun
200 papers
Decoding the role of cancer stem cells in digestive tract tumors: Mechanisms and therapeutic implications (Review).
Cao X, Geng X, Zhang C … +1 more , Li L
Int J Oncol · 2025 Jul · PMID 40576138 · Full text
Cancer stem cells (CSCs) are a distinct subpopulation of cells within tumors, characterized by their ability to self‑renew, differentiate and promote tumorigenesis. CSCs have critical roles in the initiation, progression...
Cancer stem cells (CSCs) are a distinct subpopulation of cells within tumors, characterized by their ability to self‑renew, differentiate and promote tumorigenesis. CSCs have critical roles in the initiation, progression and therapeutic resistance of digestive tract tumors, including in esophageal, gastric, colorectal and pancreatic cancer. The present review comprehensively explores the biology of CSCs, their interactions with the tumor microenvironment and their clinical relevance in predicting patient prognosis and guiding treatment strategies. The emerging therapeutic approaches that target CSCs, including pathway inhibitors, monoclonal antibodies and combination therapies, are also discussed, highlighting the potential of these strategies to improve patient outcomes in digestive tract cancer types. Additionally, future research directions and challenges in developing effective CSC‑targeted therapies are addressed, emphasizing the need for innovative strategies to overcome treatment resistance and increase therapeutic efficacy.
[Retracted] N6‑methyladenosine upregulates miR‑181d‑5p in exosomes derived from cancer‑associated fibroblasts to inhibit 5‑FU sensitivity by targeting NCALD in colorectal cancer.
Pan S, Deng Y, Fu J … +3 more , Zhang Y, Zhang Z, Qin X
Int J Oncol · 2025 Aug · PMID 40576135 · Full text
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that certain of the tumor images shown in Fig. 7B on p. 13 had already appeared in different form in Fig. 2E in a...
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that certain of the tumor images shown in Fig. 7B on p. 13 had already appeared in different form in Fig. 2E in a previously published paper in the journal written by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to , the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 60: 14, 2022; DOI: 10.3892/ijo.2022.5304].
Advancements in the therapeutic potential of sesquiterpenoids for the treatment of hepatocellular carcinoma (Review).
Li Y, Du X, Mao J
Int J Oncol · 2025 Jul · PMID 40539465 · Full text
Sesquiterpenoids are widely distributed in plants, animals, marine organisms and microorganisms, particularly in plants, and they exhibit various biological activities, including anti‑tumor, anti‑bacterial, anti‑inflamm...
Sesquiterpenoids are widely distributed in plants, animals, marine organisms and microorganisms, particularly in plants, and they exhibit various biological activities, including anti‑tumor, anti‑bacterial, anti‑inflammatory, antiviral and antioxidant properties. They also have the effects of protecting the liver, protecting the nerves, preventing and treating diabetes and improving immunosuppressive function. Hepatocellular carcinoma (HCC) is the main type of primary liver cancer and the third leading cause of cancer‑related death worldwide. There is accumulating evidence that HCC is an increasingly serious threat to human health and the incidence of primary liver cancer is also still increasing. For the present review, literature on sesquiterpenoids in the treatment of liver cancer from 2003 to 2024 was searched through electronic databases. A total of 46 sesquiterpenoids were identified for HCC treatment. It was found that sesquiterpenoids play a therapeutic role in HCC by inhibiting proliferation, inducing apoptosis, inhibiting invasion and metastasis of HCC cells, regulating the body's immune function and decreasing the resistance of tumor cells. Sesquiterpenoids are promising drugs, which may create more opportunities for the treatment of liver cancer. However, research on how sesquiterpenoids act on HCC is not systematic and most reports are also limited to mixtures, while there is only a small number of reports of new sesquiterpene monomers for treating HCC. Therefore, it is necessary to further discover new components and study their biological activities, and to gradually conduct in‑depth studies and clinical application in the future. The present study reviewed the research progress of sesquiterpene‑rich natural products in the treatment of HCC in the past two decades.
Protein lactylation and immunotherapy in gliomas: A novel regulatory axis in tumor metabolism (Review).
Luo T, Liu L, Wang H … +1 more , Wen S
Int J Oncol · 2025 Jul · PMID 40539457 · Full text
Gliomas are the most common primary brain tumors, and exhibit highly heterogeneous and aggressive biological behaviors. Metabolic reprogramming is a hallmark of gliomas, and lactate accumulation serves a critical role in...
Gliomas are the most common primary brain tumors, and exhibit highly heterogeneous and aggressive biological behaviors. Metabolic reprogramming is a hallmark of gliomas, and lactate accumulation serves a critical role in tumor progression. In addition to its traditional role as a metabolic byproduct, lactate has been recognized as a signaling molecule that modifies proteins through lactylation, which is a novel post‑translational modification. Lactate‑induced lactylation of histone and non‑histone proteins is emerging as a key epigenetic and metabolic regulator that influences glioma development, immune evasion, angiogenesis and therapeutic resistance. The present review provides mechanistic insights into protein lactylation, its role in glioma progression and its potential therapeutic implications. Targeting lactate metabolism and lactylation‑modifying enzymes holds promise for improving glioma treatment outcomes.
[Retracted] Fbxw7 regulates hepatocellular carcinoma migration and invasion via Notch1 signaling pathway.
Wang X, Zhang J, Zhou L … +8 more , Sun W, Zheng ZG, Lu P, Gao Y, Yang XS, Zhang ZC, Tao KS, Dou KF
Int J Oncol · 2025 Jul · PMID 40539454 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the different cell invasion and migration assay experiments shown in Fig. 5 on p. 238, as many as four pairs...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the different cell invasion and migration assay experiments shown in Fig. 5 on p. 238, as many as four pairs of overlapping data panels were identified, such that these data panels had all apparently been derived from the same original source(s); in addition, a further pair of overlapping data panels was identified comparing between Fig. 5 and the cell migration and invasion assay experiments shown in Fig. 7. Owing to the large number of duplications of data that have been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 47: 231‑243, 2015; DOI: 10.3892/ijo.2015.2981].
[Corrigendum] The mechanism of adenosine‑mediated activation of lncRNA MEG3 and its antitumor effects in human hepatoma cells.
Liu LX, Deng W, Zhou XT … +7 more , Chen RP, Xiang MQ, Guo YT, Pu ZJ, Li R, Wang GF, Wu LF
Int J Oncol · 2025 Jul · PMID 40539435 · Full text
Following the publication of the above article, an interested reader drew to the authors' attention that, for the fluorescence microscopic images shown in Fig. 4A on p. 425, the data shown for the 'Huh7 / pcDNA3.1‑MEG3'...
Following the publication of the above article, an interested reader drew to the authors' attention that, for the fluorescence microscopic images shown in Fig. 4A on p. 425, the data shown for the 'Huh7 / pcDNA3.1‑MEG3' experiment appeared to repeat some of the data shown in the 'HepG2 / pcDNA3.1‑MEG3' experiment, albeit at a different magnification. Upon examining their original data, the authors realized that they had inadvertently assembled the data in this figure incorrectly. The revised version of Fig. 4, now showing the correct images for the Control and pcDNA3.1‑MEG3 experiments for the Huh7 cell line, is shown on the next page. The authors wish to state that these errors did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 48: 421‑429, 2016; DOI: 10.3892/ijo.2015.3248].
Beyond the tumor microenvironment: Orchestrating systemic T‑cell response for next‑generation cancer immunotherapy (Review).
Lyu X, Han J, Lin C … +2 more , Zhou Y, Wang W
Int J Oncol · 2025 Jul · PMID 40511544 · Full text
Immune checkpoint blockade therapy has revolutionized cancer treatment, yet its clinical efficacy remains limited to a subset of patients with specific tumor types. The present review provides a comprehensive analysis of...
Immune checkpoint blockade therapy has revolutionized cancer treatment, yet its clinical efficacy remains limited to a subset of patients with specific tumor types. The present review provides a comprehensive analysis of T cell‑mediated antitumor immunity from both local and systemic perspectives, with particular emphasis on CD8 T cells as primary effectors. The review discusses how the complex trafficking between the tumor microenvironment (TME), surrounding lymphoid tissues and peripheral circulation creates multiple opportunities for tumors to evade immune surveillance. Within the TME, T‑cell exclusion mechanisms, antigen specificity and the spectrum of T‑cell exhaustion states, from progenitor exhausted T cells to terminally exhausted T‑cell phenotypes, are reviewed. Beyond the local TME, the crucial roles of tumor‑draining lymph nodes and tertiary lymphoid structures in maintaining sustainable antitumor immunity, as well as the significance of circulating T cells as both biomarkers and therapeutic targets, are analyzed. This systemic perspective provides insights into the dynamic nature of antitumor immunity and suggests potential strategies for next‑generation immunotherapies, including combination approaches targeting multiple immune compartments to achieve optimal therapeutic outcomes.
[Corrigendum] CCR7 regulates cell migration and invasion through MAPKs in metastatic squamous cell carcinoma of head and neck.
Liu FY, Safdar J, Li ZN … +4 more , Fang QG, Zhang X, Xu ZF, Sun CF
Int J Oncol · 2025 Jul · PMID 40511538 · Full text
Following the publication of the above article, the authors drew to the Editor's attention that, for the fluorescence microscopy experiments shown in Fig. 7 on p. 2506, they had inadvertently included the same data to sh...
Following the publication of the above article, the authors drew to the Editor's attention that, for the fluorescence microscopy experiments shown in Fig. 7 on p. 2506, they had inadvertently included the same data to show the results for the 'Control' and 'CCL19 + CCR7 mAb' experiments for E‑cadherin (top row, first and third images from the left). The Editorial Office subsequently conducted an independent assessment of the data in this paper and, regarding the scratch‑wound assay experiments shown in Fig. 5 also on p. 2506, two pairs of the images contained overlapping sections, 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 their original data, the authors have realized that Fig. 5 was also presented incorrectly, and the revised versions of Fig. 5, now containing the correct images for the 'CCL19+PD98059 0 h', 'CCL19+SP600125 0 h' and 'CCL19+SP600125 24 h' experiments, and of Fig. 7, now showing the correct data for the E‑cadherin 'Control' experiment, are shown on the next page. The authors wish to state that these errors did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 45: 2502‑2510, 2014; DOI: 10.3892/ijo.2014.2674].
Impact of PD‑L1 upregulation on immune checkpoint inhibitor efficacy in triple‑negative breast cancer using a 4T1 murine model.
Park AY, Kim JH, Lee S … +4 more , Kim HS, Kim HK, Lee HB, Han W
Int J Oncol · 2025 Jul · PMID 40511536 · Full text
Triple‑negative breast cancer (TNBC) is a lethal subtype of breast cancer with a poor prognosis and limited existing treatment options. The immune checkpoint inhibitor, anti‑programmed death ligand 1 (PD‑L1), has recentl...
Triple‑negative breast cancer (TNBC) is a lethal subtype of breast cancer with a poor prognosis and limited existing treatment options. The immune checkpoint inhibitor, anti‑programmed death ligand 1 (PD‑L1), has recently emerged as a promising alternative in treating TNBC. PD‑L1 is critical in tumor immune evasion and is therefore a key target for cancer immunotherapy. Although anti‑PD‑L1 therapy is effective in breast cancer based on clinical trials, the relationship between PD‑L1 expression levels and treatment response remains unclear. To investigate this, a 4T1 breast cancer cell line that stably overexpressed PD‑L1 was established and was used to create a tumor model in mice. Mice were treated with anti‑PD‑L1 antibodies, and tumor growth was compared between the control and treated groups. PD‑L1 overexpressing tumors did not exhibit an antitumor response to anti‑PD‑L1 therapy compared with the control tumors. Additionally, immune cell infiltration and activation were significantly altered, as shown by immunohistochemical staining and bulk RNA sequencing. In PD‑L1‑overexpressing tumors that did not respond to treatment, immune cell markers and antitumor immune pathways were downregulated. These results demonstrated that excessive PD‑L1 expression creates an immunosuppressive tumor microenvironment, which impairs the efficacy of anti‑PD‑L1 therapy. The present study suggests that excessive PD‑L1 expression reduces the effectiveness of antitumor immunotherapy, and that PD‑L 1 expression levels are essential in predicting the response to antitumor immunotherapy.
[Retracted] Intestinal trefoil factor activates the PI3K/Akt signaling pathway to protect gastric mucosal epithelium from damage.
Sun Z, Liu H, Yang Z … +7 more , Shao D, Zhang W, Ren Y, Sun B, Lin J, Xu M, Nie S
Int J Oncol · 2025 Jul · PMID 40476581 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell migration assay experiments shown in Fig. 1C and 3C, three sets of data panels were found...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell migration assay experiments shown in Fig. 1C and 3C, three sets of data panels were found to contain overlapping sections of data (including four panels across the figure parts that contained the same overlapping data). A further pair of overlapping data panels were identified for the immunofluorescence experiments shown in Fig. 5. Upon receiving notification of this issue, the authors requested a corrigendum and submitted corrected versions of Figs. 1, 3 and 5. However, upon performing an independent analysis of the data in this paper in the Editorial Office, it was also noted that certain of the data in these figures had appeared subsequently in a pair of more recent publications by the same research group, and moreover, one of these images had been incorporated into one of the three revised figures submitted for the corrigendum. Owing to the large number of duplications of data identified in the published paper, and the apparent mislabelling of the authors' own data files, 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. [International Journal of Oncology 45: 1123-1132, 2014; DOI: 10.3892/ijo.2014.2527].
Molecular targets and therapies associated with poor prognosis of triple‑negative breast cancer (Review).
Kim ES
Int J Oncol · 2025 Jun · PMID 40444482 · Full text
Triple‑negative breast cancer (TNBC) is a highly aggressive and heterogeneous subtype of BC characterized by the absence of estrogen, progesterone and human EGFR2 receptors. This lack of receptors renders it unresponsive...
Triple‑negative breast cancer (TNBC) is a highly aggressive and heterogeneous subtype of BC characterized by the absence of estrogen, progesterone and human EGFR2 receptors. This lack of receptors renders it unresponsive to standard targeted therapies. Despite advances made in understanding the molecular landscape of TNBC, its poor prognosis and high recurrence rates underscore the urgent need for innovative therapeutic approaches. This review explores the effects of key prognostic markers, such as Ki‑67, programmed cell death ligand 1, BRCA1/2 mutations, E‑cadherin loss and EGFR alterations. It also examines critical pathways, including the PI3K/AKT/mTOR and mutant p53 pathways, which are prerequisites for TNBC progression and therapy resistance, and discusses the therapeutic potential of directly targeting these key molecules and their associated signaling pathways. In addition, recent advances in targeted therapies were highlighted, such as immune checkpoint inhibitors, and the statuses of emerging strategies were presented, such as chimeric antigen receptor‑T cell therapy and small inhibitory RNA‑based treatments. Given the molecular heterogeneity of TNBC, the importance of precision medicine was also discussed and it was emphasized that this approach is becoming an increasingly critical aspect of personalized treatment strategies. Resistance to existing therapies presents a major challenge to the effective treatment of TNBC, and thus, the development of future therapeutic strategies requires technical innovations. By integrating these insights, this review aims to provide a comprehensive overview of current and future means of improving TNBC outcomes.
Multifaceted roles of lactate dehydrogenase in liver cancer (Review).
Jin H, Liu Q, Li J … +2 more , Zhao S, Tuo B
Int J Oncol · 2025 Jun · PMID 40417916 · Full text
Hepatocellular carcinoma (HCC) has high morbidity and mortality rates, and metabolic reprogramming of HCC cells supports the proliferation and development of tumor cells. Lactate dehydrogenase (LDH), a key metabolic enzy...
Hepatocellular carcinoma (HCC) has high morbidity and mortality rates, and metabolic reprogramming of HCC cells supports the proliferation and development of tumor cells. Lactate dehydrogenase (LDH), a key metabolic enzyme, can maintain the rapid proliferative demand of tumor cells by promoting glycolysis and lactate production in HCC cells. In addition, LDH regulates redox homeostasis and influences lipid synthesis and signaling pathways, further promoting tumor invasion and metastasis. In the tumor microenvironment, LDH affects the function of immune cells and stromal cells by regulating the lactate concentration in and promoting the immune escape and angiogenesis of tumor cells. Since elevated levels of LDH are closely associated with tumor load, invasiveness and poor prognosis, LDH also has promising applications in the early diagnosis, treatment and prognostic assessment of HCC. The present study reviewed the roles of LDH in the occurrence, development, diagnosis, prognosis and treatment of HCC and explored its value as an important biomarker and potential therapeutic target, with the aim of providing a comprehensive reference for HCC‑related research and clinical practice.
Targeting CALR reduces energy metabolism of esophageal cancer cells and inhibits tumor‑associated fibroblast infiltration.
Miao Y, Wang X, He F … +10 more , Zhang F, Huang Y, Lai Y, Wang Y, Zhang L, Yin H, Meng X, Liu H, Li W, Yang S
Int J Oncol · 2025 Jun · PMID 40417915 · Full text
Calreticulin (CALR) supports the induction of dendritic cell maturation, which makes it a key target for effective esophageal squamous cell carcinoma (ESCC) immunotherapy. The mechanism of CALR in the immunotherapy of ES...
Calreticulin (CALR) supports the induction of dendritic cell maturation, which makes it a key target for effective esophageal squamous cell carcinoma (ESCC) immunotherapy. The mechanism of CALR in the immunotherapy of ESCC is not fully studied. The aim of the present study was to explore the contributing role of CALR in ESCC progression. The association of CALR expression with calnexin (CANX) and protein disulfide isomerase A3 (PDIA3) expression in ESCC was analyzed. The functions of CALR in ESCC cells were examined by detection of cell migration, endoplasmic reticulum (ER) stress, mitochondrial function, cytoskeletal remodeling, cell proliferation and apoptosis. The effects of CALR on tumor growth and tumor‑associated fibroblast infiltration were examined by subcutaneous xenograft assay. The expression of CALR, CANX and PDIA3 in ESCC tissue significantly increased and the expression of PDIA3 was positively associated with CANX. Overexpression of CALR resulted in enhanced cell proliferation, migration, ER stress, mitochondrial function and cytoskeletal remodeling; knockdown of CALR expression had the opposite effect. In the subcutaneous xenograft assay, knockdown CALR significantly inhibited the growth of esophageal cancer tumors, suppressed the invasion of tumor‑associated fibroblasts and decreased the expression of α‑smooth muscle actin (α‑SMA), fibroblast activation protein (FAP), fibroblast specific protein‑1 (FSP1), platelet‑derived growth factor and transforming growth factor beta (TGF‑β) in tumor tissue. These findings suggested that CALR promotes the progression of ESCC by regulating ER stress and mitochondrial function to mediate ATP production, cytoskeletal remodeling, cell proliferation and apoptosis through CANX and PDIA3. Knockdown CALR significantly inhibited tumor‑associated fibroblast infiltration and is a potential drug target for ESCC.
[Corrigendum] Biological effects of BMP7 on small‑cell lung cancer cells and its bone metastasis.
Shen W, Pang H, Xin B … +3 more , Duan L, Liu L, Zhang H
Int J Oncol · 2025 Jun · PMID 40417882 · Full text
Subsequently to the publication of the above article, the authors contacted the Editorial Office to explain that, for the cell migration and invasion assay experiments shown in Fig. 3 on p. 1358, the same data had inadve...
Subsequently to the publication of the above article, the authors contacted the Editorial Office to explain that, for the cell migration and invasion assay experiments shown in Fig. 3 on p. 1358, the same data had inadvertently been selected to show the results of the 'Migration / SBC‑3‑rhBMP7' experiment in Fig. 3A and the 'Invasion / SBC‑5' experiment in Fig. 3B. After re‑examining their original data, the authors have realized that the data were correctly shown for the 'Migration / SBC‑3‑rhBMP7' experiment in Fig. 3A. Therefore, the revised version of Fig. 3, now showing the correct data for the 'Invasion / SBC‑5' experiment in Fig. 3B, is shown on the next page. The authors are grateful to the Editor of for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 53: 1354‑1362, 2018; DOI: 10.3892/ijo.2018.4469].
Chaetocin enhances tumor necrosis factor‑related apoptosis‑inducing ligand‑mediated apoptosis by enhancing DR5 stabilization and reactive oxygen species generation in human glioblastoma cells.
Jung HJ, Kim JK, Suh SI … +1 more , Baek WK
Int J Oncol · 2025 Jun · PMID 40377008 · Full text
Chaetocin, a fungal metabolite, exerts notable antiproliferative effects against solid tumors by triggering apoptosis; however, the mechanisms underlying its effects remain unclear. As tumor necrosis factor (TNF)‑related...
Chaetocin, a fungal metabolite, exerts notable antiproliferative effects against solid tumors by triggering apoptosis; however, the mechanisms underlying its effects remain unclear. As tumor necrosis factor (TNF)‑related apoptosis‑inducing ligand (TRAIL) promotes apoptosis in certain types of tumor, the present study aimed to explore the sensitizing effects of chaetocin in TRAIL‑induced apoptosis in human glioblastoma cells and the underlying mechanism. Human glioblastoma cells (U343MG, U87MG, U251MG, and T98G) and embryonic kidney cells (HEK293) were co‑treated with chaetocin and TRAIL, followed by assessment of cell viability. The results from viability and apoptosis assays demonstrated a significant increase in caspase-dependent apoptosis in glioblastoma cells, but not in HEK293 cells, upon co-treatment with chaetocin and TRAIL. Additionally, death receptor 5 (DR5) expression analysis demonstrated that co‑treatment with chaetocin and TRAIL upregulated DR5 expression in a dose‑ and time‑dependent manner by increasing the stability of DR5 on the cell surface. In glioblastoma cells, small interfering RNA‑mediated DR5 knockdown markedly suppressed chaetocin/TRAIL‑induced apoptosis. Moreover, chaetocin enhanced reactive oxygen species (ROS) production, which facilitated TRAIL‑mediated apoptosis by enhancing DR5 upregulation. Thus, chaetocin sensitized the human glioblastoma cell lines U87MG and T98G to TRAIL‑mediated apoptosis by upregulating DR5 expression through ROS-mediated mechanisms. The present findings underscore chaetocin as a potential novel therapeutic agent for glioblastoma.
[Retracted] Notch1 induces epithelial‑mesenchymal transition and the cancer stem cell phenotype in breast cancer cells and STAT3 plays a key role.
Zhang X, Zhao X, Shao S … +5 more , Zuo X, Ning Q, Luo M, Gu S, Zhao X
Int J Oncol · 2025 Jun · PMID 40376995 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 3A and B on p. 1145 showing the results of cell invasion and migration experiments, four pairs of overla...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 3A and B on p. 1145 showing the results of cell invasion and migration experiments, four pairs of overlapping data panels were identified, affecting half the panels shown in the figure, such that these data panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original source. Owing to the large number of duplications of data that have been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 46: 1141‑1148, 2015; DOI: 10.3892/ijo.2014.2809].
[Corrigendum] New application of an old drug: Antitumor activity and mechanisms of doxycycline in small cell lung cancer.
Wang SQ, Zhao BX, Liu Y … +7 more , Wang YT, Liang QY, Cai Y, Zhang YQ, Yang JH, Song ZH, Li GF
Int J Oncol · 2025 Jun · PMID 40376983 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, in Fig. 3 on p. 1356 showing the results of cellular apoptosis experiments, the 'Doxy 5 µg/ml' and 'Doxy 10 µg...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, in Fig. 3 on p. 1356 showing the results of cellular apoptosis experiments, the 'Doxy 5 µg/ml' and 'Doxy 10 µg/ml' data panels appeared to contain overlapping data, such that these images were apparently derived from the same original source where the results of differently performed experiments were intended to have been shown. In addition, in Fig. 4A on p. 1357, showing the results of TUNEL assay experiments, the 'Doxy 10 µg/ml' and '5‑FU 25 µg/ml' data panels contained overlapping sections, similarly suggesting that these data had been derived from the same original source. The authors were able to consult their original data, and recognized how these errors occurred. The corrected versions of Figs. 3 and 4, now showing the correct data for the 'Doxy 5 µg/ml' experiment in Fig. 3 and the '5‑FU 25 µg/ml' experiment in Fig. 4A, are shown below and 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 the errors that were made in compiling this pair of figures 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. [International Journal of Oncology 48: 1353‑1360, 2016; DOI: 10.3892/ijo.2016.3375].
Current updates on the structural and functional aspects of the CRISPR/Cas13 system for RNA targeting and editing: A next‑generation tool for cancer management (Review).
Allemailem KS, Rahmani AH, Almansour NM … +4 more , Aldakheel FM, Albalawi GM, Albalawi GM, Khan AA
Int J Oncol · 2025 May · PMID 40342053 · Full text
For centuries, a competitive evolutionary race between prokaryotes and related phages or other mobile genetic elements has led to the diversification of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)...
For centuries, a competitive evolutionary race between prokaryotes and related phages or other mobile genetic elements has led to the diversification of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and CRISPR‑associated sequence (Cas) genome‑editing systems. Among the different CRISPR/Cas systems, the CRISPR/Cas9 system has been widely studied for its precise DNA manipulation; however, due to certain limitations of direct DNA targeting, off‑target effects and delivery challenges, researchers are looking to perform transient knockdown of gene expression by targeting RNA. In this context, the more recently discovered type VI CRISPR/Cas13 system, a programmable single‑subunit RNA‑guided endonuclease system that has the capacity to target and edit any RNA sequence of interest, has emerged as a powerful platform to modulate gene expression outcomes. All the Cas13 effectors known so far possess two distinct ribonuclease activities. Pre‑CRISPR RNA processing is performed by one RNase activity, whereas the two higher eukaryotes and prokaryotes nucleotide‑binding domains provide the other RNase activity required for target RNA degradation. Recent innovative applications of the type VI CRISPR/Cas13 system in nucleic acid detection, viral interference, transcriptome engineering and RNA imaging hold great promise for disease management. This genome editing system can also be employed by the Specific High Sensitivity Enzymatic Reporter Unlocking platform to identify any tumor DNA. The discovery of this system has added a new dimension to targeting, tracking and editing circulating microRNA/RNA/DNA/cancer proteins for the management of cancer. However, there is still a lack of thorough understanding of the mechanisms underlying some of their functions. The present review summarizes the recent updates on the type VI CRISPR/Cas system in terms of its structural and mechanistic properties and some novel applications of this genome‑editing tool in cancer management. However, some issues, such as collateral degradation of bystander RNA, impose major limitations on its application. Furthermore, additional challenges and future prospects for this genome editing system are described in the present review.
Strategies for neoantigen screening and immunogenicity validation in cancer immunotherapy (Review).
Feng H, Jin Y, Wu B
Int J Oncol · 2025 Jun · PMID 40342048 · Full text
Cancer immunotherapy stimulates and enhances antitumor immune responses to eliminate cancer cells. Neoantigens, which originate from specific mutations within tumor cells, are key targets in cancer immunotherapy. Neoanti...
Cancer immunotherapy stimulates and enhances antitumor immune responses to eliminate cancer cells. Neoantigens, which originate from specific mutations within tumor cells, are key targets in cancer immunotherapy. Neoantigens manifest as abnormal peptide fragments or protein segments that are uniquely expressed in tumor cells, making them highly immunogenic. As a result, they activate the immune system, particularly T cell‑mediated immune responses, effectively identifying and eliminating tumor cells. Certain tumor‑associated antigens that are abnormally expressed in normal host proteins in cancer cells are promising targets for immunotherapy. Neoantigens derived from mutated proteins in cancer cells offer true cancer specificity and are often highly immunogenic. Furthermore, most neoantigens are unique to each patient, highlighting the need for personalized treatment strategies. The precise identification and screening of neoantigens are key for improving treatment efficacy and developing individualized therapeutic plans. The neoantigen prediction process involves somatic mutation identification, human leukocyte antigen (HLA) typing, peptide processing and peptide‑HLA binding prediction. The present review summarizes the major current methods used for neoantigen screening, available computational tools and the advantages and limitations of various techniques. Additionally, the present review aimed to summarize experimental strategies for validating the immunogenicity of the predicted neoantigens, which will determine whether these neoantigens can effectively trigger immune responses, as well as challenges encountered during neoantigen screening, providing relevant recommendations for the optimization of neoantigen‑based immunotherapy.
Mechanism of SMYD2 promoting stemness maintenance of bladder cancer stem cells by regulating PYCR1 expression and PINK1/Parkin mitophagy pathway.
Chen J, Xiao S, Yan X … +2 more , Wei Y, Song W
Int J Oncol · 2025 May · PMID 40341538 · Full text
SET and MYND domain‑containing protein 2 (SMYD2), an identified protein‑lysine methyltransferase, is key for bladder cancer (BC) progression. The tumor‑formation capacity and metastatic potential of bladder cancer stem c...
SET and MYND domain‑containing protein 2 (SMYD2), an identified protein‑lysine methyltransferase, is key for bladder cancer (BC) progression. The tumor‑formation capacity and metastatic potential of bladder cancer stem cells (BCSCs) are due to their stemness characteristics. The present study explores the mechanism of SMYD2 in promoting BCSC stemness maintenance by pyrroline‑5‑carboxylate reductase 1 (PYCR1). BC cells were treated with PYCR1, SMYD2 and putative kinase 1 (PINK1) small interfering (si)RNA, pcDNA3.1‑PYCR1 and pcDNA3.1‑SMYD2. Mito‑Tracker Green and light chain‑3B (LC3B) expression, colony formation ability and tumor stemness were assessed, as well as histone H3 lysine 4 trimethylation (H3K4me3) enrichment and PYCR1, SMYD2, H3K4me3, LC3B II/I, p62, PINK1, Parkin, Nanog and SRY‑box transcription factor 2 (Sox2) expression. A nude mouse xenograft model was used for verification. PYCR1 mRNA and protein expression were elevated in BCSCs. Following PYCR1 or SMYD2 siRNA treatment, PYCR1, SMYD2 and CD44CD33 expression, cancer cell colony formation, number of tumor spheres and Nanog and Sox2 expression were decreased, but pcDNA3.1‑PYCR1 or pcDNA3.1‑SMYD2 transfection enhanced BCSC stemness maintenance. SMYD2 was associated with PYCR1 expression. SMYD2 upregulated PYCR1 expression through H3K4me3, subsequently activating the PINK1/Parkin mitophagy pathway, which supports maintenance of BCSC stemness.
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