International Journal Of Oncology[JOURNAL]
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200 papers
Therapeutic implications of targeting cancer testis antigen MAGEA1 in cervical cancer.
Kim A, Kim J, Kwak W … +6 more , Mo K, Choe S, Jeon M, Lee J, Yun JW, Yoon H
Int J Oncol · 2026 May · PMID 41823529 · Full text
MAGE family member A1 (MAGEA1), a cancer‑testis antigen (CTA), is aberrantly expressed in several malignancies such as lung and liver cancers. However, its role in cervical cancer remains to be elucidated. The present st...
MAGE family member A1 (MAGEA1), a cancer‑testis antigen (CTA), is aberrantly expressed in several malignancies such as lung and liver cancers. However, its role in cervical cancer remains to be elucidated. The present study investigated the functional significance and therapeutic potential of MAGEA1 in cervical cancer using lentiviral short hairpin RNA‑mediated knockdown, a series of functional assays, RNA sequencing (RNA‑seq), and nude mouse xenograft models. It was found that MAGEA1 was upregulated in cervical cancer cells and its knockdown substantially suppressed cell proliferation, migration, invasion, and tumor growth. RNA‑seq analysis further revealed that MAGEA1 silencing altered pathways related to apoptosis, DNA repair, and metabolism. Moreover, MAGEA1 knockdown enhanced chemosensitivity, indicating a potential role in mediating drug resistance. Collectively, the findings identified MAGEA1 as a key oncogenic driver in cervical cancer and highlighted its promise as both a prognostic biomarker and a therapeutic target, offering novel avenues for personalized treatment strategies in cervical cancer.
Smoking promotes colorectal cancer via the CKAP2L/AREG axis.
Wu S, Wu F, Li X … +3 more , Jiang Z, Liu F, Jiang Z
Int J Oncol · 2026 May · PMID 41823522 · Full text
The link between smoking and colorectal cancer (CRC) is well‑established; however, further research is needed to fully understand the specific effects of tobacco on the development of this type of cancer. The aim of the...
The link between smoking and colorectal cancer (CRC) is well‑established; however, further research is needed to fully understand the specific effects of tobacco on the development of this type of cancer. The aim of the present study was to investigate the relationship between smoking and CRC, as well as to identify key genes involved in smoking‑enhanced CRC progression. To confirm the association between smoking and CRC, analyses of clinical data from the National Health and Nutrition Examination Survey database and genome‑wide association studies data were integrated. In addition, RNA sequencing (RNA‑seq) was conducted on HCT116 cells treated with cigarette smoke extract to identify genes related to smoking. To evaluate the malignant phenotypes of CRC cells and potential molecular mechanisms by which key genes promote smoking‑enhanced CRC, a series of cell and animal experiments were performed. The positive association between smoking and CRC was confirmed by both the cross‑sectional study and Mendelian randomization analyses. Furthermore, after treatment of CRC cells with cigarette smoke extract, cell proliferation, migration and invasion were enhanced. Subsequently, cytoskeleton‑associated protein 2‑like (CKAP2L) was filtered out by bioinformatics analysis, indicating its involvement in smoking‑enhanced CRC. After suppressing CKAP2L, the results revealed that cell proliferation was inhibited, and the cell cycle was arrested at S and G2/M phases. Moreover, cell migration and invasion were suppressed after suppressing CKAP2L expression. Further RNA‑seq analysis suggested that CKAP2L promotes the expression of amphiregulin (AREG). Subsequently, the suppression of AREG resulted in a reduction in the CKAP2L‑promoted proliferation and migration of CRC cells. The results of a chromatin immunoprecipitation assay further confirmed that signal transducer and activator of transcription 3 (STAT3) regulated the transcriptional level of AREG by binding to its promoter. In addition, CKAP2L increased the phosphorylation of STAT3, which subsequently activated the AREG/EGFR pathway, leading to the progression of CRC. In conclusion, the present study demonstrated that smoking may promote CRC progression through the CKAP2L/AREG axis.
[Retracted] Knockdown of MALAT1 inhibits osteosarcoma progression via regulating the miR‑34a/cyclin D1 axis.
Duan G, Zhang C, Xu C … +3 more , Xu C, Zhang L, Zhang Y
Int J Oncol · 2026 May · PMID 41789639 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the β‑actin control bands shown in Fig. 6D on p. 25 had already been submitted for publication to a di...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the β‑actin control bands shown in Fig. 6D on p. 25 had already been submitted for publication to a different journal in an article written by different authors at different research institutes. In addition, it was also identified that invasion assay data in Fig. 4D and western blot data in Fig. 5E also subsequently appeared in articles in other journals that were written by different authors at different research institutes. Given that the abovementioned contentious data in Fig. 6D had already been submitted for publication elsewhere prior to the submission of this paper 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 54: 17‑28, 2019; DOI: 10.3892/ijo.2018.4600].
[Retracted] Design, synthesis and preclinical evaluation of NRC‑AN‑019.
Amala K, Rao AKSB, Gorantla B … +2 more , Gondi CS, Rao JS
Int J Oncol · 2026 May · PMID 41789633 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the images of the experimental mice shown in Figs. 4A and 5A, several sets of mice were positione...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the images of the experimental mice shown in Figs. 4A and 5A, several sets of mice were positioned in unexpectedly similar orientations, even though details of the luciferase imaging differed a little comparing between the affected data sets. Owing to the number of duplications of data 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. 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 42: 168‑178, 2013; DOI: 10.3892/ijo.2012.1697].
FOXM1 inhibitor, RCM‑1, enhances venetoclax mediated apoptosis through downregulation of ATP2B4 in rhabdomyosarcoma.
Merjaneh N, Lan YW, Deng Z … +7 more , Donovan J, Wang G, Do J, Juan T, Xia X, Kalinichenko VV, Kalin TV
Int J Oncol · 2026 May · PMID 41789627 · Full text
Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. Intensifying chemotherapy has failed to improve patient survival for metastatic or relapsed RMS and RMS survivors often suffer from signi...
Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. Intensifying chemotherapy has failed to improve patient survival for metastatic or relapsed RMS and RMS survivors often suffer from significant long‑term toxicities. More efficient and less toxic new therapies are critically needed. RMS expresses high levels of anti‑apoptotic protein Bcl‑2 and an oncogenic transcription factor Forkhead box protein M1 (FOXM1), which is also known to inhibit tumor cell apoptosis. The present study used a combination therapy of a recently developed non‑toxic FOXM1 inhibitor, RCM‑1 and the FDA‑approved Bcl2 inhibitor, venetoclax, which is not effective as a monotherapy in solid tumors. Compared with venetoclax alone, the combination therapy efficiently inhibited RMS growth in the animal model by decreasing tumor cell proliferation and inducing tumor cell apoptosis. RNA‑sequencing analysis demonstrated that the combination therapy uniquely decreased expression of ATPase Plasma Membrane Ca Transporting 4 (ATP2B4), a plasma membrane calcium channel that is highly expressed in RMS compared with normal muscle cells. RCM‑1, but not venetoclax treatment, inhibited ATP2B4 and enhanced the sensitivity of RMS cells to apoptosis. Knockdown of decreased RMS tumor cell proliferation, migration and colony formation . Furthermore, knockdown of increased tumor cell apoptosis, while overexpression of decreased tumor cell apoptosis . In the animal model of RMS, depletion of decreased tumor growth. In summary, combining RCM‑1 with venetoclax sensitized RMS cells to apoptosis by decreasing ATP2B4. This made ATP2B4 a promising therapeutic target for RMS and provides a rationale for exploring this combination in early‑stage clinical trials.
Pancreatic cancer EMT‑targeted therapy: Molecular mechanisms and clinical translation (Review).
Zhang G, Wu Y, Wei M … +5 more , Huang S, Wang Q, Xie Z, Liu S, Wang J
Int J Oncol · 2026 May · PMID 41789626 · Full text
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with a dismal 5‑year survival rate of ~9%, primarily due to late diagnosis, aggressive metastasis and profound resistance to convention...
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with a dismal 5‑year survival rate of ~9%, primarily due to late diagnosis, aggressive metastasis and profound resistance to conventional therapies. Epithelial‑mesenchymal transition (EMT) has been identified as a pivotal driver of these malignant phenotypes, facilitating early invasion, dissemination and treatment failure. The present review systematically elaborated on the multidimensional mechanisms underlying EMT in PDAC, emphasizing its operation as a spectrum of hybrid epithelial/mesenchymal states rather than a binary switch. Key molecular mechanisms include the activation of core transcription factors (such as Snail, ZEB, Twist), intricate crosstalk within the tumor microenvironment (such as transforming growth factor-β and hepatocyte growth factor signaling from stromal cells) and dynamic epigenetic reprogramming. Furthermore, EMT critically contributes to the acquisition of cancer stem cell properties and enhances the survival and colonization of circulating tumor cells. The present review also outlined emerging translational strategies targeting EMT‑related pathways, highlighting agents such as STNM01 that have entered early-phase clinical trials. By synthesizing unprecedented insights into EMT's plastic spectrum states and subtype‑specific regulatory networks, this work establishes a paradigm‑shifting framework for advancing EMT‑targeted therapies; offering transformative potential to overcome PDAC's historical therapeutic barriers and substantially improve patient survival outcomes. By synthesizing current insights from molecular pathways to therapeutic applications, the present review confirmed EMT as a promising therapeutic target and provides a strategic framework for advancing PDAC treatment, with the ultimate goal of improving clinical outcomes.
[Corrigendum] Leptin promotes breast cancer cell migration and invasion via IL‑18 expression and secretion.
Li K, Wei L, Huang Y … +7 more , Wu Y, Su M, Pang X, Wang N, Ji F, Zhong C, Chen T
Int J Oncol · 2026 May · PMID 41789622 · Full text
Following the publication of the above article and an Expression of Concern statement that was issued in light of concerns raised by an interested reader (doi: 10.3892/ijo.2025.5816) regarding potential duplications of d...
Following the publication of the above article and an Expression of Concern statement that was issued in light of concerns raised by an interested reader (doi: 10.3892/ijo.2025.5816) regarding potential duplications of data comparing Figs. 1D and 2E, and the apparent re‑use of β‑actin control data in Fig. 4A and B where different experimental conditions were reported, the authors have now responded to the enquiry posed by the Editorial Office. After consulting their original data, the authors have realized that the data in Fig. 2E for the MDA‑MB‑231 cell line, and the β‑actin blots in Fig. 4B, were chosen incorrectly (it was also noted by the Editorial Office, upon performing an independent analysis of the data in this paper, that, in Fig. 6C, the CD68/Lep. and CD163/CNL.+Lep. data panels appeared to contain an overlapping section of data, such that the data shown in these panels may have been derived from the same original source). The revised versions of Figs. 2 and 4 (showing the correct data for the MDA‑MB‑231 cell line in Fig. 2E and the β‑actin blots in Fig. 4B) are shown on the next two pages. Furthermore, a revised version of Fig. 6, showing replacement data for the CD68/Lep. data panel, is also shown on the third page. Note that the errors made in assembling these figures did not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 48: 2479‑2487, 2016; DOI: 10.3892/ijo.2016.3483].
RNA‑binding protein DAZAP1 promotes gastric cancer metastasis by enhancing NOTCH1 and JAG1 mRNA stability.
Peng S, Chen Y, Wu J … +17 more , Huang X, Hong L, Xie Y, Lei Y, Wei X, Yang P, Zhang J, Yang Q, Liu G, Li A, Liu S, Li J, Dai W, Hu Y, Wang J, Xiong J, Wang J
Int J Oncol · 2026 May · PMID 41789621 · Full text
DAZ‑associated protein 1 (DAZAP1), an RNA‑binding protein and modulator of alternative splicing, participates in tumorigenesis. However, the potential oncogenic function and mechanism of DAZAP1 in gastric cancer (GC) are...
DAZ‑associated protein 1 (DAZAP1), an RNA‑binding protein and modulator of alternative splicing, participates in tumorigenesis. However, the potential oncogenic function and mechanism of DAZAP1 in gastric cancer (GC) are unknown. Gene expression analysis, including mRNA and protein level assessment by reverse transcription‑quantitative PCR and western blotting, respectively, immunofluorescence, immunohistochemistry, hybridization assays, tissue microarray, RNA immunoprecipitation and sequencing and mRNA stability assay were performed, as well as colony formation, EdU, wound healing, migration and invasion assays of GC cells. DAZAP1 displayed a significant upregulation in GC cells and served as an oncogene, as demonstrated by its overexpression promoting colony formation, EdU incorporation, wound healing, migration and invasion, and its knockdown suppressing these malignant phenotypes. Additionally, DAZAP1 upregulation was positively correlated with tumor progression and poor survival in individuals with GC. Functionally, DAZAP overexpression promoted proliferation, epithelial‑mesenchymal transition (EMT) and migration/invasion of GC cells. Mechanistically, DAZAP1 physically bound NOTCH1 or JAG1 mRNA to regulate its stability. In addition, overexpression of DAZAP1 facilitated NOTCH1‑ and/or JAG1‑mediated migration via EMT in GC cells. Changes in NOTCH1 or JAG1 expression were positively correlated with DAZAP1 expression when DAZAP1 was silenced or enhanced in GC. Finally, DAZAP1 modulated the activation of the NOTCH/JAG1 signaling pathway. DAZAP1 expression facilitated migration/invasion and mediated the stabilization of NOTCH1 or JAG1 mRNA, suggesting they may participate in GC progression.
lncRNA AL445238.2‑USP4 axis regulates cell survival and stemness in colon cancer.
Lin H, Feng J, Chen P … +3 more , Hu J, Zhu L, Yuan S
Int J Oncol · 2026 Apr · PMID 41789601 · Full text
Local progression and metastasis remain the foremost impediments to long‑term survival among patients with colorectal cancer (CRC). long non‑coding RNAs (lncRNAs) have a pivotal role in the advancement of colorectal mali...
Local progression and metastasis remain the foremost impediments to long‑term survival among patients with colorectal cancer (CRC). long non‑coding RNAs (lncRNAs) have a pivotal role in the advancement of colorectal malignancies. The aim of the present study was to elucidate the functional role and underlying molecular mechanisms of the lncRNA AL445238.2 in CRC progression. In the present study, overexpression/knockdown lentiviral vectors, protein half‑life assays and co‑immunoprecipitation assays were used to explore the regulatory relationship among AL445238.2, ubiquitin‑specific protease 4 (USP4) and BCL2, combined with Transwell assays, sphere formation assays and subcutaneous xenograft models to demonstrate their effects on colon cancer proliferation and stemness both and . The experimental findings revealed that AL445238.2 was highly expressed in CRC cells. AL445238 overexpression significantly enhanced the proliferation of DLD1 and SW480 cells, reduced extracellular lactate dehydrogenase release, diminished apoptotic activity and increased cellular stemness, as evidenced by increased CD133 expression and augmented tumor sphere formation, together with enhanced mitochondrial activity. RNA pulldown and immunofluorescence assays further demonstrated a direct interaction between AL445238.2 and USP4, with the two synergistically modulating the expression of the anti‑apoptotic protein Bcl2 and the pro‑apoptotic protein BAX to suppress apoptosis. Moreover, in assays, USP4 independently promoted cell proliferation, sustained stemness and enhanced mitochondrial function, thereby increasing tumor growth. Collectively, the findings of the present study revealed that AL445238.2, through its interaction with USP4, orchestrated the regulation of cell proliferation, apoptosis, stemness maintenance and migration in CRC cells, offering novel insights into the role of lncRNAs in cancer progression and highlighting potential therapeutic targets.
IL‑6: A key player in the EGFR‑TKI‑resistant tumor microenvironment and its therapeutic implications (Review).
Wei Q, Huang C, Zhang Y … +6 more , Zeng H, Qi C, Tan S, Li W, Tian P, Li Y
Int J Oncol · 2026 Apr · PMID 41789586 · Full text
IL‑6, a pleiotropic inflammatory cytokine predominantly secreted by fibroblasts, myeloid‑derived suppressor cells, tumor‑associated macrophages and tumor cells, is associated with poor prognosis of and therapeutic resist...
IL‑6, a pleiotropic inflammatory cytokine predominantly secreted by fibroblasts, myeloid‑derived suppressor cells, tumor‑associated macrophages and tumor cells, is associated with poor prognosis of and therapeutic resistance in non‑small cell lung cancer (NSCLC). The activation of signaling pathways, including the JAK/STAT3, MAPK and PI3K/AKT pathways, promotes tumor survival. Furthermore, the IL‑6/JAK/STAT3 signaling axis has emerged as a key driver of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR‑TKI) resistance, orchestrating intricate crosstalk within the tumor microenvironment (TME) to promote cell survival and immunosuppression. The present review synthesized current evidence on the dual role of IL‑6 in mediating EGFR‑TKI resistance and blunting anti‑tumor immunity. The present review highlights the preclinical rationale for combining IL‑6 blockade with EGFR‑TKI or immune checkpoint inhibitors to overcome refractory disease. The present review also highlights the structure, molecular mechanisms and clinical insights of IL‑6 in the TME of ‑mutant NSCLC and may provide optimized therapeutic strategies for EGFR‑TKI‑refractory NSCLC.
Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil‑mediated promotion of DNA damage‑driven cytotoxicity.
Mukinovic E, Federmann S, Messling L … +5 more , Sekeres M, Mann J, Abbey L, Kassack MU, Fritz G
Int J Oncol · 2026 Apr · PMID 41789585 · Full text
The efficacy of anticancer therapeutics is limited by acquired drug resistance of tumor cells. The present study aimed to characterize and overcome resistance mechanisms to the anthracycline derivative doxorubicin (Doxo)...
The efficacy of anticancer therapeutics is limited by acquired drug resistance of tumor cells. The present study aimed to characterize and overcome resistance mechanisms to the anthracycline derivative doxorubicin (Doxo). To this end, comparative analyses of Doxo‑induced stress responses of parental A2780 ovarian carcinoma cells and Doxo‑resistant A2780ADR variants were performed. A2780ADR cells revealed cross‑resistance to multiple compounds, including anticancer drugs [cisplatin (CisPt) and etoposide (Eto)] and DNA repair/DNA damage response (DDR) inhibitors (olaparib, niraparib, entinostat, prexasertib and rabusertib). A2780ADR cells formed markedly fewer DNA double‑strand breaks (DSB) following Doxo exposure compared with parental A2780 cells, resulting in a mitigated DDR, reduced proliferation inhibition and attenuated apoptosis. Potential resistance mechanisms identified to contribute to Doxo resistance of A2780ADR cells include increased Doxo efflux due to increased multi‑drug resistance gene 1 (MDR1) expression and reduced topoisomerase IIα protein expression. Substantial resensitization of A2780ADR cells to Doxo was achieved by both the RAC1 GTPase inhibitor EHT1864, the histone deacetylase inhibitor entinostat (EST) and, most effectively, the calcium channel blocker verapamil (Ver). Notably, Ver‑mediated sensitization also pertains to Eto and CisPt. The synergistic effect of Ver in combination with Doxo, which is reflected by low combination index (CI<0.8), probably involves inhibition of MDR1‑mediated drug export, increased intracellular steady state levels of Doxo and elevated DSB formation, eventually promoting pro‑toxic mechanisms of the DDR. However, combination treatment with Doxo and Ver also increased the cytotoxic response of non‑malignant murine cardiomyocytes, murine embryonic stem cells and human induced pluripotent stem cells. Taken together, the present study suggested inhibition of MDR1‑mediated Doxo efflux by Ver a useful approach to overcome acquired drug resistance of A2780ADR cells by stimulating DDR‑related cytotoxicity, yet at the price of a potentially increased risk of normal tissue toxicity.
Mechanisms of chemoresistance in diffuse large B‑cell lymphoma and novel therapeutic strategies (Review).
Wan M, Wang X, Luo B … +3 more , Hong H, Zhu Y, Lin T
Int J Oncol · 2026 Apr · PMID 41789584 · Full text
Diffuse large B‑cell lymphoma (DLBCL), the most prevalent subtype of lymphoma, is characterized by rapid growth and a poor prognosis, with the R‑CHOP regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and pre...
Diffuse large B‑cell lymphoma (DLBCL), the most prevalent subtype of lymphoma, is characterized by rapid growth and a poor prognosis, with the R‑CHOP regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) being the standard first‑line therapy. However, 30‑40% of patients experience early relapse or refractoriness to treatment, highlighting the need to understand the mechanisms of chemoresistance. The present review synthesizes the current knowledge on the molecular mechanisms underlying chemoresistance in DLBCL, including genetic mutations, epigenetic modifications, aberrant activation of signaling pathways, alterations in drug metabolism and efflux, and upregulation of anti‑apoptotic proteins. In addition, the role of the tumor microenvironment in mediating therapeutic resistance is discussed and biomarkers associated with chemoresistance are explored. Furthermore, novel therapeutic strategies targeting chemoresistance, such as immunotherapy, metabolic modulators and epigenetic therapies, are examined. Understanding these mechanisms is crucial for developing effective treatment strategies to overcome resistance and improve patient outcomes in DLBCL.
Beyond the membrane: Internalization and compartmentalization of insulin‑like growth factor 1 receptor signaling in cancer pathogenesis and treatment (Review).
Zhang T, Li L, Du C
Int J Oncol · 2026 Apr · PMID 41716020 · Full text
The insulin‑like growth factor 1 receptor (IGF‑1R) plays a central role in tumor initiation, progression and response to treatment. IGF‑1R internalization and compartmentalization have profound effects on tumor biology,...
The insulin‑like growth factor 1 receptor (IGF‑1R) plays a central role in tumor initiation, progression and response to treatment. IGF‑1R internalization and compartmentalization have profound effects on tumor biology, extending beyond classical signaling associated with receptors at the cell membrane. Following internalization, IGF‑1R alters its intracellular localization and induces new signaling functions. These changes affect the duration and spatial dynamics of signal activation, thereby influencing tumor cell proliferation, migration and the development of drug resistance. However, the exact molecular mechanisms that mediate these processes remain elusive, and the inherent complexity of the downstream signaling network continues to limit the clinical translation of IGF‑1R‑targeted therapies. The present review systematically summarizes the current knowledge on the molecular mechanisms of IGF‑1R internalization and compartmentalization, highlighting their roles in tumor progression and treatment response. The recent advancements and persistent challenges in this field are also critically discussed, aiming to provide a theoretical foundation and new insights for the development of more efficient and effective therapeutic plans that specifically target IGF‑1R.
Role and underlying mechanisms of miR‑200 family in breast cancer (Review).
Liu J, Du H, Shi Y
Int J Oncol · 2026 Apr · PMID 41716019 · Full text
Βreast cancer (BC) is the most common malignant tumor among women. Its significant heterogeneity and complex molecular mechanisms pose major clinical challenges, including limited therapeutic efficacy and drug resistance...
Βreast cancer (BC) is the most common malignant tumor among women. Its significant heterogeneity and complex molecular mechanisms pose major clinical challenges, including limited therapeutic efficacy and drug resistance. Recently, microRNAs (miRs) have been recognized as key post‑transcriptional regulators involved in tumorigenesis and tumor progression through multiple pathways. Among these, the miR‑200 family (miR‑200a, miR‑200b, miR‑200c, miR‑429 and miR‑141) has attracted considerable attention due to its pivotal role in BC. The present review systematically summarizes the genomic characteristics, expression regulation mechanisms and biological functions of the miR‑200 family in BC. Special emphasis is given to their roles in epithelial‑mesenchymal transition, cell proliferation, apoptosis, maintenance of stemness, and remodeling of the tumor microenvironment. Furthermore, members of the miR‑200 family have potential as diagnostic and prognostic biomarkers and are closely linked to chemotherapy resistance. The present review aims to provide novel insights and a theoretical foundation for the diagnosis, treatment, and deeper investigation of BC by comprehensively examining the functional mechanisms of the miR‑200.
Role of SPAG6 in regulating physiological functions and tumorigenesis (Review).
Luo Y, Yan Q, Zhang P … +4 more , Xu H, Zhang R, Wang R, Wu Y
Int J Oncol · 2026 Apr · PMID 41685588 · Full text
Sperm‑associated antigen 6 (SPAG6) belongs to the cancer/testis antigen family. It is a microtubule‑binding protein located on chromosome 10p12.2 and it plays an important role in various physiological processes, includi...
Sperm‑associated antigen 6 (SPAG6) belongs to the cancer/testis antigen family. It is a microtubule‑binding protein located on chromosome 10p12.2 and it plays an important role in various physiological processes, including ciliary movement, immune synapse formation and neurodevelopment. Abnormal SPAG6 expression occurs in multiple malignancies and developmental disorders; however, its underlying molecular mechanisms in tumorigenesis, tumor progression, clinical outcomes and therapeutic response have not been presented. This review provides a comprehensive overview of the physiological functions of SPAG6 and its mechanisms in disease, with a focus on its expression profile, function and association with disease progression and treatment response in hematologic malignancies (e.g., myelodysplastic syndrome, acute myeloid leukemia and B‑cell acute lymphoblastic leukemia) and solid tumors (e.g., breast cancer, lung cancer and osteosarcoma). SPAG6 promotes tumor progression and drug resistance by attenuating the cell cycle and through epigenetic modifications and remodeling of the tumor immune microenvironment. In addition, it may serve as a diagnostic and prognostic marker for various diseases as well as a therapeutic target.
[Corrigendum] Podoplanin‑mediated TGF‑β‑induced epithelial‑mesen‑ chymal transition and its correlation with bHLH transcription factor DEC in TE‑11 cells.
Wu Y, Liu Q, Yan X … +6 more , Kato Y, Tanaka M, Inokuchi S, Yoshizawa T, Morohashi S, Kijima H
Int J Oncol · 2026 Apr · PMID 41685573 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the scratch‑wound assay experiments shown in Fig. 8 on p. 2318, the 'control‑siRNA/24 h' and 'podoplani...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the scratch‑wound assay experiments shown in Fig. 8 on p. 2318, the 'control‑siRNA/24 h' and 'podoplanin‑siRNA/48 h' panels contained an overlapping section of data; such that these data, which were intended to show the results from differently performed experiments, appeared to have been derived from the same original source. Upon analyzing the data independently in the Editorial Office, it came to light that, in addition to control blots, the podoplanin blots were duplicated in Fig. 2A and B, and also in Fig. 3A and B, although it wasn't clear whether this was simply the way in which the authors had chosen to arrange the data in these figures, as the reported experimental conditions were the same in the respective figure parts (note that an Expression of Concern statement was also published for this paper: doi.org/10.3892/ijo.2025.5805). Upon contacting the authors, they confirmed that the data had been included in Figs. 2 and 3 as intended, although they realized that an error had been made during the assembly of the scratch‑wound assay images shown in Fig. 8. However, the authors had retained their original data, and the data for the podoplanin‑siRNA/48 h' panel was shown incorrectly in this Figure. In the first instance, the authors wish to propose the following wording for the figure legend for Fig. 3, to clarify that the same podoplanin and β‑actin bands were intended to have been shown in Figs. 2 and 3 (the added text is highlighted in bold): 'Figure 3. The protein expression of podoplanin and EMT‑related markers was regulated by TGF‑β. TE‑11 cells were treated as indicated in Fig. 2. These cells were then lysed, and the lysates were subjected to western blot analyses of pSmad2, Smad2/3, Slug, podoplanin, vimentin, N‑cadherin, E‑cadherin, Claudin‑4, DEC1, DEC2, and β‑actin. Two representative results of at least four independent experiments with similar outcomes are shown'. Textual corrections should also be noted in this Corrigendum: First, in the figure legend for Fig. 8, the P‑value for significance should have been written as '*P<0.05', not as '*P<0.001'. Secondly, in the Results section, the '' subsection on p. 2314, sentences 5-7 in this paragraph should have been written as follows ('at 24 h' should have been included in the sixth sentence): 'In order to evaluate the ability of migration, wound‑healing assay was introduced in podoplanin siRNA‑transfected cells. Remaining wound length was measured after 0, 24 and 48 h of podoplanin siRNA transfection, and a significant difference between the control siRNA‑transfected group and the podoplanin siRNA‑ transfected group at 24 h was attained (Fig. 8). Morphologically, a small amount of the TE‑11 cells in the middle of the chamber was dead in the podoplanin‑siRNA transfected group, especially at the 24‑h time‑point'. The revised version of Fig. 8, now showing the correct data for the 'podoplanin‑siRNA/48 h' experiment, is shown on the next page. The authors confirm that the error made in assembling Fig. 8 did not have a major impact on the conclusions reported in the above article, and they thank the Editor of for allowing them the opportunity to publish a Corrigendum. Furthermore, all the authors agree to the publication of this Corrigendum, and apologize to the readers for any inconvenience caused. [International Journal of Oncology 48: 2310‑2320, 2016; DOI: 10.3892/ijo.2016.3445].
Emerging roles of RNA mA modification in multiple myeloma pathogenesis and treatment resistance (Review).
Maimaitiyiming Y, Hu S, Bai D … +4 more , Guan Y, Bu N, Hao W, Maimaiti M
Int J Oncol · 2026 Apr · PMID 41685571 · Full text
Multiple myeloma (MM) is an incurable hematologic malignancy characterized by the clonal expansion of plasma cells in the bone marrow. Despite advances in therapeutic agents, including proteasome inhibitors, immunomodula...
Multiple myeloma (MM) is an incurable hematologic malignancy characterized by the clonal expansion of plasma cells in the bone marrow. Despite advances in therapeutic agents, including proteasome inhibitors, immunomodulatory drugs and immunotherapies, relapse driven by treatment resistance remains a major clinical challenge. This underscores the critical need to elucidate additional molecular mechanisms that drive MM pathogenesis and therapeutic failure. The emerging field of epitranscriptomics, which studies post‑transcriptional RNA modifications, offers a promising perspective. Among these modifications, N6‑methyladenosine (mA), the most abundant internal mRNA modification, has been implicated in regulating nearly every aspect of RNA metabolism. Growing evidence indicates that dysregulation of the mA modification machinery plays a pivotal role in MM heterogeneity, disease progression and drug resistance. The present review synthesized current knowledge on how specific mA regulators contribute to MM oncogenesis by modulating key signaling pathways, interactions with the bone marrow microenvironment and responses to therapy. It also discussed the potential of targeting mA pathways as a therapeutic strategy to overcome treatment resistance and improve patient outcomes. By highlighting recent advances and future directions, the present review underscored mA modification as an important frontier in the battle against MM.
[Corrigendum] The p85α regulatory subunit of PI3K mediates cAMP‑PKA and retinoic acid biological effects on MCF7 cell growth and migration.
Donini CF, Di Zazzo E, Zuchegna C … +6 more , Di Domenico M, D'Inzeo S, Nicolussi A, Avvedimento EV, Coppa A, Porcellini A
Int J Oncol · 2026 Apr · PMID 41645761 · Full text
Following the publication of the above article, an interested reader drew the authors' attention to the fact, for the wound‑healing assay data shown in Fig. 6 on p. 1632, the 'T16 h/p85 WT' and 'T16 h + RA/p85 D' panels...
Following the publication of the above article, an interested reader drew the authors' attention to the fact, for the wound‑healing assay data shown in Fig. 6 on p. 1632, the 'T16 h/p85 WT' and 'T16 h + RA/p85 D' panels appeared to contain an overlapping section, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. Upon contacting the authors, they realized that Fig. 6 had been inadvertently assembled incorrectly. The revised version of Fig. 6, now showing the correct data for the 'T16 h + RA/p85 D' panel, is shown on the next page. Note that this error 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 40: 1627‑1635, 2012; DOI: 10.3892/ijo.2012.1383].
Advances in the study of the breast carcinoma exosomal microRNAs: From basic mechanisms to clinical applications (Review).
Chen ZM, Huang P, Yang DY … +2 more , Lin S, Cai SQ
Int J Oncol · 2026 Apr · PMID 41614405 · Full text
Breast carcinoma remains a major global health burden requiring innovative diagnostic and therapeutic strategies. Exosomal miRNAs have emerged as key factors in breast carcinoma that influence tumor progression, metastas...
Breast carcinoma remains a major global health burden requiring innovative diagnostic and therapeutic strategies. Exosomal miRNAs have emerged as key factors in breast carcinoma that influence tumor progression, metastasis and treatment resistance. Recent studies have elucidated their mechanisms of action, including their roles in regulating oncogenic and tumor‑suppressive pathways, modulating the tumor microenvironment and promoting chemo‑resistance. Advances in miRNA‑based therapies such as miRNA mimics and inhibitors have shown promise in combination treatments, enhancing their therapeutic efficacy. Furthermore, exosomal miRNAs play a role in breast carcinoma calcification, offering novel insights into tumor progression. Unlike previous reviews that focus on a single function or therapeutic potential of miRNAs, the present review systematically integrated the multilevel role of exosomal miRNAs in breast cancer from the two dimensions of oncogenicity and tumor inhibition and the regulatory mechanism of breast carcinoma calcification and proposes that the exosomal miRNA calcification axis may be a key link connecting tumor metabolism and pathological calcification. Despite the potential of miRNAs, challenges remain in optimizing exosome isolation techniques and standardizing miRNA detection methods for clinical applications. Future research should focus on refining miRNA‑based liquid biopsies, developing delivery systems that target exosomes to enhance therapeutic efficacy and early detection strategies and ultimately improving patient survival and quality of life. The present review comprehensively explored the roles of exosomal miRNAs and highlighted their importance in breast carcinoma research. The present review illustrated the potential of exosomal miRNAs as non‑invasive biomarkers and therapeutic targets in precision medicine.
<p>KMO downregulation promotes hepatocellular carcinoma growth via 3‑HAA‑mediated mitochondrial mass and function imbalances</p>.
Liu M, Zhang X, Hu Y … +8 more , Niu L, Guo L, Zhao G, Lu F, Jia F, Li L, Wu H, Zhu J
Int J Oncol · 2026 Mar · PMID 41543194 · Full text
<p>Kynurenine (Kyn) 3‑monooxygenase (KMO) is a key enzyme of the tryptophan (Try)‑Kyn pathway and is located on the outer membrane of mitochondria. Notably, it has not yet been elucidated as to whether KMO is involved in...
<p>Kynurenine (Kyn) 3‑monooxygenase (KMO) is a key enzyme of the tryptophan (Try)‑Kyn pathway and is located on the outer membrane of mitochondria. Notably, it has not yet been elucidated as to whether KMO is involved in hepatocellular carcinoma (HCC) progression by affecting mitochondria. In the present study, KMO was revealed to be downregulated in HCC patients and this downregulation was associated with a poor prognosis. Notably, the downregulation of KMO promoted the proliferation and migration of HCC cells and increased mitochondrial mass. The levels of the Try metabolite 3‑hydroxyanthranilic acid (3‑HAA) were elevated in HCC cells overexpressing KMO. The results indicated that 3‑HAA may inhibit HCC cell growth promoted by KMO downregulation and reverse the KMO downregulation‑induced increase in mitochondrial mass. Furthermore, KMO and 3‑HAA were shown to regulate the expression of the transcription factor nuclear receptor subfamily 4 group A member 1 (NR4A1) and reduce NR4A1 mitochondrial translocation, thus inhibiting the growth of HCC cells. In summary, the current study elucidated that low KMO expression in HCC affects mitochondrial mass and function by reducing the level of the Try metabolite 3‑HAA, downregulating the expression of NR4A1 and promoting its mitochondrial translocation, which in turn may promote the progression of HCC. These findings provide new insights into the treatment of HCC, potentially targeting the mitochondria and the Try‑Kyn pathway.</p>.
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