Dendritic cell (DC)‑based vaccines have emerged as a promising immunotherapy against a broad range of cancers. DCs are sentinel antigen‑presenting cells that play a pivotal role in cancer immunosurveillance by recognizing tumor antigens via innate immune responses and subsequently stimulating adaptive T‑cell‑mediated anti‑tumor responses. Autologous DC‑based vaccines prime the individual's immune system to recognize and destroy tumor cells, aiming to achieve durable anti‑tumor immunity and impede tumor relapse. The safety and effectiveness of DC‑based vaccines for cancer treatment have been demonstrated in several clinical studies, either as monotherapy (such as Sipuleucel‑T) or in combination with other therapies such as chemotherapy and immune checkpoint blockade. The present review provides a comprehensive overview of the current progress and clinical applications of DC‑based vaccines for colorectal cancer (CRC). Various subsets of DCs and their biological roles in anti‑tumor immunity are explored in detail and the mechanistic insights into DC‑based vaccine development are discussed. Additionally, the present review highlighted the outcomes of recent clinical trials of autologous DC‑based vaccines for advanced CRC, as well as the challenges and strategies for overcoming them in the development and clinical applications for CRC. Taken together, the potential and limitations of DC‑based vaccines for CRC are underscored in the present review to provide an improved understanding and guide future directions in developing efficacious DC‑based therapeutic vaccines for CRC.
Following the publication of the above paper, and an Expression of concern statement (doi: 10.3892/ijo.2025.5808) that was published to draw the readers' attention to the fact that, for the immunohistochemistry images shown in Fig. 6, the 'Control/PCNA' and 'Control/p27kip1' panels appeared to be duplicates of each other, the authors have now responded concerning this issue. After having examined their original data, the authors have realized that this figure was inadvertently assembled incorrectly; specifically, the Control/p27kip1 panel, as shown correctly, was duplicated in the Figure as the Control/PCNA panel. The revised version of Fig. 6, now showing the correct data for the Control/PCNA 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 International Journal of Oncology 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 36: 913‑920, 2010; DOI: 10.3892/ijo_00000570].
Lung cancer is one of the most common and deadly forms of cancer worldwide, with >80% of cases being non‑small cell lung cancer. Its recurrence and drug resistance have been major challenges in clinical treatment, posing a serious threat to the lives of patients. The present study found that high xeroderma pigmentosum group C (XPC) expression markedly reduced the proliferation capacity and stem cell characteristics of the lung cancer cell lines A549‑XPC and H460‑XPC. In addition, XPC overexpression led to a decreased in the proportion of cells in the G2/M phase proportion, suggesting alterations in the cell cycle process. MTS assays showed that XPC overexpressing cells demonstrated markedly higher sensitivity to chemotherapy drugs compared with control cells. Furthermore, the clonogenic and anchorage‑independent spheroid formation capacities of the cells were markedly inhibited with high XPC expression and the phosphorylation levels of the JAK/STAT pathway and the expression levels of stemness‑associated markers were markedly altered. In vivo studies validated the effect of high XPC expression on tumorigenicity using a subcutaneous tumor model, with tumor volumes of 134.04±46.77 mm³ and 324.64±85.31 mm³ and weights of 164.24±76.16 mg and 434.70±115.72 mg for subcutaneously injected A549‑XPC and A549‑CTR cells, respectively. High expression of XPC in the A549 cells significantly affected tumor volume (P<0.05) and weight (P<0.01) in vivo. The present findings suggested that high XPC expression is associated with reduced proliferation, migration and stem cell‑like properties in lung cancer cells, enhances their sensitivity to chemotherapy drugs and suppresses tumor growth in vivo. These observations supported further investigation of XPC as a potential therapeutic target and prognostic marker for lung cancer, offering new strategies to improve treatment outcomes and prolong patient survival.
Following the publication of the above paper, an interested reader has drawn the Editor's attention to the fact that the tubulin control blots featured in Fig. 3 on p. 88 were strikingly similar to the control blots subsequently featured in a figure in another paper that was published by the same research group in the journal Oncotarget, where the experimental conditions were reported to be different. A subsequent investigation of the data in this paper undertaken by the Editorial Office revealed that various of the western blots included in Figs. 2A and B, 3E and F, and 4C and D appeared to have been duplicated within and/or between these figure parts; moreover, various of the data in these figure parts were remarkably similar to data which appeared (either previously or subsequently relative to the publication date of this article) in other papers written by different authors at different research institutes. Given that the contentious data mentioned above have apparently re‑appeared in a range of other publications, the Editor of International Journal of Oncology 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 50: 85‑92, 2017; DOI: 10.3892/ijo.2016.3797].
Lung cancer is among the most prevalent and fatal cancers worldwide, with its progression heavily shaped by the tumor microenvironment (TME). As key immune cell populations within the TME of lung cancer, macrophages are involved in the entire process of tumor initiation and development. Macrophage polarization serves as a critical link between inflammation and tumorigenesis and is broadly divided into classically activated M1 and alternatively activated M2 phenotypes. These phenotypes exert tumor‑suppressive and tumor‑promoting effects, respectively, by secreting distinct cytokine profiles. MicroRNAs (miRNAs/miRs) are a class of endogenous small non‑coding RNAs that play broad roles in the malignant progression of lung cancer by regulating various cellular processes, including proliferation, resistance to apoptosis, and metabolic reprogramming. Emerging evidence suggests that miRNAs such as miR‑335‑5p, miR‑106a‑5p and miR‑99b regulate M1/M2 macrophage polarization by targeting key pathways in lung cancer. Through these regulatory events, miRNAs exert synergistic effects on multiple tumor hallmarks, including proliferation, invasion, migration, apoptosis, angiogenesis, cell cycle progression, stemness maintenance, and epithelial‑mesenchymal transition. Collectively, these events drive lung cancer progression and influence therapeutic efficacy. The present review synthesizes recent discoveries to explore the relationship between macrophage polarization and lung cancer, with a specific focus on miRNA‑mediated regulatory mechanisms in lung cancer therapy. Ultimately, the present review aimed to provide new insight and a reference point to inform future prevention and treatment strategies for lung cancer.
Following the publication of the above article, an interested reader drew to the Editor's attention that the β‑actin control protein band featured in the right‑hand lane of Fig. 1A on p. 54 appeared to be strikingly similar to the β‑actin control protein band featured in the right‑hand lane of Fig. 2B on the same page, albeit after vertical flipping and with possible horizontal and vertical resizing. Owing to the lack of availability of the raw western blot data due to the time that has elapsed since this paper was published, the authors have repeated the experiments and provided new western blots for these figures, which fully confirm the veracity of the findings presented in the originally published study. The revised versions of Figs. 1 and 2 are shown on the next page. In response to an additional query, the authors also wished to point out that the raw data from the PCR analysis (which were presented to the Editorial Office for inspection) confirmed that the data were correctly assembled from the original electropherograms, and that the part of Fig. 4C associated with the A2780/ADR cells was composed of two parts that came from the same experiment and the same run. They were put together as such, simply because they were loaded in two separate parts of the gel. The authors thank the Editor of International Journal of Oncology for granting them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 47: 51‑60, 2015; DOI: 10.3892/ijo.2015.2987].
Immune escape and therapeutic resistance remain major obstacles to durable benefit from cancer immunotherapy, yet transcript‑based or abundance‑based biomarkers often fail to capture the regulatory states that determine effective immune control. Post‑translational modifications (PTMs) form a dynamic protein‑state layer that rapidly reshapes protein stability, trafficking, complex assembly, and signaling persistence under tumor‑intrinsic and therapy‑imposed stress. In the present review, a biomarker‑oriented framework is proposed in which PTM biology is interpreted through three recurrent immune constraints: Checkpoint competence, tumor visibility and stress‑conditioned immune‑state programming. Within this framework, programmed death‑ligand 1 is viewed as a protein‑state biomarker problem rather than a static expression marker; tumor visibility is defined by durable antigen‑presentation competence and interferon‑linked reinforcement; and stress‑driven immune dysfunction is interpreted through metabolite‑sensitive PTM rewiring and chromatin‑coupled suppressive stabilization. Rather than cataloguing PTMs comprehensively in cancer immunity, the present review focuses on five core exemplar PTM axes, glycosylation, palmitoylation, ubiquitin editing, phosphorylation and lactylation, because they repeatedly map to rate‑limiting immune constraints, are supported by mechanistic evidence, and represent candidate assay‑compatible or intervention‑relevant state variables at differing levels of translational maturity. It is further outlined how integrated proteogenomic, immuno‑peptidomic, and spatial datasets can be used to discover candidate PTM‑state biomarkers, validate mechanism‑proximal readouts in prespecified pretreatment and on‑treatment settings, and prioritize single or co‑dominant state constraints for patient stratification, pharmacodynamic monitoring, and rational combination design. By organizing PTM biology around measurable state variables rather than modification class alone, the present review provides a phase‑aware translational framework for candidate biomarker discovery, fit‑for‑purpose validation, constraint‑guided stratification, and therapeutic prioritization in cancer immunotherapy.
Shikonin (SHK) possesses potent antitumor activity; however, its severe non‑selective toxicity greatly limits the feasibility of conventional systemic administration for cancer therapy. Likewise, mild photothermal therapy (PTT) has intrinsic limitations, including inadequate induction of immunogenic cell death (ICD) and compensatory activation of immunosuppressive pathways, such as increased IDO1 activity and PD‑L1 expression. In the present study, low‑dose SHK and gold nanorods were co‑encapsulated within a supramolecular hydrogel (mPECT) and administered by intratumoral injection to achieve localized combination therapy with mild PTT. Mild PTT rapidly triggered antitumor immune activation within the immunosuppressive tumor microenvironment, whereas SHK sustained this response by suppressing PTT‑induced IDO1 activation and PD‑L1 upregulation and by markedly enhancing ICD. The mPECT hydrogel enabled prolonged local retention and controlled release of SHK, minimizing rapid systemic exposure while preserving therapeutic efficacy at the tumor site. This localized combination of SHK and mild PTT elicited a robust adaptive antitumor immune response that not only inhibited primary tumor growth but also suppressed the progression of untreated distant tumors and generated durable antitumor immune memory. These findings indicate that a single intratumoral administration of low‑dose SHK‑loaded hydrogel combined with mild PTT can induce potent systemic antitumor immunity, supporting the further development of localized SHK‑based therapeutic strategies for the treatment of immune‑cold tumors.
Osteosarcoma (OS) is a highly aggressive bone tumor with limited therapeutic options. As a key component of the N6‑methyladenosine (m6A) methyltransferase complex, KIAA1429 contributes to tumor progression; however, its role in OS remains unclear. For the present study, four human OS cell lines (MG63, 143B, U2OS and Saos‑2) and an osteoblast cell line (hFOB1.19) were cultured in vitro, and KIAA1429 was knocked down in 143B and U2OS cells. To evaluate functional effects, cell proliferation was assessed using a Cell Counting Kit‑8 assay, apoptosis was evaluated by flow cytometry, migration was assessed by Transwell assay and invasion was analyzed using a wound healing assay. Subsequently, ferroptosis was induced using erastin, and analyzed by western blotting, ELISA, C11‑BODIPY staining and m6A‑modified RNA immunoprecipitation‑quantitative PCR. In addition, actinomycin D was used to inhibit transcription and to assess mRNA stability. The interaction between KIAA1429 and solute carrier family 7 member 11 (SLC7A11) was validated using a dual‑luciferase reporter assay. Furthermore, a xenograft model was established in BALB/c nude mice to assess tumor growth and ferroptosis markers, and tumor histology and proliferation were examined using hematoxylin and eosin staining and immunohistochemistry. The results revealed that KIAA1429 was significantly upregulated in OS cells, whereas its knockdown markedly suppressed malignant cellular behaviors. Downregulation of KIAA1429 also enhanced erastin‑induced ferroptosis. Mechanistically, KIAA1429 knockdown reduced m6A modification and decreased the stability of SLC7A11 mRNA, leading to its downregulation. Rescue experiments demonstrated that SLC7A11 overexpression reversed the effects of KIAA1429 knockdown on ferroptosis and malignant phenotypes. In vivo, KIAA1429 knockdown inhibited tumor growth and promoted ferroptosis, effects that were reversed by SLC7A11 overexpression. In conclusion, KIAA1429 knockdown may suppress OS progression by inhibiting m6A‑dependent SLC7A11 expression, thereby promoting ferroptosis. Targeting the KIAA1429/SLC7A11 axis may thus represent a promising therapeutic strategy for OS.
Stearoyl‑CoA desaturase‑1 (SCD1) has emerged as a critical nexus linking lipid metabolic reprogramming to the regulation of cell death. Frequently overexpressed in digestive system malignancies ‑ including gastric, liver and colorectal cancers ‑ SCD1 represents a promising therapeutic target. This review systematically examined how SCD1, through its lipid‑modifying functions, governs three key forms of regulated cell death ‑ ferroptosis, autophagy and apoptosis ‑ thereby driving malignant progression and mediating therapy resistance in digestive cancers. Building on this mechanistic framework, the specific contributions of these regulatory pathways to tumor biology and their association with drug resistance were delineated. Current preclinical therapeutic strategies targeting SCD1 were then highlighted, encompassing both monotherapy and combination approaches with ferroptosis inducers, chemotherapeutic agents or targeted drugs. Finally, key challenges and outline future directions for drug development and clinical translation in this rapidly evolving field were discussed.
Thyroid cancer is the most common endocrine malignancy worldwide, with its incidence increasing markedly over the past several decades, while mortality trends have shown complex patterns. High‑risk refractory thyroid cancers (including radioactive iodine‑refractory differentiated thyroid cancer, poorly differentiated thyroid cancer, anaplastic thyroid carcinoma, progressive medullary thyroid carcinoma and locally advanced disease) pose major challenges in clinical management. The present review systematically reviewed recent epidemiological trends in thyroid cancer and provided an in‑depth exploration of the molecular regulatory mechanisms of key signaling pathways, including MAPK, PI3K/AKT, Janus kinase/STAT, WNT/β‑catenin and NF‑κB, along with their roles in the pathogenesis and progression of thyroid cancer. Based on this, the latest clinical research advances in targeted therapies for high‑risk, refractory thyroid cancer are elaborated on, covering multikinase inhibitors, B‑Raf proto‑oncogene, serine/threonine kinase/mitogen‑activated protein kinase kinase inhibitors, immunotherapy combinations, innovative targeted strategies and redifferentiation approaches. Finally, future directions are discussed based on the 'total treatment' paradigm and strategies to overcome drug resistance, aiming to provide a systematic reference for basic research and clinical translation in thyroid cancer.
Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy with limited options for early diagnosis and poor clinical outcomes. In the present study, PIWI‑interacting RNA (piR)‑164552 was identified as a novel oncogenic regulator in HNSCC. piR‑164552 was found to be markedly upregulated in tumor tissues and serum exosomes and its expression promoted the proliferation, migration, invasion and tumorigenicity of HNSCC cells both in vitro and in vivo. Mechanistic analyses revealed that piR‑164552 interacted with RNA‑binding motif protein 4 (RBM4) and positively regulated RBM4 protein levels, which in turn enhanced the expression of eukaryotic initiation factor 4E‑like 2 (EIF4E2), forming a piR‑164552/RBM4/EIF4E2 axis. Integrated transcriptomic and translatomic profiling further demonstrated that this axis orchestrated extensive reprogramming of mRNA metabolism, ribosome biogenesis and cancer‑associated signaling pathways, underscoring its multilayered role in tumor progression. The present findings highlighted the diagnostic potential of piR‑164552 and uncovered its key contribution to the molecular network driving HNSCC, providing new insights into biomarker development and therapeutic strategies.
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the three breast cancer cell lines investigated in their study, it was surprising that they should have detected caspase‑3 expression in the MCF‑7 cell line, as reported for example in Fig. 6, since it has been shown that MCF‑7 cells do not express caspase‑3 (see the paper by Reiner U. Jänicke and colleagues entitled 'MCF‑7 breast carcinoma cells do not express caspase‑3'. Breast Cancer Res Treat vol. 117.1 (2009); p. 219‑221). In their response, the authors acknowledge that the prevailing consensus in the literature, established by the seminal work of Jänicke et al in an article they published in 1998 in Journal of Biological Chemistry holds that MCF‑7 cells harbor a 47‑bp deletion in exon 3 of the CASP3 gene, resulting in a frameshift mutation and a premature stop codon, with consequent absence of detectable functional protein. The authors' own article acknowledged this controversy by citing conflicting reports (references 13 and 39 compared with references 41‑43); however, they also recognize in retrospect that this should have prompted a more circumspect interpretation of their own data. Following a critical re‑evaluation of their methodology, the authors wish to draw attention to the following limitations of the present work: (1) The band detected in MCF‑7 cells using antibody H‑277 cannot be unambiguously attributed to caspase‑3, and cross‑reactivity with co‑expressed proteins of similar molecular weight, most notably caspase‑7, cannot be excluded. (2) The DDRT‑PCR amplicon obtained from MCF‑7 cells with the reported primers may correspond to the aberrant CASP3 transcript arising from the exon 3 deletion, and does not necessarily represent a translation‑competent mRNA. Sequencing of this amplicon was not performed, and would be required to resolve this question. (3) The conclusions of the article on caspase‑3 expression in MCF‑7 cells should therefore be read with these methodological caveats in mind. Importantly, these limitations do not affect the principal findings of the study concerning MDA‑MB‑231 and MCF‑10F cell lines, for which the experimental evidence remains methodologically sound. The authors are grateful to the Editorial Board of International Journal of Oncology for the rigor of the review process, and also for the opportunity to address these concerns transparently. They also thank the reader of the article for drawing these concerns to their attention. [International Journal of Oncology 49: 753‑762, 2016; DOI: 10.3892/ijo.2016.3558].
Endometrial cancer (EC) has become an increasing clinical concern as the incidence is rising, and treatment options available for advanced disease or recurrent disease are limited. In the present study, the anticancer potential of punicalagin (PCG), a natural ellagitannin polyphenol that comes from pomegranate, was characterized using both in vitro and in vivo models in EC. Two EC cell lines (Ishikawa and SNU‑539) treated with increasing doses of PCG showed dose‑dependent inhibition of cell proliferation and demonstrated a decrease in colony formation. PCG inhibited Transwell migration and an increase in E‑cadherin expression, indicating an inhibition of epithelial‑mesenchymal transition. Further experimental work characterized the mechanisms by which PCG acted and revealed that it decreased the mitochondrial membrane potential and subsequently increased levels of reactive oxygen species, which led to apoptosis as shown by increased BAX expression and Hoechst/PI staining. In addition, PCG showed signs of autophagy, especially in the Ishikawa cells, as indicated by increased levels of LC3‑IIB and the formation of autophagic vacuoles. In vivo studies using a xenograft mouse model showed that treatment with PCG significantly reduced tumor volume and weight, whereas body weight was not significantly affected, thus highlighting strong anticancer efficacy coupled with very low toxicity. Overall, the present study highlights PCG as a promising natural compound with multitarget anticancer activity against EC and warrants further preclinical and clinical research as a potential treatment option.
Non‑small cell lung cancer (NSCLC), as the main type of lung cancer, is characterized by high heterogeneity and a complex tumor microenvironment (TME), which are key factors contributing to therapeutic resistance, recurrence and metastasis. In recent years, the interaction between neural stem cells (NSCs) and NSCLC, known as the 'NSC‑NSCLC axis', has gradually become a research hotspot at the intersection of tumor biology and cancer neuroscience. The present review summarizes the extensive overlap between NSCs and NSCLC stem cells in terms of molecular markers and signaling pathways, and discusses the possible mechanisms through which NSCLC cells 'hijack' NSC programs to enhance stemness, therapeutic resistance and metastatic potential. The present review further discusses how the TME actively recruits NSCs and drives their functional reprogramming, thereby promoting tumor progression through the paracrine secretion of neurotrophic factors, the induction of angiogenesis, remodeling of the immune microenvironment and the formation of synapse‑like connections. In addition, the regulatory networks of neurotransmitters, neurotrophic factors and neuropeptides in NSCLC are reviewed, with particular emphasis on evaluating the potential and challenges of emerging therapies targeting neurotransmitter receptors, perineural invasion, neuroendocrine differentiation and brain metastasis. Unlike previous reviews that focused predominantly on a single mechanism or flux, the present review adopts an integrated perspective of the 'neural stem cell‑non‑small cell lung cancer axis' to link three tiers: Molecular hijacking, microenvironment remodeling and clinical translation. The present review further highlights translational research priorities, including targeting neurotransmitter receptors, perineural invasion, neuroendocrine transformation and brain metastasis. Additionally, it is proposed that single‑cell and spatial omics are poised to advance this field from phenomenological description toward precise subtyping, providing a novel therapeutic strategy for NSCLC shifting from 'tumor eradication' to 'reprogramming the tumor microecology'.
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 2E on p. 264, the Transwell invasion assay results shown in the 'T98G‑AHIF KD' data panel appeared to potentially contain an overlapping section with the 'U251‑NC' data panel in Fig. 3E. After having re‑examined their original data, the authors have realized that Fig. 3 of the above paper was inadvertently assembled incorrectly. The revised version of Fig. 3, now showing replacement data for Fig. 3E (the Transwell results for the U251‑NC and U251‑AHIF‑OE experiments), is featured on the next page. Note that the error made in assembling Fig. 3 did not adversely affect either the results or the overall conclusions reported in this study. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of International Journal of Oncology for allowing them the opportunity to publish this. They also wish to apologize to the readership of the Journal for any inconvenience caused. [International Journal of Oncology 54: 261‑270, 2019; DOI: 10.3892/ijo.2018.4621].
Prostate cancer (PCa) remains a leading cause of cancer‑related mortality in men despite advances in screening and localized treatment. The clinical heterogeneity of PCa, ranging from indolent disease to aggressive, lethal phenotypes, underscores the urgent need for reliable biomarkers that improve diagnosis, prognostication and therapeutic decision‑making. While prostate‑specific antigen testing has reduced mortality, its limited specificity has resulted in overdiagnosis and overtreatment. The present review provides a comprehensive overview of contemporary and emerging biomarkers that support a precision‑medicine approach to PCa management. The present review summarizes established and novel diagnostic, prognostic and predictive biomarkers, including serum‑ and urine‑based assays, genomic and transcriptomic signatures and multiparametric imaging. Particular emphasis is placed on liquid biopsy technologies (circulating tumor cells, circulating tumor DNA and extracellular vesicles), which offer minimally invasive, real‑time insights into tumor burden, molecular evolution and treatment resistance, although their clinical implementation remains context‑dependent and is currently most established in advanced disease settings rather than routine early‑stage management. The present review discusses the strengths and limitations of these platforms, highlighting disease‑stage dependency, technical variability and sensitivity constraints. Beyond tumor‑intrinsic markers, tissue‑based immune biomarkers that capture the tumor immune microenvironment, including immune cell density, spatial organization, checkpoint expression and immune‑related gene signatures, are explored. Evidence indicates that 'immune‑hot' tumors characterized by CD8+ T‑cell infiltration and interferon‑γ signaling are associated with improved outcomes, whereas immunosuppressive macrophage‑ or regulatory T‑cell‑dominant profiles predict poor prognosis. However, these associations are not uniform across studies and PCa remains largely resistant to immunotherapy, underscoring the need to improve the understanding of immune evasion mechanisms and the contextual limitations of immune biomarkers. Furthermore, the present review examines the emerging role of germline human leukocyte antigen class I genotype as a prognostic and predictive biomarker, explicitly integrating it with tissue‑based immune contexture and liquid biopsy readouts by proposing immunoediting as a unifying mechanistic framework that links allele‑specific antigen presentation to immune infiltration. Finally, the present review highlights the prognostic significance of preexisting tumor‑antigen‑specific CD8+ T cells, which reflect an active antitumor immune response and predict a favorable progression‑free survival and responsiveness to immunotherapeutic strategies. Collectively, the present review underscores the need for standardized, multimodal biomarker integration and prospective validation to enable personalized, immune‑aware management of PCa.
Multiple myeloma (MM) is a malignant disorder of plasma cells. Combinations of bortezomib (BTZ) with other therapeutic agents remain the mainstay of MM treatment. However, the rising incidence of drug resistance among patients with MM underscores an urgent need for novel therapeutic strategies. The present study identified triptonide (TN), a small‑molecule monomer extracted from the traditional Chinese herb Tripterygium wilfordii Hook. f., as a synergistic agent that enhanced the anti‑MM activity of BTZ, following a screening of 198 compounds from a ubiquitination‑focused library. TN effectively inhibited cell proliferation, induced apoptosis, and reduced cell viability in MM cells. Furthermore, the synergistic anti‑MM effect between TN and BTZ was validated across MM cell lines, primary MM cells, and xenograft mouse models of MM. Mechanistic investigations revealed that TN synergizes with BTZ by enhancing DNA damage through the suppression of TRIP13‑mediated DNA repair pathways, including non‑homologous end joining and homologous recombination. Notably, TRIP13 knockdown attenuated TN‑induced DNA damage and apoptosis, and diminished the synergistic effect of TN and BTZ on MM cells. Collectively, TN represents a novel anti‑MM agent, and the combination of TN with BTZ constitutes a promising therapeutic strategy for the treatment of MM.
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding Figs. 2A and 4B (and possibly also Fig. 4A), certain of the gel lanes within these figure parts (showing numbered cultures) appeared to contain duplicated data (specifically, lanes 2‑4 and 8‑10 in Fig. 2A, lanes 5 and 6 in Fig. 4A, and lanes 1‑4 and 7‑10 in Fig. 4B). Upon performing an independent analysis of the data in this paper, it also came to light that the β‑actin data in Fig. 3A and the Desmin data in Fig. 3E had appeared in a previous paper published in American Journal of Pathology that featured entirely different authors, although comparing the affiliations of the papers, one of the universities was the same. Given the apparent duplications of data within this paper itself and the re‑use of data that had originally appeared in a different article, the Editor of International Journal of Oncology has decided that it 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 satisfactory reply. The corresponding author, Claudio Festuccia, takes full responsibility for the raised concerns and clarifies that the other co-authors were not directly involved in the preparation of the submitted figures. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 42: 2116‑2122, 2013; DOI: 10.3892/ijo.2013.1892].
