International Journal of Oncology

Journal Information
ISSN / EISSN : 1019-6439 / 1791-2423
Published by: Spandidos Publications (10.3892)
Total articles ≅ 11,940
Current Coverage
SCOPUS
LOCKSS
MEDICUS
MEDLINE
PUBMED
SCIE
Archived in
SHERPA/ROMEO
Filter:

Latest articles in this journal

Jiecheng Ye, Wanying Deng, Ying Zhong, Hui Liu, Baoyin Guo, Zixi Qin, Peiwen Li, Xueyun Zhong, Lihui Wang
International Journal of Oncology, Volume 61, pp 1-15; https://doi.org/10.3892/ijo.2022.5384

Abstract:
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide with a low 5‑year survival rate due to the lack of effective therapeutic strategies. Accumulating evidence has indicated that maternal embryonic leucine zipper kinase (MELK) is highly expressed in several tumors and associated with tumor development. However, the biological effects of MELK in ESCC remain unknown. In the present study, cell phenotypical experiments and animal metastasis assays were performed to detect the influence of MELK knockdown in vitro and in vivo. The potential molecular mechanism of MELK‑mediated ESCC metastasis was further investigated by western blotting and immunofluorescence staining. The results revealed that the expression of MELK in human ESCC tissues was higher than that in adjacent normal tissues and was positively associated with the poor prognosis of patients. Reducing MELK expression resulted in growth inhibition and suppression of the invasive ability of ESCC cells in vitro and in vivo. MELK inhibition induced alterations of epithelial‑mesenchymal transition‑associated proteins. Mechanistically, MELK interacted with IκB kinase (IKK) and promoted the phosphorylation of IKK, by which MELK regulated activation of the NF‑κB pathway. Collectively, the present study revealed the function and mechanism of MELK in the cell metastasis of ESCC, which may be a potential therapeutic target for ESCC.
Michal Zuzčák,
International Journal of Oncology, Volume 61, pp 1-16; https://doi.org/10.3892/ijo.2022.5383

Abstract:
Pancreatic cancer (PC) has one of the highest fatality rates and the currently available therapeutic options are not sufficient to improve its overall poor prognosis. In addition to insufficient effectiveness of anticancer treatments, the lack of clear early symptoms and early metastatic spread maintain the PC survival rates at a low level. Metabolic reprogramming is among the hallmarks of cancer and could be exploited for the diagnosis and treatment of PC. PC is characterized by its heterogeneity and, apart from molecular subtypes, the identification of metabolic subtypes in PC could aid in the development of more individualized therapeutic approaches and may lead to improved clinical outcomes. In addition to the deregulated utilization of glucose in aerobic glycolysis, PC cells can use a wide range of substrates, including branched‑chain amino acids, glutamine and lipids to fulfil their energy requirements, as well as biosynthetic needs. The tumor microenvironment in PC supports tumor growth, metastatic spread, treatment resistance and the suppression of the host immune response. Moreover, reciprocal interactions between cancer and stromal cells enhance their metabolic reprogramming. PC stem cells (PCSCs) with an increased resistance and distinct metabolic properties are associated with disease relapses and cancer spread, and represent another significant candidate for therapeutic targeting. The present review discusses the metabolic signatures observed in PC, a disease with a multifaceted and often transient metabolic landscape. In addition, the metabolic pathways utilized by PC cells, as well as stromal cells are discussed, providing examples of how they could present novel targets for therapeutic interventions and elaborating on how interactions between the various cell types affect their metabolism. Furthermore, the importance of PCSCs is discussed, focusing specifically on their metabolic adaptations.
Retraction
Huaying Dong, Wei Wang, Ru Chen, Yu Zhang, Kejian Zou, Mulin Ye, Xionghui He, Fan Zhang, Jing Han
International Journal of Oncology, Volume 61, pp 1-1; https://doi.org/10.3892/ijo.2022.5382

Abstract:
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the TUNEL assay data shown in Fig. 6C were strikingly similar to images that had already appeared in Fig. 8B in another article that appeared in the journal Oncotarget [Chen W, Xu X-K, Li J-L, Kong K-K, Li H, Chen C, He J, Wang F, Li P, Ge X-S and Li F-C: MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression. Oncotarget 8: 22783-22799, 2017]. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to International Journal of Oncology, the Editor has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors did provide an explanation to account for the duplication of the data, although this was not accepted by the Editorial Board. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 53: 1013-1026, 2018; DOI: 10.3892/ijo.2018.4467]
Shuyue Yang, Jiaxin Wang, Shidong Wang, Anni Zhou, ,
International Journal of Oncology, Volume 61, pp 1-17; https://doi.org/10.3892/ijo.2022.5381

Abstract:
Hepatocellular carcinoma (HCC) is the most common malignancy of hepatocytes accounting for 75‑85% of primary hepatic carcinoma cases. Small extracellular vesicles (sEVs), previously known as exosomes with a diameter of 30‑200 nm, can transport a variety of biological molecules between cells, and have been proposed to function in physiological and pathological processes. Recent studies have indicated that the cargos of sEVs are implicated in intercellular crosstalk among HCC cells, paratumor cells and the tumor microenvironment. sEV‑encapsulated substances (including DNA, RNA, proteins and lipids) regulate signal transduction pathways in recipient cells and contribute to cancer initiation and progression in HCC. In addition, the differential expression of sEV cargos between patients facilitates the potential utility of sEVs in the diagnosis and prognosis of patients with HCC. Furthermore, the intrinsic properties of low immunogenicity and high stability render sEVs ideal vehicles for targeted drug delivery in the treatment of HCC. The present review article summarizes the carcinogenic and anti‑neoplastic capacities of sEVs and discusses the potential and prospective diagnostic and therapeutic applications of sEVs in HCC.
Retraction
Qi Wang, Jiaqi Wang, Songtao Niu, Songsong Wang, Yibin Liu, Xiaoya Wang
International Journal of Oncology, Volume 61, pp 1-1; https://doi.org/10.3892/ijo.2022.5380

Abstract:
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that several of the panels showing flow cytometric assay data in Figs. 2D, 5D and 6E, western blotting data featured in Fig. 7, and certain of the cell migration assay data panels included in Fig. 5E and F and Fig. 6G were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to International Journal of Oncology, 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: 1884‑1896, 2019; DOI: 10.3892/ijo.2019.4759]
, Nadia Maggi, Alessandra Tozzi, Muriel Disler, Ricardo Coelho, Francis Jacob, Viola Heinzelmann‑Schwarz
International Journal of Oncology, Volume 61, pp 1-14; https://doi.org/10.3892/ijo.2022.5379

Abstract:
Poly (ADP‑ribose) polymerase (PARP)‑inhibitors (PARPi) such as olaparib and niraparib are currently used as a treatment option for BRCA‑deficient tumors and also show efficacy in platinum‑sensitive tumors. However, resistance to PARPi occurs in numerous patients and in particular acquired PARPi resistance presents a major obstacle in the treatment of these tumors. In the present study, it was investigated whether stepwise exposure of ovarian cancer cells to escalating concentrations of olaparib produced subcells with acquired resistance to PARPi and/or acquired cross‑resistance to platinum compounds, paclitaxel, and doxorubicin. To this aim, the sensitivity of fourteen ovarian cancer cell lines, including nine with TP53‑mutations and five carrying BRCA‑mutations, to olaparib and niraparib was determined and a subset of seven cell lines was selected to investigate the potential of olaparib to produce resistance. It was identified that escalating olaparib did neither produce subcells with acquired PARPi‑resistance nor did it produce acquired cross‑resistance to platinum compounds, doxorubicin, and paclitaxel. This finding was independent of the cells' TP53 and BRCA mutation status. CRISPR‑Cas9 mediated deletion of PARP1 did not affect sensitivity to PARPi, platinum compounds, doxorubicin, and paclitaxel. In addition, olaparib sensitivity correlated with niraparib sensitivity, but BRCA‑mutated cells were not more sensitive to PARPi. Moreover, PARPi sensitivity associated with cross‑sensitivity not only to platinum compounds but also to anthracylines, paclitaxel, and inhibitors of histone deacetylases. These in vitro data indicated that olaparib exposure is unlikely to produce an acquired resistance phenotype and that PARPi‑sensitive ovarian cancer cells are also cross‑sensitive to non‑platinum and even to compounds not directly interacting with the DNA.
, Johann Kern, Karen Bieback, Claudia Scherl, Nicole Rotter, Anne Lammert
International Journal of Oncology, Volume 61, pp 1-22; https://doi.org/10.3892/ijo.2022.5378

Abstract:
Immunotherapy has evolved into a powerful tool in the fight against a number of types of cancer, including head and neck squamous cell carcinomas (HNSCC). Although checkpoint inhibition (CPI) has definitely enriched the treatment options for advanced stage HNSCC during the past decade, the percentage of patients responding to treatment is widely varying between 14‑32% in second‑line setting in recurrent or metastatic HNSCC with a sporadic durability. Clinical response and, consecutively, treatment success remain unpredictable in most of the cases. One potential factor is the expression of target molecules of the tumor allowing cancer cells to acquire therapy resistance mechanisms. Accordingly, analyzing and modeling the complexity of the tumor microenvironment (TME) is key to i) stratify subgroups of patients most likely to respond to CPI and ii) to define new combinatorial treatment regimens. Particularly in a heterogeneous disease such as HNSCC, thoroughly studying the interactions and crosstalking between tumor and TME cells is one of the biggest challenges. Sophisticated 3D models are therefore urgently needed to be able to validate such basic science hypotheses and to test novel immuno‑oncologic treatment regimens in consideration of the individual biology of each tumor. The present review will first summarize recent findings on immunotherapy, predictive biomarkers, the role of the TME and signaling cascades eliciting during CPI. Second, it will highlight the significance of current promising approaches to establish HNSCC 3D models for new immunotherapies. The results are encouraging and indicate that data obtained from patient‑specific tumors in a dish might be finally translated into personalized immuno‑oncology.
Xing Huang, Yan Huang, Zheng Lv, Tao Wang, Huayi Feng, Hanfeng Wang, Songliang Du, Shengpan Wu, Donglai Shen, Chenfeng Wang, et al.
International Journal of Oncology, Volume 61, pp 1-17; https://doi.org/10.3892/ijo.2022.5377

Abstract:
Cell division cycle‑associated 5 (CDCA5) protein, which is involved in cohesion, contributes to cell cycle regulation and chromosome segregation by maintaining genomic stability. Accumulating evidence indicates that CDCA5 expression is upregulated in a number of types of cancer associated with a poor prognosis. However, the biological function of CDCA5 in clear cell renal cell carcinoma (ccRCC) remains largely unknown. In the present study, The Cancer Genome Atlas data mining revealed that CDCA5 was more highly expressed in ccRCC than in adjacent normal tissues. Importantly, such a high expression was associated with a higher risk of distant metastasis and poorer clinical outcomes. Moreover, the clinical and prognostic value of CDCA5 expression was further investigated using immunohistochemistry on tissue microarrays containing paired tumor tissues and adjacent normal tissues from 137 patients with ccRCC. Functional analyses revealed that CDCA5 knockdown significantly inhibited the proliferation and migration of ccRCC cells, and suppressed the growth of xenografts in nude mice. Mechanistically, CDCA5 knockdown induced severe DNA damage with the persistent accumulation of γ‑H2A histone family member X foci, resulting in G2/M cell cycle arrest and finally, in chromosomal instability and apoptosis. CDCA5 knockdown significantly decreased the phosphorylation levels of Stat3 and NF‑κB, suggesting that CDCA5 plays a role in regulating the inflammatory response. Collectively, the findings of the present study indicate that ccRCC cells require CDCA5 for malignant progression, and that CDCA5 inhibition may enhance the outcomes of patients with high‑risk ccRCC.
Retraction
Jianjie Zhao, Zhirong Li, Yi Chen, Shu Zhang, LingJi Guo, Bo Gao, Yan Jiang, Wuguo Tian, Shuai Hao, Xiaohua Zhang
International Journal of Oncology, Volume 61, pp 1-1; https://doi.org/10.3892/ijo.2022.5376

Abstract:
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that various panels showing the data from flow cytometry experiments in Figs. 2D, 4D and 5D, and certain of the tumor images featured in Fig. 7A, were strikingly similar to data appearing in different form in other articles by different authors. Furthermore, overlapping data panels were identified within this paper comparing the cell migration assay images between Figs. 2C and 4F. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to International Journal of Oncology, 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. [the original article was published in International Journal of Oncology 54: 315‑325, 2019; DOI: 10.3892/ijo.2018.4615]
In-Hye Ham, Lei Wang, Dagyeong Lee, Jongsu Woo, Tae Hoon Kim, Hye Young Jeong, Hye Jeong Oh, Kyeong Sook Choi, Hoon Hur
International Journal of Oncology, Volume 61, pp 1-12; https://doi.org/10.3892/ijo.2022.5375

Abstract:
The present study aimed to investigate whether the Janus‑activated kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) signaling pathway is a critical mechanism underlying the cancer‑associated fibroblast (CAF)‑induced chemoresistance of gastric cancer (GC). In addition, the present study tried to suggest a natural product to compromise the effects of CAF on the chemoresistance of GC. The results of cell proliferation assay revealed that the conditioned medium (CM) collected from CAFs further increased resistance to 5‑fluorouracil (5‑FU) in GC cell lines. Secretome analysis revealed that the levels of several secreted proteins, including C‑C motif chemokine ligand 2, C‑X‑C motif chemokine ligand 1, interleukin (IL)‑6 and IL‑8, were increased in the CM from CAFs co‑cultured with cancer cells compared to CM from cancer cells. Western blot analysis revealed that CAFs activated the JAK/STAT3 signaling pathway in cancer cells. The experimental models revealed that curcumin abrogated the CAF‑mediated activation of the JAK/STAT3 signaling pathway in GC cells. In vivo data revealed the synergistic effects of curcumin with 5‑FU treatment in xenograft GC tumors. These data strongly suggest that the suppression of the JAK/STAT3 signaling pathway counteracts the CAF‑induced chemoresistance of GC cells. It is suggested that curcumin may be a suitable natural product which may be used to overcome chemoresistance by inhibiting the CAF‑induced activation of the JAK/STAT3 signaling pathway in GC.
Back to Top Top