Lung cancer (LC) is the second most frequently diagnosed malignancy worldwide and has the highest mortality rate among all types of cancer. Despite advancements in treatment strategies, the overall survival rate for affe...Lung cancer (LC) is the second most frequently diagnosed malignancy worldwide and has the highest mortality rate among all types of cancer. Despite advancements in treatment strategies, the overall survival rate for affected individuals remains low. Ferroptosis, a form of regulated cell death characterized by iron‑dependent lipid peroxidation and accumulation of reactive oxygen species, serves a role in LC. The present review aimed to explore the dual role of ferroptosis in LC, examining both its pathological and therapeutic implications. Ferroptosis contributes to tumor progression, modulates the immune microenvironment and influences treatment resistance. Conversely, it also enhances the efficacy of immunotherapy, increases radiosensitivity and decreases chemotherapy resistance. The present study aimed to summarize the potential of ferroptosis‑based strategies, including the use of nanomaterials and combination therapy, to inform future research and therapeutic approaches.
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the TEM microscopic data featured in Fig. 3C on p. 3443, the RIP assay data in Fig. 4A and the we...Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the TEM microscopic data featured in Fig. 3C on p. 3443, the RIP assay data in Fig. 4A and the western blot data in Fig. 4D on p. 3444 were strikingly similar to data that had appeared in other articles written by different authors at different research institutes, which had either already been published before this article was received at , or were submitted for publication at around the same time (one of which has subsequently been retracted). Owing to the fact that certain of the abovementioned data had already been published prior to the receipt of this article at , the Editor has decided that this paper should be retracted from the Journal. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 40: 3438‑3446, 2018; DOI: 10.3892/or.2018.6762].
Upper tract urothelial carcinoma (UTUC), a relatively rare but highly malignant tumor arising from the renal pelvis and the urothelial layer of the ureter, accounts for 5‑10% of all urothelial malignancies. The lack of s...Upper tract urothelial carcinoma (UTUC), a relatively rare but highly malignant tumor arising from the renal pelvis and the urothelial layer of the ureter, accounts for 5‑10% of all urothelial malignancies. The lack of specific early symptoms commonly results in a delayed diagnosis, with >60% of cases being diagnosed at an advanced stage of the disease. Lymph node involvement can critically affect the clinical outcomes, thus serving as a key prognostic indicator, guiding both staging protocols and treatment strategies. Lymphadenectomy, typically performed alongside radical nephroureterectomy, not only assists in evaluating the extent of the regional metastases, but also plays a critical role in guiding both staging and treatment planning. Although several studies have suggested that a more extensive lymph node dissection (LND) can improve cancer‑specific survival and disease‑free survival rates, there is still no consensus on the optimal extent of dissection or a universally accepted surgical template. The present review aims to summarize the existing evidence on the efficacy of LND in UTUC, thus emphasizing its potential in staging, outcome prediction and possible survival benefits. The review also aims to address the challenges caused by inconsistent LND practices and the limited availability of robust prospective data. Furthermore, it discusses novel biomarkers that could improve patient classification, and proposes future research directions to improve the management of UTUC through more personalized and evidence‑driven LND strategies.
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that one of the colony‑formation assay images shown in Fig. 2D for the SKOV3 experiments was strikingly similar to the...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that one of the colony‑formation assay images shown in Fig. 2D for the SKOV3 experiments was strikingly similar to the 'SKOV3/0 µM LY294002' image shown in Fig. 5E, if one of the dishes were to be rotated 90°. Upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that the data shown for the MMP9 blot (A2780 cell line) in Fig. 4E was strikingly similar to the p‑mTOR blot (again for the A2780 cell line) in Fig. 5B, suggesting that one of these figures had been assembled incorrectly. The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 41: 917‑927, 2019; DOI: 10.3892/or.2018.6888].
Circular RNAs (circRNAs) are stable, conserved non‑coding RNA molecules with key roles in gene regulation. Because of their tissue‑specific expression patterns and involvement in various cellular processes, circRNAs are...Circular RNAs (circRNAs) are stable, conserved non‑coding RNA molecules with key roles in gene regulation. Because of their tissue‑specific expression patterns and involvement in various cellular processes, circRNAs are relevant in cancer biology, specifically for colorectal cancer (CRC) diagnosis. The present review systematically examines the roles of circRNAs in CRC pathogenesis and their potential as diagnostic biomarkers and therapeutic targets for CRC, focusing on the key circRNAs involved in CRC development and progression, their molecular mechanisms and clinical value, as well as advances in circRNA‑based therapeutic strategies and challenges in the clinical translation of circRNA application.
5‑Fluorouracil (5‑FU), a cornerstone chemotherapeutic agent used for colorectal cancer therapy, has long been established as a first‑line treatment. However, clinical evidence has suggested that a substantial proportion...5‑Fluorouracil (5‑FU), a cornerstone chemotherapeutic agent used for colorectal cancer therapy, has long been established as a first‑line treatment. However, clinical evidence has suggested that a substantial proportion of patients develop resistance to 5‑FU, notably compromising its therapeutic efficacy. The present study aimed to investigate whether loperamide (LOP) can enhance the sensitivity of colorectal cancer cells to 5‑FU and to elucidate the potential underlying molecular mechanism. First, the IC values of LOP were determined in the 5‑FU‑sensitive HCT8 and 5‑FU‑resistant HCT8R colorectal cancer cell lines, using the Cell Counting Kit‑8 assay to evaluate LOP‑induced alterations in 5‑FU sensitivity. The effects of LOP on cell proliferation were subsequently analyzed using 5‑ethynyl‑2'‑deoxyuridine and colony formation assays. Cell migration was assessed through wound healing and Transwell migration assays, and apoptosis was evaluated using flow cytometric analysis with PI/Annexin V staining. Western blot analysis was performed to measure the expression levels of the autophagy‑associated proteins microtubule‑associated protein 1 light chain 3 (LC3) and Beclin, and autophagosome formation following LOP treatment was visualized. The role of autophagy in LOP‑mediated reversal of drug resistance was further examined using autophagy inhibitors. Finally, xenograft experiments in nude mice were performed to investigate the effects of LOP on the 5‑FU sensitivity of HCT8R cells. Compared with in the parental cell line, HCT8R cells exhibited enhanced migratory capabilities and resistance to 5‑FU. Notably, LOP was revealed to potentiate the sensitivity of HCT8R cells to 5‑FU, as evidenced by reduced rates of cell proliferation, suppressed migratory ability, increased levels of apoptosis, and decreased tumor weight and volume in subcutaneous xenografts in mice. LOP was also shown to induce upregulation of autophagy marker proteins, leading to the accumulation of autophagosomes within the cells. Blocking autophagy with 3‑methyladenine led to a reversal of the inhibitory effect of LOP on HCT8R cell migration. LOP was also shown to enhance the sensitivity of HCT8R cells to 5‑FU by activating cellular autophagy, thereby suppressing resistant cell proliferation and migration, promoting apoptosis and reversing drug resistance. Taken together, these findings provide novel insights into the mechanisms underlying 5‑FU resistance, thereby highlighting potential therapeutic strategies for colorectal cancer.
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Figs. 2D and 4C, several of the panels appeared to show simila...Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Figs. 2D and 4C, several of the panels appeared to show similar groupings of dots, which would not have been anticipated if these experiments had been performed discretely under different experimental conditions, suggesting a fundamental flaw either in the way in which these experiments were performed, or in how the results were outputted. The Editor of has decided that this paper 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. [Oncology Reports 37: 1227-1234, 2017; DOI: 10.3892/or.2016.5290].
Cervical cancer (CC) poses a substantial global health challenge and it ranks as the fourth most prevalent malignancy among women worldwide. Management strategies include surgical intervention, radiotherapy, chemotherapy...Cervical cancer (CC) poses a substantial global health challenge and it ranks as the fourth most prevalent malignancy among women worldwide. Management strategies include surgical intervention, radiotherapy, chemotherapy and emerging systemic treatments. Although advancements in immunotherapy and targeted therapies have been achieved, the aggressive metastatic nature of the disease, coupled with immune evasion and drug resistance, continues to limit overall survival rates. Therefore, there remains an urgent need to identify novel treatment modalities and more effective therapeutic agents. As fundamental regulators of epigenetic modifications, histone alterations serve a critical role in controlling gene expression, DNA repair mechanisms and cellular differentiation. These modifications include acetylation, methylation, phosphorylation, ubiquitination, ADP‑ribosylation and glycosylation, as well as the more recently identified lactylation and palmitoylation. By restructuring chromatin and facilitating interactions among histones, DNA and regulatory proteins, these modifications exert a substantial influence on cellular functions. Aberrant histone modifications contribute to tumorigenesis, tumor heterogeneity and resistance to conventional anticancer therapies, making them a key focus of oncological research. In recent years, therapeutic strategies targeting histone modifications have gained increasing attention in the treatment of CC. Among these epigenetic alterations, histone acetylation and deacetylation have been extensively studied, with numerous histone deacetylase inhibitors showing promise in preclinical studies. The present review explores the patterns of histone modifications in CC, emphasizing their molecular roles in tumor progression, metastasis and therapeutic resistance. Additionally, histone modification‑driven therapeutic targets are examined, laying the groundwork for future precision medicine approaches in CC treatment.
Subsequently to the publication of the above paper, the authors contacted the Editorial Office to explain that, for the Transwell migration and invasion assay experiments shown in Fig. 4 on p. 573, the data panel for the...Subsequently to the publication of the above paper, the authors contacted the Editorial Office to explain that, for the Transwell migration and invasion assay experiments shown in Fig. 4 on p. 573, the data panel for the '94T778 / Lenti‑shTYMS‑1' experiment shown in Fig. 4A was selected incorrectly. The authors have re‑examined their original data, and realize how this error occurred. The revised (and corrected) version of Fig. 4 shown on the next page. The authors sincerely apologize for the error introduced during the preparation of this figure, although they confirm that this did not grossly affect either the results or the conclusions reported in this study. They also thank the Editor of for granting them the opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 44: 565‑576, 2020; DOI: 10.3892/or.2020.7635].
Comprehensive genomic profiling (CGP) aims to assist clinicians with the diagnosis, treatment decisions and early detection of recurrence in patients with cancer. CGP using tumor tissue is widely implemented, whereas cir...Comprehensive genomic profiling (CGP) aims to assist clinicians with the diagnosis, treatment decisions and early detection of recurrence in patients with cancer. CGP using tumor tissue is widely implemented, whereas circulating tumor DNA (ctDNA) analysis is a noninvasive method that uses peripheral blood. This pilot study included eight patients with locally advanced tumors (two each of breast, lung, pancreatic, and head and neck cancers). The concordance of somatic variants with tumor tissues and paired ctDNA from pre‑ and post‑resection samples was evaluated. This study demonstrated that the overall concordance rate in all genes between tissue and postoperative blood was high (94.2%), but the concordance rate in genes with somatic variants was low (4.76%). In patient 8 with head and neck cancer, the variant was concordant between the tissue and blood after surgery. The patient was found to have a small lung tumor at 10 months after surgery, indicating recurrence in the lung. In patient 6 with pancreas cancer, the variant was concordant between the blood before and after surgery, but no recurrence was observed. In patient 5 with pancreas cancer, recurrence was identified; however, the somatic variants were not concordant between the tissue and blood. Furthermore, a case, such as patient 8, of recurrence with somatic variants matching the tissue and postoperative blood was encountered, suggesting that detecting a somatic variant in postoperative ctDNA matching the same variant in the tissue may predict recurrence. However, since the major limitation of this study was the limited sample size, subsequent studies with larger sample sizes and more extensive research designs are warranted. The study was entered in the Japan Registry of Clinical Trials (April 10, 2023; no. 072230003).
Osteopontin (OPN) is an extracellular matrix protein secreted by various types of cells, and serves multiple physiological roles such as modulating bone cell maturation, immune responses, tissue repair and regeneration....Osteopontin (OPN) is an extracellular matrix protein secreted by various types of cells, and serves multiple physiological roles such as modulating bone cell maturation, immune responses, tissue repair and regeneration. Aberrant OPN expression contributes to tumor genesis and development. This indicates that OPN serves a crucial role in tumor genesis and could serve as a potential target for tumor interventions. The present review firstly introduces the molecular structure, receptors and physiological functions of OPN. Subsequently, the present review elaborately addresses the pivotal role served by OPN, and its mechanism in tumor initiation and progression, metastasis, and drug resistance. Furthermore, the present review summarizes currently reported OPN‑based tumor intervention strategies. Lastly, the present review also provides perspectives on how to deepen the insights into the exact role of OPN in tumorigenesis, with the aim of aiding the development of novel strategies for tumor therapeutics. The present review broadens the knowledge regarding the pathophysiological role of OPN, so that novel OPN‑based cancer treatment strategies may be proposed.
Liver metastasis is a common complication in colorectal cancer (CRC), with its presence and progression significantly shortening patient survival. Therefore, a deeper understanding of the underlying mechanisms driving li...Liver metastasis is a common complication in colorectal cancer (CRC), with its presence and progression significantly shortening patient survival. Therefore, a deeper understanding of the underlying mechanisms driving liver metastasis in CRC is essential to identify more effective and actionable therapeutic targets and improve prognosis. Liver metastasis in CRC is a multifaceted and dynamic process. Tumor cells with invasive properties communicate with the surrounding microenvironment through mechanisms such as immune checkpoint molecules and cytokines, thereby establishing a supportive niche for their colonization and proliferation. Moreover, suppressive immune cells may enhance the invasiveness of tumor cells. The interplay between tumor cells and the microenvironment is an interdependent process. Targeting these interactions offers promising potential for novel therapeutic strategies. The present review outlined mechanisms of colorectal cancer liver metastasis, emphasizing the immune microenvironment's role, current treatment approaches, and future development prospects.
microRNA‑214‑3p (miRNA‑214‑3p) can be mapped to the human chromosome 1q24.3 and is ~22 nucleotides in length. It has been garnering considerable attention due to its aberrant expression profile in various different types...microRNA‑214‑3p (miRNA‑214‑3p) can be mapped to the human chromosome 1q24.3 and is ~22 nucleotides in length. It has been garnering considerable attention due to its aberrant expression profile in various different types of cancer and its apparent role in regulating tumor progression. In malignant tumors, miRNA‑214‑3p can serve as a tumor suppressor or oncogene. This can be mediated by mainly inhibiting the expression of target genes by binding to the 3'‑untranslated region of target mRNAs, thereby regulating multiple downstream cellular processes, such as cell proliferation, metastasis, invasion and apoptosis. However, the role of miRNA‑214‑3p in cancer remains unclear. Therefore, in the present review, the role of miRNA‑214‑3p in cancer was summarized, whilst analyzing its potential as a biomarker for cancer diagnosis, prognosis and response to treatment. In addition, the present review evaluates its effects on sensitivity to chemotherapy, targeted therapy and radiotherapy. The current proposed strategies for the systemic delivery of miRNA‑214‑3p in cancer were also discussed.
Intrahepatic cholangiocarcinoma (ICC) is a highly aggressive biliary cancer originating within the liver with a high incidence, high degree of malignancy and extremely poor prognosis. Protein tyrosine phosphatase 4A1 (PT...Intrahepatic cholangiocarcinoma (ICC) is a highly aggressive biliary cancer originating within the liver with a high incidence, high degree of malignancy and extremely poor prognosis. Protein tyrosine phosphatase 4A1 (PTP4A1) plays a carcinogenic role in numerous tumors. However, the role of PTP4A1 in the progression of ICC has not been fully elucidated. The aim of the present study was to clarify the function of PTP4A1 in ICC. Cell Counting Kit‑8 assay, 5‑ethynyl‑2'‑deoxyuridine staining and a cell colony formation assay were performed to detect cell proliferation and viability. Wound healing and Transwell assays were used to analyze cell migration and invasion. The interaction of PTP4A1 with phosphatase and tensin homolog (PTEN) was validated by immunofluorescence and co‑immunoprecipitation assays. Reverse transcription‑quantitative PCR, western blotting and immunohistochemistry were used to evaluate the mRNA and protein expression levels. The present study demonstrated that PTP4A1 was highly expressed and associated with invasive pathological features in ICC. Furthermore, PTP4A1 promoted ICC cell proliferation, migration and invasion both and . Mechanistically, PTP4A1 interacts with PTEN, contributes to the suppression of PTEN phosphorylation and promotes the activation of the PI3K/AKT/glycogen synthase kinase 3 alpha pathway. In addition, the present results demonstrated that the promotion of cell proliferation, migration and invasion by PTP4A1 was dependent on the regulation of the PTEN/PI3K/AKT/GSk3α pathway in ICC. Collectively, these data revealed that PTP4A1 is a promising target for ICC therapeutics.
Esophageal cancer, one of the most prevalent types of cancer worldwide, frequently exhibits distant metastases. The adipokine visfatin is implicated in cancer progression and metastasis. However, the mechanisms by which...Esophageal cancer, one of the most prevalent types of cancer worldwide, frequently exhibits distant metastases. The adipokine visfatin is implicated in cancer progression and metastasis. However, the mechanisms by which visfatin regulates motility in esophageal cancer remain unclear. Bioinformatics analysis showed levels of visfatin were higher in patients with metastatic esophageal cancer than in those with primary esophageal cancer. Cell motility assay revealed that visfatin stimulation enhanced the migration and invasion of esophageal cancer cells. Treatment with or without visfatin (30 ng/ml) in KYSE410 cells followed by miRNA sequencing, revealed that miR‑3613‑5p controlled visfatin‑induced cell motility. Further cell migration, invasion, qPCR and western blot assay shows that visfatin promoted esophageal cancer cell migration by decreasing miR‑3613‑5p expression and subsequently increasing vascular endothelial zinc finger 1/versican production. Thus, the visfatin/miR‑3613‑5p axis may be a promising target for inhibiting esophageal cancer cell migration and invasion.
Following the publication of the above article, the authors drew to the Editor's attention that, concerning the histological images shown in Fig. 5B on p. 890, two pairs of the data panels showed overlapping sections, su...Following the publication of the above article, the authors drew to the Editor's attention that, concerning the histological images shown in Fig. 5B on p. 890, two pairs of the data panels showed overlapping sections, such that these data were derived from the same original source where the panels were intended to show the results from differently performed experiments. Upon examining their original data, the authors realized that inadvertent errors were made in assembling the data in this figure. The corrected version of Fig. 5, now showing replacement data for the liver and lung images in Fig. 5B, is shown on the next page. Note that this error did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Oncology Reports 36: 886‑892, 2016; DOI: 10.3892/or.2016.4866].
Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, exhibits diverse biological activities and notable antitumor properties. Lung cancer (LC), a leading malignancy of the respiratory system, is predomi...Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, exhibits diverse biological activities and notable antitumor properties. Lung cancer (LC), a leading malignancy of the respiratory system, is predominantly classified into small cell LC and non‑small cell LC. The increasing incidence and mortality rates of LC have spurred considerable interest in the chemo‑preventive potential of UA. Accumulating evidence demonstrates that UA markedly inhibits LC cell proliferation and induces apoptosis. Mechanistically, UA induces cell cycle arrest at the G0/G1 phase, thereby suppressing LC cell invasion, migration and tumor growth. Furthermore, UA has shown synergistic effects when combined with other therapeutic agents, including mitotic kinase inhibitors and multifunctional nanomedicines, effectively overcoming drug resistance in LC cells. These multifaceted mechanisms collectively contribute to the chemo‑preventive efficacy of UA against LC. Consequently, UA represents a promising candidate for LC prevention and therapy. The present review comprehensively summarizes the anticancer effects and molecular mechanisms of UA in LC, offering insights to guide future research and facilitate the development of innovative therapeutic strategies.
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell migration and invasion assay experiments shown in Fig. 3C and D on p. 1791, two pairs of the d...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell migration and invasion assay experiments shown in Fig. 3C and D on p. 1791, two pairs of the data panels appeared to be overlapping, suggesting that the same data may have been used in this figure to represent data that were intended to show the results from differently performed experiments. Although the authors responded to the original emailed request from the Editorial Office concerning these data and repeated the experiments shown in this figure, upon performing an independent analysis of the original (published) figures in the office, it came to light that Figs. 1 and 4 also contained probable anomalies. In Fig. 1C and D, there were cells/small areas of the images located in the bottom left hand corners of the images that were strikingly similar, to the extent that this would have been difficult to attribute to coincidence. Furthermore, in the case of Fig. 4, the gel slices in Fig. 4B showed evidence of possible cutting‑and‑splicing events. Owing to the fact that these probable anomalies were also identified that could have affected the interpretation of two additional figures in the published article, the Editor of has decided that this paper should be retracted from the Journal due to 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. [Oncology Reports 34: 1787‑1794, 2015; DOI: 10.3892/or.2015.4143].
Cancer has become one of the leading causes of death in most countries. While immune checkpoint inhibitors (ICIs) have revolutionized cancer therapeutics by harnessing antitumor immunity, their clinical application is co...Cancer has become one of the leading causes of death in most countries. While immune checkpoint inhibitors (ICIs) have revolutionized cancer therapeutics by harnessing antitumor immunity, their clinical application is constrained by intrinsic resistance in most patients and limited responsiveness across specific tumor types. Rational combination strategies may enhance therapeutic outcomes. Antibody‑drug conjugates (ADCs) are an optimal therapeutic partner for synergistic combination with ICIs. ADCs enhance ICI efficacy by inducing immunogenic cell death, which activates tumor‑specific immune responses, remodeling the immunosuppressive tumor microenvironment, and amplifying ICI‑mediated immune cell activation. ADC‑ICI combinations have encouraging antitumor activity across multiple types of solid malignancies. The present review systematically evaluates the synergistic potential of ADC and ICI combination in solid tumor management.
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot data shown in Figs. 1C and 5C on p. 2186 and p. 2188 respectively were strikingly sim...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot data shown in Figs. 1C and 5C on p. 2186 and p. 2188 respectively were strikingly similar to data that had already been published in articles written by different authors at different research institutes, or which had been included in articles that were already under consideration for publication. Upon investigating this matter independently in the Editorial Office, we were able to confirm the reader's concerns. Therefore, due to the fact that the contentious western blot 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. [Oncology Reports 32: 2183‑2190, 2014; DOI: 10.3892/or.2014.3423].