Wen L, Zhang J, Ju B
… +7 more, Ran Z, Zhang H, Liao Y, Cao L, Hou Q, Hu J, Yang J
Int J Oncol
· 2025 Jun · PMID 40341416
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Oxaliplatin (OXA) is a first‑line chemotherapy agent for hepatocellular carcinoma (HCC); however, its application is hindered by low therapeutic sensitivity and severe adverse effects. Acteoside (ACT) has both antitumor...Oxaliplatin (OXA) is a first‑line chemotherapy agent for hepatocellular carcinoma (HCC); however, its application is hindered by low therapeutic sensitivity and severe adverse effects. Acteoside (ACT) has both antitumor and hepatoprotective properties. Therefore, the present study investigated the mechanisms underlying the synergistic and toxicity‑reducing effects of ACT as an adjuvant to OXA in HCC therapy. Liver cancer cell lines and a xenograft mouse model were treated with ACT and/or OXA. Cell Counting kit‑8, Transwell invasive assay, wound healing assay, cell cycle and apoptosis detection assays assessed cell viability, migration, invasion, cell cycle progression and apoptosis to evaluate the synergistic effects of the combination therapy. studies examined tumor growth, cell proliferation, survival time and blood biochemical indices. The effects of ACT on OXA‑induced toxicity were also evaluated. Transcriptomics and metabolomics analyses were integrated to elucidate the mechanisms by which ACT enhances OXA efficacy and mitigates its toxicities. The results revealed that ACT synergized with OXA to inhibit HCC progression both and . ACT significantly alleviated OXA‑induced toxicity, particularly neurotoxicity. Mechanistically, phosphatidylinositol signaling system‑associated genes/proteins exerted important roles in the anti‑HCC effects of ACT. Western blotting revealed that ACT‑induced upregulation of INPP4B inhibited the PI3K/AKT signaling pathway, which may underlie its ability to enhance the therapeutic efficacy of OXA and reduce its toxic effects. In conclusion, ACT enhanced efficacy and reduced the toxicity of OXA in the treatment of HCC, potentially via the regulation of INPP4B to inhibit the PI3K/AKT signaling pathway.
Wang HY, Tu YS, Long J
… +5 more, Zhang HQ, Qi CL, Xie XB, Li SH, Zhang YJ
Int J Oncol
· 2025 Jun · PMID 40341375
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Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 1A and Fig. 3A and B showing the results of Transwell invasion and migration experiments, the majority o...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 1A and Fig. 3A and B showing the results of Transwell invasion and migration experiments, the majority of the data panels were identified as having overlapping sections, such that the affected data panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original sources. Owing to the large number of duplications of data that have been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 47: 641‑649, 2015; DOI: 10.3892/ijo.2015.3034].
Int J Oncol
· 2025 May · PMID 40314093
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Lymphoma is a malignancy of the immune system, which originates from lymphatic tissues and lymph nodes. Diffuse large B‑cell lymphoma (DLBCL) is a common type of non‑Hodgkin lymphoma, occurring in 30‑40% of all cases, wh...Lymphoma is a malignancy of the immune system, which originates from lymphatic tissues and lymph nodes. Diffuse large B‑cell lymphoma (DLBCL) is a common type of non‑Hodgkin lymphoma, occurring in 30‑40% of all cases, which has persistent clinical challenges. The treatment of DLBCL is challenging due to its diverse genetic and biological characteristics and complex clinical physiology. Despite advancements in overall prognosis, 20‑25% of patients continue to experience relapse and 10‑15% of patients experience refractory disease. Vitamin C is a water‑soluble vitamin with antioxidant properties and notable pharmacological activity, with potential applications in cancer therapy. Pharmacological doses of vitamin C (1‑4 g/kg) can induce apoptosis in malignant cells by inhibiting and/or reversing gene mutations that are associated with hematological malignancies. For example, 10‑25% of patients with myeloid malignancies have tet methylcytosine dioxygenase 2 (TET2) gene mutations and vitamin C can regulate blood stem cell frequency and leukemia production by enhancing TET2 function. Consequently, pharmacological doses of vitamin C can inhibit the development and progression of hematological malignancies. Therefore, the present review aimed to investigate the role of vitamin C in the pathophysiology and treatment of DLBCL, whilst highlighting the potential challenges and future perspectives.
Gil EY, Jo UH, Jeong H
… +9 more, Whang YM, Woo OH, Cho KR, Seo JH, Kim A, Lee ES, Koh I, Kim YH, Park KH
Int J Oncol
· 2025 May · PMID 40242973
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Following the publication of this paper, and a corrigendum that was subsequently published to take account of anomalies that were identified with the assembly of western blot data in Fig. 5B (doi: 10.3892/ijo.2017.3900),...Following the publication of this paper, and a corrigendum that was subsequently published to take account of anomalies that were identified with the assembly of western blot data in Fig. 5B (doi: 10.3892/ijo.2017.3900), a concerned reader drew to the Editor's attention that, regrettably, there remained possible issues with the duplication of data in the revised version of Fig. 5 provided by the authors in the Corrigendum; in addition, potential anomalies were also noted with the western blot assay data in the originally published versions of Fig. 2A and B. After having performed an independent review of the data in these figures in the Editorial Office, the concerns of the reader were found to be validated. Therefore, the Editor of has decided that this paper should now 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. [International Journal of Oncology 41: 611‑620, 2012; DOI: 10.3892/ijo.2012.1470].
Chen Y, Zhang Y, Yang H
… +7 more, Liu Q, Sui R, Shi J, Liang H, Liu J, Xu H, Piao H
Int J Oncol
· 2025 May · PMID 40242972
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Glioblastoma (GBM) is a disease with high morbidity and poor prognosis. The combination of traditional Chinese and Western medicine and cuproptosis are known to serve important roles in the treatment of GBM. However, tar...Glioblastoma (GBM) is a disease with high morbidity and poor prognosis. The combination of traditional Chinese and Western medicine and cuproptosis are known to serve important roles in the treatment of GBM. However, targeting cuproptosis to treat GBM by combining traditional Chinese and Western medicine has not been extensively investigated. Therefore, the present study focused on the diagnosis and treatment of GBM based on cuproptosis. Through a bioinformatics approach, a cuproptosis‑related prognostic model was first constructed. Next, this prognostic model was found to be closely related to immune infiltration, DNA mutation and DNA methylation through multi‑omics analysis. The present study indicated the cell clusters in GBM tissues and the risk scores in each cluster based on single‑cell sequencing data derived from Gene Expression Omnibus. Notably, by screening the CellMiner database, EMD‑1204831 was found to exhibit a high correlation with the risk score. Next, through network pharmacology and molecular docking analysis, the risk score‑related gene collagen type XXII α1 chain (COL22A1) was identified as the target of kaempferol, which is the active component of Ginseng. Notably, kaempferol could decrease the proliferation of GBM cells by inhibiting COL22A1 expression in cell experiments. Finally, kaempferol and EMD‑1204831 had an obvious inhibitory effect on the growth of GBM and sensitized GBM to cuproptosis inducers via COL22A1 in cell and animal experiments. Overall, the present study revealed a cuproptosis‑related combined regimen for GBM.
Chen F, Qi S, Zhang X
… +3 more, Wu J, Yang X, Wang R
Int J Oncol
· 2025 May · PMID 40183411
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Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the immunofluorescence assay data shown in Figs. 3C on p. 1189 and 4E on p. 1190 were strikingly simil...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the immunofluorescence assay data shown in Figs. 3C on p. 1189 and 4E on p. 1190 were strikingly similar to data appearing in different form in another pair of articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to . Given that the abovementioned data had already apparently been published previously, the Editor of has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 54: 1183-1194, 2019; DOI: 10.3892/ijo.2019.4707].
Sun MX, Zhu HC, Yu Y
… +6 more, Yao Y, Li HY, Feng FB, Wang QY, Liu RJ, Sun CG
Int J Oncol
· 2025 May · PMID 40145557
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The focus on breast cancer treatment has shifted from the cytotoxic effects of single drugs on tumor cells to multidimensional multi‑pathway synergistic intervention strategies targeting the tumor microenvironment (TME)....The focus on breast cancer treatment has shifted from the cytotoxic effects of single drugs on tumor cells to multidimensional multi‑pathway synergistic intervention strategies targeting the tumor microenvironment (TME). The activation of the Wnt signaling pathway in the TME of breast cancer cells serves a key regulatory role in tissue homeostasis and is a key driver of the carcinogenic process. Modulating the crosstalk between the Wnt pathway and TME of breast cancer is key for understanding the biological behavior of breast cancer and advancing the development of novel antitumor drugs. The present review aimed to summarize the complex mechanisms of the Wnt signaling pathway in the breast cancer TME, interactions between the Wnt signaling pathway and components of the breast cancer TME and breast cancer‑associated genes, as well as the interactions between the Wnt signaling pathway and other signaling cascades at the molecular level. Furthermore, the present review aimed to highlight the unique advantages of the Wnt signaling pathway in the macro‑regulation of the TME and the current therapeutic strategies targeting the Wnt signaling pathway, their potential clinical value and future research directions in breast cancer treatment.
Li J, Li Y, Fu L
… +7 more, Chen H, Du F, Wang Z, Zhang Y, Huang Y, Miao J, Xiao Y
Int J Oncol
· 2025 May · PMID 40116120
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The emergence of resistance to antitumor drugs in cancer cells presents a notable obstacle in cancer therapy. Metabolic reprogramming is characterized by enhanced glycolysis, disrupted lipid metabolism, glutamine depende...The emergence of resistance to antitumor drugs in cancer cells presents a notable obstacle in cancer therapy. Metabolic reprogramming is characterized by enhanced glycolysis, disrupted lipid metabolism, glutamine dependence and mitochondrial dysfunction. In addition to promoting tumor growth and metastasis, metabolic reprogramming mediates drug resistance through diverse molecular mechanisms, offering novel opportunities for therapeutic intervention. Non‑coding RNAs (ncRNAs), a diverse class of RNA molecules that lack protein‑coding function, represent a notable fraction of the human genome. Due to their distinct expression profiles and multifaceted roles in various cancers, ncRNAs have relevance in cancer pathophysiology. ncRNAs orchestrate metabolic abnormalities associated with drug resistance in cancer cells. The present review provides a comprehensive analysis of the mechanisms by which metabolic reprogramming drives drug resistance, with an emphasis on the regulatory roles of ncRNAs in glycolysis, lipid metabolism, mitochondrial dysfunction and glutamine metabolism. Furthermore, the present review aimed to discuss the potential of ncRNAs as biomarkers for predicting chemotherapy responses, as well as emerging strategies to target ncRNAs that modulate metabolism, particularly in the context of combination therapy with anti‑cancer drugs.
Wang Y, Guo W, Li Z
… +17 more, Wu Y, Jing C, Ren Y, Zhao M, Kong L, Zhang C, Dong J, Shuang Y, Sun S, Chen J, Wu C, Qiao Y, Qu X, Wang X, Zhang L, Jin R, Zhou X
Int J Oncol
· 2025 May · PMID 40116088
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Following the publication of the above paper, and a corrigendum that has already been published (doi.org/10.3892/ijo.2023.5528) to attend to errors that were made in the assembly of Figs. 2 and 8, it was drawn to the Edi...Following the publication of the above paper, and a corrigendum that has already been published (doi.org/10.3892/ijo.2023.5528) to attend to errors that were made in the assembly of Figs. 2 and 8, it was drawn to the Editor's attention by a concerned reader that two pairs of data panels featuring overlapping data existed comparing Figs. 1C and 2D in the above paper with Fig. 2 in a paper published in the journal , which was published before the above paper had been submitted, even though this earlier paper did contain many of the same authors. Given that this further issue has come to light, and owing to the number of duplications of data and errors made in assembling figures that have now been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the originally 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 52: 1149‑1164, 2018; DOI: 10.3892/ijo.2018.4293].
Yan H, He Q, Gao Y
… +5 more, He X, Luo H, Shao L, Dong J, Li F
Int J Oncol
· 2025 May · PMID 40084702
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Lactate and protein lactylation serve a key role in tumor pathogenesis. Solute carrier 4A7 (SLC4A7), a key transporter, participates in cellular acid homeostasis. However, its impact on lactate transport and protein lact...Lactate and protein lactylation serve a key role in tumor pathogenesis. Solute carrier 4A7 (SLC4A7), a key transporter, participates in cellular acid homeostasis. However, its impact on lactate transport and protein lactylation in solid tumors, particularly lung adenocarcinoma (LUAD), remains largely unexplored. In the present study, lactylome analysis, Transwell and wound healing assay, animal experiments were conducted to validate functional regulation mediated by SLC4A7 in LUAD. SLC4A7 inhibited tumor progression, including metastasis, invasion and proliferation. Mechanistically, SLC4A7 decreased both intracellular and extracellular lactate accumulation and inhibited overall protein lactylation, as confirmed by lactylome analysis. Analyzing the lactylome revealed that SLC4A7 suppressed lysine lactylation of numerous genes like HSP90AA1 and pathways such as focal adhesion associated with carcinogenesis. Additionally, low expression levels of SLC4A7 in LUAD cancer stem cells were validated using tumor tissue samples from patients with LUAD. Moreover, the inhibitory role of SLC4A7 in regulating tumor stemness was verified. Collectively, the present results uncovered the inhibitory effect exerted by SLC4A7 on tumor progression via its regulation of lactate transport, protein lactylation and stemness properties. Targeting SLC4A7 may hold promise as a novel therapeutic strategy for LUAD.
Liu K, Bie J, Zhang R
… +6 more, Xiong R, Peng L, Luo Y, Yang S, Feng G, Song G
Int J Oncol
· 2025 Apr · PMID 40084687
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Cisplatin is one of the principal chemotherapeutic agents used for esophageal cancer (EC) treatment; however, EC mortality remains high. It is therefore imperative to find new therapeutic targets and approaches to potent...Cisplatin is one of the principal chemotherapeutic agents used for esophageal cancer (EC) treatment; however, EC mortality remains high. It is therefore imperative to find new therapeutic targets and approaches to potentiate the chemotherapeutic efficacy of cisplatin. Angiotensin II receptor type 1 (AGTR1) is a potential therapeutic target in multiple cancer types. In the present study, RNA‑sequencing analysis of EC and normal esophageal tissues was performed and AGTR1 was identified as a differentially expressed gene that is markedly downregulated in recurrent and metastasized EC. AGTR1 upregulation in the esophageal squamous cell carcinoma cell lines, KYSE‑150 and EC109, promoted their chemosensitivity to cisplatin both and . Additionally, AGTR1 suppressed the metastasis‑relevant traits of EC cells, as evidenced by the reduced migration, invasion and wound healing of EC cells with higher AGTR1 expression levels. Moreover, AGTR1 overexpression in EC cells upregulated intracellular Ca levels, reduced ATP levels and mitochondrial membrane potentials, which was accompanied by enhanced mitochondrial pathway apoptosis. Notably, either AGTR1 overexpression or treatments with the calcium channel blocker, fendiline, caused Ca influx and promoted mitochondria‑dependent apoptosis in KYSE‑150 cells . These effects were augmented when both AGTR1 overexpression and fendiline stimulation were imposed in the absence or presence of cisplatin treatments. Furthermore, fendiline administration enhanced the chemosensitivity of cisplatin in an EC xenograft mouse model. Collectively, these findings offer an alternative treatment option and provide mechanistic insights into using fendiline to potentiate the chemotherapy efficacy of cisplatin in treating EC.
Int J Oncol
· 2025 Apr · PMID 40052577
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Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that a pair of data panels (namely, the A549T‑eto/FERO, 1 mM and FERO, 12 h panels) in the cell viability experiments...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that a pair of data panels (namely, the A549T‑eto/FERO, 1 mM and FERO, 12 h panels) in the cell viability experiments shown in Fig. 1B on p. 1235 were partially overlapping, where the data had apparently been derived from the same original source. After having performed an independent review of the data in the Editorial Office, also in Fig. 1B, another pair of overlapping data panels were identified; moreover, strikingly similar data for the α‑P‑glycoprotein blots had been included in different figures (Figs. 1C and 3B), and there appeared to be a splicing event/break in the continuity of the α‑actin bands shown for the control data in Figs. 1C and 3B that wasn't apparent elsewhere for the proteins of interest shown in these figure parts. Owing to these possible anomalies and the duplications of the data that have been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 44: 1233‑1242, 2014; DOI: 10.3892/ijo.2014.2297].
Shangguan F, Ma N, Chen Y
… +5 more, Zheng Y, Ma T, An J, Lin J, Yang H
Int J Oncol
· 2025 Apr · PMID 40052552
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Pancreatic cancer (PC) is one of the most malignant tumors, with a 5‑year survival rate <10%. Chemosynthetic drugs are widely used in the treatment of PC; however, their toxicity and side effects often reduce the quality...Pancreatic cancer (PC) is one of the most malignant tumors, with a 5‑year survival rate <10%. Chemosynthetic drugs are widely used in the treatment of PC; however, their toxicity and side effects often reduce the quality of life for patients. MTT and colony formation assay were performed to detect cell growth and viability in PC cells. Levels of ROS in whole cell and mitochondria were analyzed through flow cytometry. ATP production was evaluated using an ATP Assay Kit. Cellular bioenergetics were analyzed with a Seahorse XFe96 Analyzer, and changes in target molecules were monitored by western blotting. The present study reports that fucoxanthin (FX), a carotenoid derived from aquatic brown seaweed, significantly inhibits PC by inhibiting cell proliferation and inducing cell death via the non‑classical pathway. FX switches mitochondrial respiration to aerobic glycolysis in PC cells. Furthermore, FX decreases whole‑cell ATP levels, which indicates that promotion of glycolysis does not compensate for FX‑induced ATP depletion in mitochondria. Moreover, FX decreased the reduced glutathione/oxidized glutathione ratio observed under glucose‑limited conditions. These alterations caused by FX may decrease metabolic flexibility, indicating higher sensitivity to glucose‑limited (GL) conditions. FX increased the cytotoxicity of cisplatin (DDP) and the expression of solute carrier family 31 member 1 (SLC31A1) in PC cells. Furthermore, the knockdown of SLC31A1 can attenuate cytotoxicity caused by the combination of FX and DDP. It was inferred that FX increased the sensitivity of PC cells to DDP), potentially by upregulating SLC31A1 expression. In conclusion, FX exhibited potent antitumor effects by reprogramming energy metabolism and inducing a distinct form of regulated cell death. Therefore, combining FX with GL treatment or DDP presents a promising therapeutic strategy for PC.
Hou R, Wu X, Wang C
… +7 more, Fan H, Zhang Y, Wu H, Wang H, Ding J, Jiang H, Xu J
Int J Oncol
· 2025 Apr · PMID 40017131
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Cancer is the second leading cause of death among humans worldwide. Despite remarkable improvements in cancer therapies, drug resistance remains a significant challenge. The tumor microenvironment (TME) is intimately ass...Cancer is the second leading cause of death among humans worldwide. Despite remarkable improvements in cancer therapies, drug resistance remains a significant challenge. The tumor microenvironment (TME) is intimately associated with therapeutic resistance. Tumor‑associated neutrophils (TANs) are a crucial component of the TME, which, along with other immune cells, play a role in tumorigenesis, development and metastasis. In the current review, the roles of TANs in the TME, as well as the mechanisms of neutrophil‑mediated resistance to cancer therapy, including immunotherapy, chemotherapy, radiotherapy and targeted therapy, were summarized. Furthermore, strategies for neutrophil therapy were discussed and TANs were explored as potential targets for cancer treatment. In conclusion, the need to explore the precise roles, recruitment pathways and mechanisms of action of TANs was highlighted for the purpose of developing therapies that precisely target TANs and reverse drug resistance.
Dai C, Qianjiang H, Fu R
… +3 more, Yang H, Shi A, Luo H
Int J Oncol
· 2025 Apr · PMID 40017127
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Long non‑coding RNAs (lncRNAs) are key players in the regulation of gene expression by mediating epigenetic and epitranscriptomic modification. Dysregulation of lncRNAs is implicated in tumor initiation, progression and...Long non‑coding RNAs (lncRNAs) are key players in the regulation of gene expression by mediating epigenetic and epitranscriptomic modification. Dysregulation of lncRNAs is implicated in tumor initiation, progression and metastasis. lncRNAs modulate chromatin structure and gene transcription by recruiting epigenetic regulators, including DNA‑ or histone‑modifying enzymes. Additionally, lncRNAs mediate chromatin remodeling and enhancer‑promoter long‑range chromatin interactions to control oncogene expression by recruiting chromatin organization‑associated proteins, thereby promoting carcinogenesis. Furthermore, lncRNAs aberrantly induce oncogene expression by mediating epitranscriptomic modifications, including RNA methylation and RNA editing. The present study aimed to summarize the regulatory mechanisms of lncRNAs in cancer to unravel the complex interplay between lncRNAs and epigenetic/epitranscriptomic regulators in carcinogenesis. The present review aimed to provide a novel perspective on the epigenetic and epitranscriptomic roles of lncRNAs in carcinogenesis to facilitate identification of potential biomarkers and therapeutic targets for cancer diagnosis and treatment.
Zheng Y, Wang K, Mao W
… +4 more, Zhang G, Han X, Li H, Wang Y
Int J Oncol
· 2025 Apr · PMID 39981934
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Non‑small cell lung cancer (NSCLC) exhibits a high incidence and mortality rate worldwide. Elevated cytokinesis cyclin 25 homologous protein C (CDC25C) expression is correlated with a poor prognosis in patients with NSCL...Non‑small cell lung cancer (NSCLC) exhibits a high incidence and mortality rate worldwide. Elevated cytokinesis cyclin 25 homologous protein C (CDC25C) expression is correlated with a poor prognosis in patients with NSCLC. Transcriptional regulation and post‑transcriptional modification are critical mechanisms governing gene expression, with aberrations in these processes increasingly recognized as pivotal contributors to cancer pathogenesis. The present study elucidated that the transcriptional activator, signal transducer and activator of transcription 3, directly interacts with the CDC25C promoter, thereby modulating its expression. Moreover, multi‑omics analysis was employed to identify the genes involved in the N6‑methyladenosine (mA) methylation‑mediated post‑transcriptional regulation of CDC25C. The findings indicated that downregulation of alkB homolog 5 RNA demethylase in NSCLC leads to a marked increase in the mA modification of CDC25C mRNA. It was also shown that YTH N6‑methyladenosine RNA binding protein (YTHDF) 3 and YTHDF2 compete to bind to CDC25C mRNA, thereby promoting or inhibiting its expression. Thus, the present study revealed that dysregulated expression of the CDC25C gene in NSCLC is influenced by multifaceted regulatory layers encompassing both transcriptional and post‑transcriptional mechanisms.
Li Z, Deng L, Cheng M
… +4 more, Ye X, Yang N, Fan Z, Sun L
Int J Oncol
· 2025 Mar · PMID 39981904
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Liver metastasis is the leading cause of colorectal cancer (CRC)‑related mortality. Microbiota dysbiosis serves a role in the pathogenesis of colorectal liver metastases. Bile acids (BAs), cholesterol metabolites synthes...Liver metastasis is the leading cause of colorectal cancer (CRC)‑related mortality. Microbiota dysbiosis serves a role in the pathogenesis of colorectal liver metastases. Bile acids (BAs), cholesterol metabolites synthesized by intestinal bacteria, contribute to the metastatic cascade of CRC, encompassing colorectal invasion, migration, angiogenesis, anoikis resistance and the establishment of a hepatic pre‑metastatic niche. BAs impact inflammation and modulate the immune landscape within the tumor microenvironment by activating signaling pathways, which are used by tumor cells to facilitate metastasis. Given the widespread distribution of BA‑activated receptors in both tumor and immune cells, strategies aimed at restoring BA homeostasis and blocking metastasis‑associated signaling are of importance in cancer therapy. The present study summarizes the specific role of BAs in each step of colorectal liver metastasis, elucidating the association between BA and CRC progression to highlight the potential of BAs as predictive biomarkers for colorectal liver metastasis and their therapeutic potential in developing novel treatment strategies.
Int J Oncol
· 2025 Apr · PMID 39981901
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Malignant tumors are non-communicable diseases that impact human health and quality of life. Identifying and targeting the underlying genetic drivers is a challenge. Heme oxygenase-1 (HO-1), a stress-inducible enzyme als...Malignant tumors are non-communicable diseases that impact human health and quality of life. Identifying and targeting the underlying genetic drivers is a challenge. Heme oxygenase-1 (HO-1), a stress-inducible enzyme also known as heat shock protein 32, plays a crucial role in maintaining cellular homeostasis. It mitigates oxidative stress-induced damage and exhibits anti-apoptotic properties. HO-1 is expressed in a wide range of malignancies and is associated with tumor growth. However, the precise role of HO-1 in tumor development remains controversial. Drugs, both naturally occurring and chemically synthesized, can inhibit tumor growth by modulating HO-1 expression in cancer cells. The present review aimed to discuss biological functions of HO-1 pharmacological therapies targeting HO-1.
Zhang C, Xu W, Pan W
… +6 more, Wang N, Li G, Fan X, Xu X, Shen S, Das UN
Int J Oncol
· 2025 Apr · PMID 39981900
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Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the flow cytometric plots shown in Fig. 9A on p. 1628, a pair of data panels showed a surprisingly high leve...Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the flow cytometric plots shown in Fig. 9A on p. 1628, a pair of data panels showed a surprisingly high level of partially overlapping data, given that the results from differently performed experiments were intended to have been shown in these figure parts. Upon performing an independent analysis of the data in this paper, a series of further issues concerning the data were noted; first in Fig. 9B, a separate pair of flow cytometric plots appeared to have been duplicated in their entireties. In addition, two pairs of data panels in Fig. 6A and B (showing the senescence of gastric cancer cells) contained overlapping sections of data; the control panels for the migration assay data in Fig. 7A and B were overlapping, albeit the orientation of the overlapping data sections was different. Owing to the large number of duplications of data, and other potential anomalies, 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 42: 1620‑1629, 2013; DOI: 10.3892/ijo.2013.1850].
Int J Oncol
· 2025 Mar · PMID 39981889
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Malignant mesothelioma (MM) is a rare but aggressive cancer linked to asbestos exposure and characterized by advanced‑stage disease at presentation. Despite advances in treatment, prognosis remains abysmal, highlighting...Malignant mesothelioma (MM) is a rare but aggressive cancer linked to asbestos exposure and characterized by advanced‑stage disease at presentation. Despite advances in treatment, prognosis remains abysmal, highlighting the imperative for the development of novel biomarkers and treatment approaches. Telomere biology plays a pivotal role in the tumorigenic process and has emerged as a key area in oncology research. Short telomeres have been associated with genomic instability, and substantially shorter telomere length (TL) has been identified in MM, showcasing the potential of TL in risk assessment, early detection, and disease progression monitoring. MM predominantly maintains TL through telomerase activity (TA), which in research has been identified in >90% of MM cases, underscoring the potential of TA as a biomarker in MM. Telomerase reverse transcriptase (TERT) polymorphisms may serve as valuable biomarkers, with research identifying associations between single nucleotide polymorphisms (SNPs) and the risk and prognosis of MM. Additionally, TERT promoter mutations have been associated with poor prognosis and advanced‑stage disease, with the non‑canonical functions of TERT hypothesized to contribute to the development of MM. TERT promoter mutations occur in ~12% of MM cases; C228T, C250T and A161C are the most common, while the distribution and frequency differ depending on histological subtype. Research reveals the promise of the various approaches therapeutically targeting telomerase, with favorable results in pre‑clinical models and inconclusive findings in clinical trials. The present review examines the role of telomere biology in MM and its implications in diagnosis, prognosis, and therapy.