International journal of oncology最新文献

Following the publication of the above article, an interested reader drew to the authors' attention that certain of the in vitro image panels shown in Fig. 3B (featuring the effects of adding five different concentrations of omeprazole on acridine orange/ethidium bromide‑stained HCA‑7 cells) and Fig. 4 (showing western blotting experiments) on p. 173 and 174 respectively contained overlapping data panels, where results that were intended to represent the results of differently performed experiments had apparently been derived from the same original sources. Specifically, the image panels for 0 and 50 µM/ml omeprazole (Fig. 3Ba and Bb), and 100 and 200 µM/ml omeprazole (Fig. 3Bc and Bd), in Fig. 3B were strikingly similar; and the bands shown for p21 and cyclin A in Fig. 4A and B respectively were also similar, albeit each set of protein bands were turned through 180° relative to the other. After having examined their original data, the authors realized that these figures had been inadvertently assembled incorrectly. The revised versions of Figs. 3 (showing the data correctly for the 0, 100 and 300 µM/ml omeprazole experiments) and 4 (with the cyclin A data omitted) are shown on the next page. Note that the edits made to these figures do not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of International Journal of Oncology for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 40: 170‑175, 2012; DOI: 10.3892/ijo.2011.1214].

Metastatic hepatocellular carcinoma (HCC) seriously threatens patients' prognosis. It was previously suggested that the insulin growth factor binding protein (IGFBP) family could serve as cancer suppressors in the development and metastasis of HCC. However, the role of IGFBP4 and its underlying molecular mechanism in HCC metastasis is elusive. In the present study, it was found that IGFBP4 is significantly downregulated in HCC, whose expression is positively correlated with the prognosis of patients with HCC. Overexpression of IGFBP4 restrained migration abilities and cancer metastasis of HCC cells both in vitro and in vivo. Furthermore, it was found that IGFBP4 represses HCC metastasis by inhibiting epithelial‑mesenchymal transition. Molecular mechanism studies showed that overexpression of IGFBP4 obviously suppresses NOTCH1 signaling in HCC. As for the upstream regulatory mechanism, it was revealed that downregulation of IGFBP4 in HCC was caused by CpG islands' hyper‑methylation‑dependent degradation mediated by MYBBP1A. Inhibition of MYBBP1A limited HCC metastatic ability and silence of IGFBP4 at the same time restored HCC metastatic potentials. Clinical data demonstrated that low expression of IGFBP4 was found in patients with HCC, especially with lymphatic metastasis. High MYBBP1A expression and low IGFBP4 expression in HCC were correlated with poor survival of patients with HCC. Summarily, in the present study, it was revealed that MYBBP1A/IGFBP4/NOTCH1 pathway could play a crucial role in the progression and metastasis of HCC, which stimulates novel therapeutic and diagnostic strategies against metastatic HCC.

Resistance to cytarabine is a major obstacle to the successful treatment of acute myeloid leukemia (AML). The present study aimed to explore the mechanism by which sirtuin 1 (SIRT1) reverses the cytarabine resistance of leukemia cells. Cell viability was investigated using the EdU proliferation assay. The expression levels of molecules were determined by reverse transcription‑quantitative PCR, western blotting, and immunofluorescence staining. Flow cytometry was used to detect reactive oxygen species and apoptosis levels, The levels of superoxide dismutase, glutathione and malondialdehyde were examined by ELISA. Mitochondrial damage was investigated by transmission electron microscopy. Furthermore, tumor growth was evaluated in a xenograft model. The results revealed that SIRT1 expression was significantly upregulated in drug‑resistant leukemia cells. By contrast, knockdown of SIRT1 reversed cytarabine resistance in HL60 cells by promoting ferroptosis. Mechanistically, SIRT1 could regulate the translocation of HMGB1 from the nucleus to the cytoplasm in cytarabine‑resistant HL60 (HL60/C) cells. Furthermore, knockdown of HMGB1 inhibited the expression of ACSL4. In addition, knockdown of SIRT1 expression could inhibit the growth of HL60/C cells in vivo and reverse cytarabine resistance. In conclusion, the present results demonstrated that SIRT1 inhibition could be a promising strategy to overcome cytarabine resistance in AML.

Developing novel anti‑angiogenic agents with minimal toxicity is notably challenging for cancer therapeutics. The discovery and development of peptides, whether derived from natural sources or synthesized, has potential for developing anti‑angiogenic agents characterized by their ability to penetrate cancer cells, high specificity and low toxicity. The present study identified a Bryopsis plumose‑derived anticancer and anti‑angiogenesis marine‑derived peptide 06 (MP06). A 22‑amino acid peptide was synthesized and conjugated with fluorescein isothiocyanate (FITC‑MP06) for intracellular localization in H1299 non‑small cell lung cancer cells. Regulatory effects of this peptide on the viability, migration and self‑renewal of lung cancer cells was assessed. Furthermore, anti‑angiogenic effect of MP06 was investigated by monitoring vascular tube formation in human umbilical vein endothelial cells and a zebrafish model. Aquaporin (AQP)3, a membrane channel in various tissues, is involved in regulating stemness, epithelial‑mesenchymal transition (EMT) and angiogenesis. MP06 downregulated AQP3 expression. Consistently, AQP3 knockdown by RNA silencing downregulated its gene expression, leading to a decrease in stemness, EMT and angiogenesis properties in H1299 cells. MP06 could thus serve as a novel therapeutic target with anticancer and angiogenesis properties for non‑small cell lung cancer.

Ferroptosis is a novel form of regulated cell death that plays a key role in inhibiting tumor malignancy. The ferroptosis signalling cascade provides new opportunities for lung cancer therapy. Non‑coding RNA (ncRNA)‑mediated epigenetic modification can influence the vulnerability of cancer cells to ferroptosis in non‑small‑cell lung cancer (NSCLC). The present review describes the core molecular mechanisms underlying ferroptosis and the role of epigenetic mechanisms in regulating ferroptosis in NSCLC, as well as developments in understanding the ncRNA‑induced mechanisms that affect ferroptosis in NSCLC. The present review aimed to enhance understanding of the epigenetic mechanisms mediated by ncRNAs that modulate ferroptosis in NSCLC, highlighting a novel therapeutic strategy for NSCLC via the ncRNA‑ferroptosis axis.

Leukemia is a cancer that starts in blood stem cells in the bone marrow. Today, the proper diagnosis and prognosis of leukemia are essential in mitigating the morbidity and mortality associated with this malignancy. The advent of novel biomarkers, particularly those related to minimal residual disease, has paved the way for personalized therapeutic strategies and enables the quantitative assessment of patient responses to treatment regimens. Novel diagnostic and targeted drug delivery may be helpful for the improved management of leukemia. Genetic clinical parameters, such as chromosomal abnormalities, are crucial in diagnosing and guiding treatment decisions. These genetic markers also provide valuable prognostic information, helping to predict patient outcomes and tailor personalized treatment plans. In the present review, the studies on the diagnostic and prognostic parameters of leukemia were analyzed. The prognosis of leukemia was investigated in most of the studies, and the remaining were performed on diagnosis. The clinical and laboratory prognostic parameters were the most common, followed by diagnostic hematological parameters, diagnostic blood parameter studies, and diagnostic immunological parameters. Clinical and laboratory prognostic and hematologic parameters were the most extensively studied. The methods used to diagnose and prognose the leukemia cases in these studies were predominantly clinical hematology. Numerous surface proteins and receptors, including CD45, CD27, CD29, CD38, CD27, CD123, CD56 and CD25, react similarly in various kinds of leukemia, which are ideal for targeted drug delivery. Drug delivery to leukemia cells encounters several significant obstacles, including heterogeneity, that hinder the effectiveness of treatment. Nanocarriers play a critical role in targeted drug delivery for leukemia by enhancing the precision of treatments directed at surface proteins and receptors. Additionally, they can be functionalized with targeting drugs and antibodies to target specific tissues and cells.

Aldehyde dehydrogenase 1 family member A1 (ALDH1A1) is a member of the aldehyde dehydrogenase gene subfamily that encode enzymes with the ability to oxidize retinaldehyde. It was recently shown that high ALDH1A1 RNA abundance correlates with a poor prognosis in acute myeloid leukemia (AML). AML is a hematopoietic malignancy associated with high morbidity and mortality rates. Although there are a number of agents that inhibit ALDH activity, it would be crucial to develop methodologies for adjustable genetic interference, which would permit interventions on several oncogenic pathways in parallel. Intervention in multiple oncogenic pathways is theoretically possible with microRNAs (miRNAs or miRs), a class of small non‑coding RNAs that have emerged as key regulators of gene expression in AML. A number of miRNAs have shown the ability to interfere with ALDH1A1 gene expression directly in solid tumor cells, and these miRNAs can be evaluated in AML model systems. There are indications that a few of these miRNAs actually do have an association with AML disease course, rendering them a promising target for genetic intervention in AML cells.

Ovarian cancer (OC) is the most common and deadly malignant tumor of the female reproductive system. When OC cells detach from the primary tumor and enter the ascitic microenvironment, they are present as individual cells or multicellular spheroids in ascites. These spheroids, composed of cancer and non‑malignant cells, are metastatic units and play a crucial role in the progression of OC. However, little is known about the mechanism of spheroid formation and dissemination. Tumor‑associated macrophages (TAMs) in the center of spheroids are key in spheroid formation and metastasis and provide a potential target for OC therapy. The present review summarizes the key biological features of spheroids, focusing on the role of TAMs in spheroid formation, survival and peritoneal metastasis, and the strategies targeting TAMs to provide new insights in treating OC.

Bladder cancer (BC) is a common malignancy and its most prevalent type is urothelial carcinoma, which accounts for ~90% of all cases of BC. The current treatment options for BC are limited, which necessitates the development of alternative treatment strategies. Hyperthermia (HT), as an adjuvant cancer therapy, is known to improve the efficacy of chemotherapy or radiotherapy. The present study aimed to investigate the anti‑tumor effects of HT on cell survival, invasiveness, chemoresistance and immune evasion in human BC cell lines (5637, T24 and UMUC3). Calcein AM staining was performed to analyze the cytotoxicity of natural killer (NK) cells against human BC cells following HT treatment. Cell migration and invasion affected by HT were analyzed using Transwell migration and invasion assays. It was found that HT inhibited the proliferation of BC cells by downregulating the phosphorylation of protein kinase B. Moreover, HT effectively enhanced the sensitivity of BC cells to the chemotherapy drug cisplatin (DDP) and reduced the chemoresistance of DDP‑resistant cells by downregulating the expression of cadherin‑11. It was further demonstrated that HT inhibited the migration and invasion of BC cells and enhanced the cytotoxic effects of NK cells. In summary, the antineoplastic effects of HT were mediated through three main mechanisms: Enhancement of the chemosensitivity of BC cells and mitigation of DDP‑induced chemoresistance, suppression of the invasive potential of BC cells and reinforcement of the anticancer response of NK cells. Thus, HT appears to be a promising adjunctive therapy for human BC.

Significant advancements have been made in cancer therapy; however, limitations remain with some conventional approaches. Adjuvants are agents used alongside primary treatments to enhance their efficacy and the treatment outcomes of patients. Modern lifestyles contribute to deficiencies in melatonin and vitamin D. Limited sun exposure affects vitamin D synthesis, and artificial light at night suppresses melatonin production. Both melatonin and vitamin D possess anti‑inflammatory, immune‑boosting and anticancer properties, rendering them potential adjuvants of interest. Studies suggest melatonin and vitamin D supplementation may address antioxidant imbalances in lip, oral and pharyngeal cancers. Moreover, promising results from breast, head and neck, brain, and osteosarcoma research indicate potential for tumor growth inhibition, improved survival, and a better quality of life of patients with cancer. The radioprotective properties of melatonin and vitamin D are another exciting area of exploration, potentially enhancing radiotherapy effectiveness while reducing side effects. For its part, the sleep‑promoting effects of melatonin may indirectly benefit patients with cancer by influencing the immune system. Thus, the prevalence of vitamin D and melatonin deficiencies highlights the importance of supplementation, as lower levels can worsen side‑effects from cancer treatments. The present review explores the potential of combining melatonin and vitamin D as synergistic adjuvants for cancer therapy. These agents have shown promise individually in cancer prevention and treatment, and their combined effects warrant investigation. Therefore, large‑scale controlled trials are crucial to definitively determine the optimal dosage, safety and efficacy of this combination in improving the lives of patients with cancer.