International journal of oncology最新文献

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.

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.

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 International Journal of Oncology 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].

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.

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 (m⁶A) 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 m⁶A 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.

Long non‑coding (lnc)RNAs participate in colorectal cancer (CRC) occurrence and progression. The present study aimed to investigate whether lncRNA ABHD11‑AS1 regulates malignant biological behavior of CRC cells. Bioinformatic analysis, reverse transcription‑quantitative PCR and in situ hybridization revealed that ABHD11‑AS1 expression was decreased in CRC samples and associated with an unfavorable prognosis. ABHD11‑AS1 overexpression significantly decreased proliferation, migration and invasion of CRC cells, whereas ABHD11‑AS1 inhibition had the opposite effects. ABHD11‑AS1 interacted with EGFR to inhibit EGFR phosphorylation and attenuate EGFR/ERK signaling, which in turn suppressed the malignant biological behavior of CRC cells. The tumor suppressor function of ABHD11‑AS1 was attenuated by the EGFR agonist NSC228155. Finally, resveratrol (RSV) inhibited CRC cell proliferation, migration and invasion, which may be associated with RSV‑induced decrease in SPT6 homolog, histone chaperone and transcription elongation factor protein expression and increase in ABHD11‑AS1 transcript levels. ABHD11‑AS1 inhibited the phosphorylation of EGFR and decreased EGFR/ERK signaling by interacting with EGFR, thereby delaying the progression of CRC. The ABHD11‑AS1/EGFR/ERK axis may be a novel therapeutic target for preventing CRC progression.

Colorectal cancer (CRC) is a prevalent malignancy and a significant proportion of patients with CRC develop liver metastasis (CRLM), which is a major contributor to CRC‑related mortality. The present review aimed to comprehensively examine the pathogenetic development and diagnosis of CRLM and the clinical therapeutic approaches for treatment of this disease. The molecular mechanisms underlying CRLM were discussed, including the role of the tumour microenvironment and epithelial‑mesenchymal transition. The present review also highlighted the importance of early detection and the current challenges in predicting the development of CRLM. Various treatment strategies were reviewed, including surgical resection, chemotherapy and immunotherapy, and the potential of novel therapies, such as selective internal radiation therapy and Traditional Chinese Medicine. Despite recent advancements in treatment options, the treatment of CRLM remains a therapeutic challenge due to the complexity of the liver microenvironment and the heterogeneity of CRC. The present review emphasized the need for a multidisciplinary approach and the integration of emerging therapies to improve patient outcomes.

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.

Following the publication of this paper, a concerned reader drew to the attention of the Editorial Office that, for the photomicrographs shown in Fig. 2B on p. 8, the same image had apparently been selected to represent the images for cerebrum and cerebellum from the brain. Secondly, the same image for the prostate tissue in Fig. 2B was used as the 'Matched normal' data in Fig. 3C on p. 9, and thirdly, the si3 and si3+CT images selected for Fig. 7B on p. 13 appeared to be derived from the same original source. Finally, after having performed an independent analysis of the data in the Editorial Office, it was noted that, for the wound healing assay data shown in Fig. 8E on p. 14, overlapping sections were identified comparing the CT and Overexp panels in the lower panel of images in this figure, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. After having considered these issues, owing to the number of instances of apparently misassembled data that have been identified in this paper, and also on the basis of an overall lack of confidence in the presented data, the Editor of International Journal of Oncology has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 62: 38, 2023; DOI: 10.3892/ijo.2023.5486].

Acute myeloid leukemia (AML) is the most prevalent form of leukemia in adults. The cornerstone of first‑line chemotherapy for AML has poor survival rates, underscoring the urgent need for development of novel therapeutic agents. Differentiation therapy targets the blockade of differentiation in myeloid progenitor cells. The present study screened 100 plant extracts native to South Korea to search for those with differentiation‑inducing activity in AML. Differentiation‑inducing activity was assessed by measuring CD11b expression using fluorescence activated cell sorting. Of these, Corydalis incisa (Thunb.) Pers. (CIP) exhibited the highest efficacy. CIP induced myeloid differentiation, decreased viability and increased cell apoptosis and cell cycle arrest in HL‑60, U937 and THP‑1 cells. Furthermore, ultra‑performance liquid chromatography‑quadrupole time‑of‑flight mass spectrometry identified norchelerythrine as the primary anti‑leukemic compound in CIP. Norchelerythrine induced differentiation and promoted cell cycle arrest and apoptosis, mirroring the tumor‑suppressive effects of CIP, and notably decreased cell viability in patients with various genetic abnormalities. The present mechanistic study showed that norchelerythrine stimulated reactive oxygen species generation, leading to activation of DNA damage signaling and upregulation of p21^cip1, a cyclin‑dependent kinase inhibitor. Overall, norchelerythrine isolated from CIP may be a novel therapeutic option in AML.