International journal of oncology最新文献

Ferroptosis, a recently discovered type of programmed cell death triggered by excessive accumulation of iron‑dependent lipid peroxidation, is linked to several malignancies, including non‑small cell lung cancer. Long non‑coding RNAs (lncRNAs) are involved in ferroptosis; however, data on their role and mechanism in cancer therapy remains limited. Therefore, the aim of the present study was to identify ferroptosis‑associated mRNAs and lncRNAs in A549 lung cancer cells treated with RAS‑selective lethal 3 (RSL3) and ferrostatin‑1 (Fer‑1) using RNA sequencing. The results demonstrated that lncRNA lung cancer‑associated transcript 1 (LUCAT1) was significantly upregulated in lung adenocarcinoma and lung squamous cell carcinoma tissues. Co‑expression analysis of differentially expressed mRNAs and lncRNAs suggested that LUCAT1 has a crucial role in ferroptosis. LUCAT1 expression was markedly elevated in A549 cells treated with RSL3, which was prevented by co‑incubation with Fer‑1. Functionally, overexpression of LUCAT1 facilitated cell proliferation and reduced the occurrence of ferroptosis induced by RSL3 and Erastin, while inhibition of LUCAT1 expression reduced cell proliferation and increased ferroptosis. Mechanistically, downregulation of LUCAT1 resulted in the downregulation of both GTP cyclohydrolase 1 (GCH1) and ferroptosis suppressor protein 1 (FSP1). Furthermore, inhibition of LUCAT1 expression upregulated microRNA (miR)‑34a‑5p and then downregulated GCH1. These results indicated that inhibition of LUCAT1 expression promoted ferroptosis by modulating the downregulation of GCH1, mediated by miR‑34a‑5p. Therefore, the combination of knocking down LUCAT1 expression with ferroptosis inducers may be a promising strategy for lung cancer treatment.

Although annexin A1 (ANXA1), a 37 kDa phospholipid‑binding anti‑inflammatory protein expressed in various tissues and cell types, has been investigated extensively for its regulatory role in cancer biology, studies have mainly focused on its intracellular role. However, cancer cells and stromal cells expressing ANXA1 have the ability to transmit signals within the tumor microenvironment (TME) through autocrine, juxtacrine, or paracrine signaling. This bidirectional crosstalk between cancer cells and their environment is also crucial for cancer progression, contributing to uncontrolled tumor proliferation, invasion, metastasis and resistance to therapy. The present review explored the important role of ANXA1 in regulating the cell‑specific crosstalk between various compartments of the TME and analyzed the guiding significance of the crosstalk effects in promotion or suppressing cancer progression in the development of cancer treatments. The literature shows that ANXA1 is critical for the regulation of the TME, indicating that ANXA1 signaling between cancer cells and the TME is a potential therapeutic target for the development of novel therapeutic approaches for impeding cancer development.

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the immunohistochemical data shown in Fig. 1C on p. 236, and immunofluorescence data featured in Figs. 2G and 5G on p. 237 and 239 respectively, were strikingly similar to data that had appeared in other articles written by different authors at different research institutes which had already been published.  In view of the fact that certain of the data in the above article had already been published at the time of the paper's submission, the Editor of International Journal of Oncology has decided that this paper should be retracted from the publication. 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 56: 232‑242, 2020; DOI: 10.3892/ijo.2019.4922].

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 1D on p. 1134, the data panels showing the results for the 'Control' and '1 μmol/l GW9662' experiments (on the left hand side of the figure) were overlapping, such that these data had been derived from the same original source where they were intended to show the results from differently performed experiments. The authors were able to re‑examine their original data, and realize that the data for the '1 μmol/l GW9662' panel had been selected incorrectly. The corrected version of Fig. 1, now featuring the correct data for the '1 μmol/l GW9662' experiment in Fig. 1D, is shown on the next page, The authors confirm their error did not grossly affect either the results of the conclusions reported in the paper, and are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum. They also apologize to the readership for any inconvenience caused. [International Journal of Oncology 46: 1131-1140, 2015; DOI: 10.3892/ijo.2015.2829].

Circular RNA (circRNA) was first observed in the cytoplasm of eukaryotic cells in 1979, but it was not characterized in detail until 2012, when high‑throughput sequencing technology was more advanced and available. Consequently, the mechanism of circRNA formation and its biological function have been progressively elucidated by researchers. circRNA is abundant in eukaryotic cells and exhibits a certain degree of organization, timing and disease‑specificity. Additionally, it is poorly degradable, meeting the characteristics of an ideal clinical biomarker. In the present review, the recent research progress of circRNAs in digestive tract malignant tumors was primarily discussed. This included the roles, biological functions and clinical significance of circRNA, providing references for its research value and clinical potential in gastrointestinal cancer.

YTHDF1, an N6‑methyladenosine (m6A)‑binding protein, is significantly upregulated in glioma tissues. The present study investigated the molecular mechanism underlying the regulatory effects of YTHDF1 on the viability, invasion and self‑renewal of glioma stem cells (GSCs). Glioma and normal brain tissues were collected, and reverse transcription‑quantitative PCR and western blotting were used to measure the gene and protein expression levels, respectively. Methylated RNA immunoprecipitation‑PCR was used to assess the m6A modification level of the target gene. Subsequently GSCs were induced, and YTHDF1 and LINC00900 gene regulation was carried out using lentiviral infection. The viability, invasion and self‑renewal of GSCs were assessed by Cell Counting Kit‑8, Transwell and sphere formation assays, respectively. Binding between YTHDF1 and LINC00900 was verified by RNA immunoprecipitation and RNA pull‑down assays. The targeted binding of microRNA (miR)‑1205 to the LINC00900/STAT3 3'‑UTR was verified using a luciferase reporter assay. The results revealed that YTHDF1 and LINC00900 expression levels were significantly upregulated in glioma tissues, and a high m6A modification level in LINC00900 transcripts was detected in glioma tissues. Overexpression of YTHDF1 promoted GSC viability, invasion and self‑renewal, whereas knockdown of YTHDF1 had the opposite effects. In addition, YTHDF1 maintained the stability of LINC00900 and upregulated its expression through binding to it, thereby promoting GSC viability, invasion and self‑renewal. Furthermore, LINC00900 promoted GSC viability, invasion, self‑renewal and tumor growth by regulating the miR‑1205/STAT3 axis. In conclusion, YTHDF1 promotes GSC viability and self‑renewal by regulating the LINC00900/miR‑1205/STAT3 axis.

Breast cancer arises from the malignant transformation of mammary epithelial cells under the influence of various carcinogenic factors, leading to a gradual increase in its prevalence. This disease has become the leading cause of mortality among female malignancies, posing a significant threat to the health of women. The timely identification of breast cancer remains challenging, often resulting in diagnosis at the advanced stages of the disease. Conventional therapeutic approaches, such as surgical excision, chemotherapy and radiotherapy, exhibit limited efficacy in controlling the progression and metastasis of the disease. Regulated cell death (RCD), a process essential for physiological tissue cell renewal, occurs within the body independently of external influences. In the context of cancer, research on RCD primarily focuses on cuproptosis, ferroptosis and pyroptosis. Mounting evidence suggests a marked association between these specific forms of RCD, and the onset and progression of breast cancer. For example, a cuproptosis vector can effectively bind copper ions to induce cuproptosis in breast cancer cells, thereby hindering their proliferation. Additionally, the expression of ferroptosis‑related genes can enhance the sensitivity of breast cancer cells to chemotherapy. Likewise, pyroptosis‑related proteins not only participate in pyroptosis, but also regulate the tumor microenvironment, ultimately leading to the death of breast cancer cells. The present review discusses the unique regulatory mechanisms of cuproptosis, ferroptosis and pyroptosis in breast cancer, and the mechanisms through which they are affected by conventional cancer drugs. Furthermore, it provides a comprehensive overview of the significance of these forms of RCD in modulating the efficacy of chemotherapy and highlights their shared characteristics. This knowledge may provide novel avenues for both clinical interventions and fundamental research in the context of breast cancer.

Since its discovery, the role of the transcription factor, signal transducer and activator of transcription 3 (STAT3), in both normal physiology and the pathology of numerous diseases, including cancer, has been extensively studied. STAT3 is aberrantly activated in different types of cancer, fulfilling a critical role in cancer progression. The biological process, epithelial‑mesenchymal transition (EMT), is indispensable for embryonic morphogenesis. During the development of cancer, EMT is hijacked to confer motility, tumor cell stemness, drug resistance and adaptation to changes in the microenvironment. The aim of the present review was to outline recent advances in knowledge of the role of STAT3 in EMT, which may contribute to the understanding of the function of STAT3 in EMT in various types of cancer. Delineating the underlying mechanisms associated with the STAT3‑EMT signaling axis may generate novel diagnostic and therapeutic options for cancer treatment.

Fungi inhabit different anatomic sites in the human body. Advances in omics analyses of host‑microbiome interactions have tremendously improved our understanding of the effects of fungi on human health and diseases such as tumors. Due to the significant enrichment of specific fungi in patients with malignant tumors, the associations between fungi and human cancer have attracted an increasing attention in recent years. Indeed, cancer type‑specific fungal profiles have been found in different tumor tissues. Importantly, fungi also influence tumorigenesis through multiple factors, such as host immunity and bioactive metabolites. Microbiome interactions, host factors and fungal genetic and epigenetic factors could be involved in fungal enrichment in tumor tissues and/or in the conversion from a commensal fungus to a pathogenic fungus. Exploration of the interactions of fungi with the bacterial microbiome and the host may enable them to be a target for cancer diagnosis and treatment. In the present review, the associations between fungi and human cancer, cancer type‑specific fungal profiles and the mechanisms by which fungi cause tumorigenesis were discussed. In addition, possible factors that can lead to the enrichment of fungi in tumor tissues and/or the conversion of commensal fungi to pathogenic fungi, as well as potential therapeutic and preventive strategies for tumors based on intratumoral fungi were summarized.