Oncology reports最新文献

Further to the publication of the above paper, a concerned reader drew to our attention that, in Figs. 1A and 4A, the same loading controls for the RT‑PCR experiments portrayed had apparently been incorporated into these figures, even though the experimental results (i.e., for the DEC1 bands) were otherwise different. In addition, the control GAPDH bands featured in the western blots in Figs. 3A and 3B for the SMMC‑7721 and BRL‑7402 cell lines respectively were strikingly similar, albeit the bands appeared to have been vertically flipped in Fig. 3A relative to Fig. 3B, and possibly stretched. The Editorial Office subsequently investigated this matter, and were able to confirm the concerns of the reader. After having considered the various issues that have been brought to light with this paper, in spite of a request from the authors that a Corrigendum be published, the Editor of Oncology Reports has determined that the article should be retracted on account of a lack of overall 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 30: 2957‑2962, 2013; DOI: 10.3892/or.2013.2774].

The present review aimed to elucidate the roles of extracellular matrix (ECM) components in the progression of vulvar squamous cell carcinoma (VSCC) and explore potential therapeutic avenues for this type of malignancy. This exploration holds promise for identifying precise molecular targets within the ECM milieu, thus facilitating the development of innovative therapeutic modalities tailored to disrupt these interactions and ultimately improve patient outcomes in VSCC. The dysregulated ECM serves as a potent driver of SCC tumor progression, orchestrating key processes such as angiogenesis, inflammation and stromal cell behavior. Yet, the exploration of ECM role in VSCC is still in its early stages. Recent research highlights the critical role of ECM organization and expression within the tumor microenvironment (TME) in influencing key aspects of VSCC, including tumor staging, grading, metastasis, invasion and patient survival. Cancer‑associated fibroblasts play a pivotal role in this dynamic by engaging in reciprocal interactions with VSCC cells, leading to significant ECM alterations and creating an immune‑suppressive TME. This hinders antitumor immunity and fosters therapeutic resistance in VSCC treatment. The dysregulated ECM in VSCC drives tumor progression, metastasis and affects patient survival. Targeting ECM, along with emerging therapies such as immune checkpoint blockade, offers promise for improved VSCC treatment outcomes.

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 Fig. 4 on p. 521 were strikingly similar to data that had already appeared in a pair of figures in a previously published article written by different authors at different research institutes in the journal Molecular Cancer Therapeutics. In addition, there was an unexpected issue with the appearance of the shading surrounding one of the tumor images featured in Fig. 7, such that this figure appeared to contain an anomaly. Owing to the fact that contentious western blot data in the above article had already been published prior to its submission to Oncology Reports, 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 43: 516‑524, 2020; DOI: 10.3892/or.2019.7425].

BH3 mimetics are small‑molecule inhibitors of the antiapoptotic Bcl‑2 family and have therapeutic efficacy against hematological malignancies. BH3 mimetic A‑1331852 suppresses colorectal cancer cell proliferation. Progressive resistance to the widely used anticancer agent fluorouracil (5‑FU) is a key reason for colorectal cancer recurrence; therefore, the present study tested if A‑1331852 can suppress the proliferation of 5‑FU‑resistant colorectal cancer cells. A 5‑FU‑resistant colorectal cancer cell line was derived from HCT116 cells and compared with the parental line. Expression levels of the antiapoptotic Bcl‑2 proteins Bcl‑xL and myeloid cell leukemia 1 (Mcl‑1) were determined via western blotting, proliferation in the presence of 5‑FU and following small interfering (si)RNA‑mediated Bcl‑xL or Mcl‑1 knockdown was assessed by WST‑1 assay and sensitivity to A‑1331852‑induced apoptosis was assessed via western blotting and DNA fragmentation assay. In addition, a xenograft mouse model of 5‑FU‑resistant colorectal cancer was established via subcutaneous inoculation of 5‑FU‑resistant HCT116 cells to examine the in vivo antitumor efficacy of A‑1331852. Compared with the parental line, 5‑FU‑resistant cells overexpressed Bcl‑xL. Knockdown of Bcl‑xL by siRNA and treatment with A‑1331852 suppressed proliferation and induced the apoptosis of both 5‑FU‑resistant and parental HCT116 cells, but the potency of both effects was stronger in 5‑FU‑resistant than parental HCT116 cells. Furthermore, A‑1331852 suppressed the growth of xenograft tumors derived from 5‑FU‑resistant cells by inducing apoptosis. Overall, the present findings suggested that Bcl‑xL upregulation contributes to 5‑FU resistance of colorectal cancer and targeted inhibition by A‑1331852 may be an effective treatment strategy.

Gastrointestinal (GI) cancers, which have notable incidence and mortality, are impacted by metabolic reprogramming, especially the increased production and accumulation of lactate. Lactylation, a post‑translational modification driven by lactate, is a crucial regulator of gene expression and cellular function in GI cancer. The present review aimed to examine advancements in understanding lactate and lactylation in GI cancer. The mechanisms of lactate production, its influence on the tumor microenvironment and the clinical implications of lactate levels as potential biomarkers were explored. Furthermore, lactylation was investigated, including its biochemical foundation, primary targets and functional outcomes. The present review underscored potential therapeutic strategies targeting lactate metabolism and lactylation. Challenges and future directions emphasize the potential of lactate and lactylation as innovative therapeutic targets in GI cancer to improve clinical outcomes.

Gastric cancer (GC) is characterized by a complex and heterogeneous tumor microenvironment (TME) that significantly influences disease progression and treatment outcomes. The tumor stroma, which is composed of a variety of cell types such as cancer‑associated fibroblasts, immune cells and vascular components, displays significant spatial and temporal diversity. These stromal elements engage in dynamic crosstalk with cancer cells, shaping their proliferative, invasive and metastatic potential. Furthermore, the TME is instrumental in facilitating resistance to traditional chemotherapy, specific treatments and immunotherapy strategies. Understanding the underlying mechanisms by which the GC microenvironment evolves and supports tumor growth and therapeutic resistance is critical for developing effective treatment strategies. The present review explores the latest progress in understanding the intricate interactions between cancer cells and their immediate environment in GC, highlighting the implications for disease pathogenesis and therapeutic interventions.

Pancreatic ductal adenocarcinoma (PDAC) is a malignant neoplasm that typically manifests with subtle clinical manifestations in its early stages and frequently eludes diagnosis until the advanced phases of the disease. The limited therapeutic options available for PDAC significantly contribute to its high mortality rate, highlighting the urgent need for novel biomarkers capable of effectively identifying early clinical manifestations and facilitating precise diagnosis. The pivotal role of cellular exosomes in both the pathogenesis and therapeutic interventions for PDAC has been underscored. Furthermore, researchers have acknowledged the potential of exosomes as targeted drug carriers against regulatory cells in treating PDAC. The present article aims to provide a comprehensive review encompassing recent advancements in utilizing exosomes for elucidating mechanisms underlying disease development, patterns of metastasis, diagnostic techniques and treatment strategies associated with PDAC.

Lung cancer remains a leading cause of global cancer‑related deaths, therefore the identification of prognostic factors for lung cancer is critical. Casein kinase 2 alpha (CK2α) is one of the driver kinases in various cancers, and it was previously demonstrated that CK2α localization was associated with a poor prognosis in invasive breast cancer. In the present study, the importance of CK2α in the nucleolus was explored as a potential prognostic marker for surgically resected early‑stage lung adenocarcinoma. The present study included 118 patients who underwent pulmonary lobectomy between 2014 and 2018 in Fukushima Medical University Hospital (Fukushima, Japan), and in whom CK2α localization in tumor samples was assessed by immunohistochemistry. Patient and tumor characteristics, including pathological stage, histological type and histological grade, were analyzed. Recurrence‑free survival (RFS) and overall survival were evaluated in relation to nucleolar CK2α staining. CK2α staining in the nucleoli was observed in 50.8% of lung adenocarcinoma tumors. Positive nucleolar CK2α staining was independent of pathological stage, histological type and histological grade. Patients with positive nucleolar CK2α staining exhibited significantly worse RFS compared with patients with negative staining. Multivariate analysis identified nucleolar CK2α staining and lymph node metastasis as independent poor prognostic factors. The results of the present study suggested that nucleolar CK2α staining is a novel and independent prognostic factor in surgically resected early‑stage lung adenocarcinoma. These findings indicated the potential of nucleolar CK2α as a predictive biomarker for future recurrence, and a guide to treatment decisions. Further research is required, particularly in understanding the molecular mechanisms linking nucleolar CK2α to recurrence.

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the flow cytometric plots shown in Fig. 5A and B on p. 2572, each figure part contained a pair of duplicated data panels; specifically, the panels depicting the 'NC/5‑FU' and the 'shTRIM11/Gemcitabine' experiments in Fig 5A (MCF‑7 cells), and the 'NC/Paclitaxel' and 'shTRIM11/Adriamycin' experi-ments in Fig. 5B (MDA‑MB‑231 cells), were apparently identical. The authors were able to re‑examine their original data files, and realize that this figure was inadverently assembled incorrectly. The revised version of Fig. 5, now showing the correct data for the 'shTRIM11/Gemcitabine' experiment in Fig 5A and the 'NC/Paclitaxel' experiment in Fig. 5B, is shown on the next page. Note that the revisions made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 41: 2567‑2574, 2019; DOI: 10.3892/or.2019.7015].

N6‑methyladenosine (m⁶A) is the predominant chemical modification of eukaryotic mRNA, dynamically mediated by the RNA methyltransferase, methyltransferase-like 3 (METTL3). m⁶A modification plays a critical role in cancer progression through post‑transcriptional regulation in various types of cancer. However, the role of METTL3 and its associated m⁶A modification in colorectal tumorigenesis remains to be fully elucidated. In the present study, it was demonstrated that METTL3 expression and the m⁶A levels were both upregulated in colorectal cancer (CRC) and positively associated with clinical progression, based on the bioinformatics analysis of cancer databases. Furthermore, knockdown and overexpression of METTL3 notably affected CRC cell viability, apoptosis and migration in vitro. Similarly, xenograft animal models confirmed that METTL3 promoted CRC tumorigenicity in vivo. Mechanistically, it was revealed that the m⁶A modification of matrix metallopeptidase 9 (MMP9) mRNA mediated by METTL3 promoted its expression in CRC by decreasing its degradation. Collectively, the findings of the present study suggested that the METTL3/MMP9 axis could serve as a novel promising therapeutic candidate for CRC.