Oncology reports最新文献

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be a number of anomalies in the presentation of data, including both tabulated data and data in figures: First, a discrepancy was noted between the numbers of males and females reported in the Materials and methods section on p. 1681 (47 females and 47 males) and yet, in Table I, showing clinicopathological characteristics of the patients, different numbers of male and female patients were reported. Secondly, data in Fig. 1 on p. 1683 had been misassembled: Experiments with COX‑2 and 5‑LOX are shown, but the panels for the x40 and x100 magnified images are presented the wrong way around. Thirdly, regarding the western blotting data, there were a couple of instances where it appeared that different exposures of gels had been undertaken in an attempt to show the same data for different experimental conditions. Fourthly, western blotting data featured internally in Fig. 4C on p. 1686 appeared to be strikingly similar, such that the same data may have been used to show the results for differently performed experiments. Fifthly, the data shown in the left‑hand columns for the scratch‑wound assay experiments in Figs. 2A and 5A were the same, even though different experiments were intended to have been portrayed in these figures. Finally, after having conducted an independent investigation of this paper in the Editorial Office, the presence of overlapping sections was also noted comparing the Transwell cell invasion assay data in Figs. 3 and 5. Given the identification of these various issues in the paper, the Editor of Oncology Reports has decided that this article should be retracted from the Journal on account of the uncertainties, and an overall 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. [Oncology Reports 35: 1680‑1688, 2016; DOI: 10.3892/or.2015.4506].

Glioma, a type of brain tumor, is influenced by mechanical forces in its microenvironment that affect cancer progression. However, our understanding of the contribution of compression and its associated mechanisms remains limited. The objective of the present study was to create an environment in which human brain glioma H4 cells experience pressure and thereby investigate the compressive mechanosensors and signaling pathways. Subsequent time‑lapse imaging and wound healing assays confirmed that 12 h of compression significantly increased cell migration, thereby linking compression with enhanced cell motility. Compression upregulated the expression of Piezo1, a mechanosensitive ion channel, and growth differentiation factor 15 (GDF15), a TGF‑β superfamily member. Knockdown experiments targeting PIEZO1 or GDF15 using small interfering RNA resulted in reduced cell motility, with Piezo1 regulating GDF15 expression. Compression also upregulated CTLA4, a critical immune checkpoint protein. The findings of the present study therefore suggest that compression enhances glioma progression by stimulating Piezo1, promoting GDF15 expression and increasing CTLA4 expression. Thus, these findings provide important insights into the influence of mechanical compression on glioma progression and highlight the involvement of the Piezo1‑GDF15 signaling pathway. Understanding tumor responses to mechanical forces in the brain microenvironment may guide the development of targeted therapeutic strategies to mitigate tumor progression and improve patient outcomes.

Colorectal cancer (CRC) ranks fifth in terms of incidence rate and mortality among malignant tumors in China. Oxaliplatin (OXA) is a first‑line drug for the clinical treatment of CRC, but its antitumor effect is limited because of the development of drug resistance. The present study aimed to investigate whether the traditional Chinese medicine Huaier can regulate the Wnt/β‑catenin signaling pathway by affecting the expression of METTL3, thereby promoting the sensitivity of HCT‑8/L cells to OXA. The expression of METTL3 was analyzed based on the UCSC Xena and Gene Expression Omnibus databases. Silent METTL3 and overexpression METTL3 models were constructed, and Cell Counting Kit‑8 and flow cytometry were used to detect the effects of Huaier on the viability and apoptosis of HCT‑8/L cells. Western blotting, reverse transcription‑quantitative PCR, nuclear cytoplasmic separation and immunofluorescence were used to detect the effects of Huaier on the expression of METTL3, Pgp, Wnt/β‑catenin signaling pathway‑related proteins, apoptosis‑related proteins and related mRNA. The results demonstrated that patients with high expression levels of METTL3 had a shorter overall survival period. The expression level of METTL3 significantly increased in drug‑resistant CRC cells. Silencing METTL3 promoted apoptosis of CRC cells and increased their sensitivity to OXA by inhibiting the Wnt/β‑catenin signaling pathway. Huaier downregulated the expression of METTL3, thereby promoting apoptosis of drug‑resistant CRC cells and increasing their sensitivity to OXA by inhibiting the Wnt/β‑catenin signaling pathway.

Long noncoding RNAs (lncRNAs) serve pivotal roles in cancer biology. The present study investigated the oncogenic roles of lncRNAs in renal cell carcinoma (RCC) and their potential as prognostic biomarkers. The lncRNA leucine‑rich repeat containing 75 A‑antisense RNA1 (LRRC75A‑AS1) was identified through lncRNA microarray as a potential lncRNA that may predict the efficacy of immune checkpoint inhibitor therapy and cancer progression in RCC. The present study subsequently assessed the expression of LRRC75A‑AS1 in 212 patients with clear cell RCC (ccRCC) who underwent nephrectomy, and performed in vitro functional analysis of LRRC75A‑AS1 in RCC cell lines. Additionally, the interactions between LRRC75A‑AS1, microRNA (miR)‑370‑5p and ADAMTS5 were explored. LRRC75A‑AS1 was revealed to be significantly upregulated in ccRCC tissues compared with in adjacent normal tissues, and high LRRC75A‑AS1 expression was associated with poor prognosis, including lower progression‑free survival, in patients with RCC. The knockdown of LRRC75A‑AS1 in RCC cell lines resulted in reduced cell proliferation and invasion, highlighting its role in promoting tumorigenesis. Furthermore, the interaction among LRRC75A‑AS1, miR‑370‑5p and ADAMTS5 was suggested as a regulatory mechanism underlying RCC progression. These findings indicated that LRRC75A‑AS1 may function as an oncogene in RCC, promoting cell proliferation and invasion. Its significant upregulation in ccRCC tissues and association with poor prognosis underscore its potential as a prognostic biomarker for RCC. Understanding the regulatory interactions among LRRC75A‑AS1, miR‑370‑5p and ADAMTS5 may provide new insights into the molecular mechanisms underlying RCC and facilitate the identification of novel therapeutic targets.

The health of individuals is seriously threatened by intestinal cancer, which includes pancreatic, colorectal, esophageal, gastric and gallbladder cancer. Most gastrointestinal cancers do not have typical and specific early symptoms, and lack specific and effective diagnostic markers and treatment methods. It is critical to understand the etiology of gastrointestinal cancer and develop more efficient methods of diagnosis and treatment. The cyclic GMP‑AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway serves a crucial role in the occurrence, progression and treatment of gastrointestinal cancer. The present review focuses on the latest progress regarding the role and mechanism of the cGAS/STING pathway in gastrointestinal cancer, and discusses treatment approaches and related applications based on the cGAS/STING signaling pathway. In order to improve the knowledge of the connection between the cGAS/STING pathway and gastrointestinal cancer, aid the diagnosis and treatment of gastrointestinal cancer, and lessen the burden on patients and society, the present review also discusses future research directions and existing challenges regarding cGAS/STING in the study of gastrointestinal cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the BrdU incorporation assay data shown in Fig. 7C were strikingly similar to data that had already appeared in another article written by different authors at different research institutes [Lu M, Qin X, Zhou Y, Li G, Liu Z, Geng X and Yue H: Long non‑coding RNA LINC00665 promotes gemcitabine resistance of Cholangiocarcinoma cells via regulating EMT and stemness properties through miR‑424‑5p/BCL9L axis. Cell Death Dis 12: 72, 2021]. Owing to the fact that the contentious 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 48: 207, 2022; DOI: 10.3892/or.2022.8422].

Following the publication of this paper, after having performed an independent analysis of the data shown in the various of the figures in the Editorial Office, it was identified that, in Fig. 5A and B on p. 1232 showing the results of Transwell invasion and migration experiments, the majority of the data panels exhibited overlapping sections of data, such that the affected 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 Oncology Reports 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. [Oncology Reports 33: 1227‑1234, 2015; DOI: 10.3892/or.2015.3729].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be overlapping sections of data in the three Transwell invasion assay images shown in Fig. 4A, and in the 3D sphere formation assay data shown in Fig. 5, on p. 2068; moreover, certain of the data featured in one of the data panels in Fig. 4A also appeared in a subsequent publication by the same research group in the journal Scientific Reports. The authors requested the publication of a corrigendum to acount for the errors made in assembling the data in Figs. 4 and 5; however, after careful consideration of the matter, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal on account of the number of issues that were identified, and a general lack of confidence in the 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. [Oncology Reports 43: 2062‑2072, 2020; DOI: 10.3892/or.2020.7549].

Amplification of human epidermal growth factor 2 receptor (HER2) and overexpression of estrogen receptor (ER) and/or progesterone receptor (PR) are key determinants in the treatment planning for human breast cancer (BC). Currently, targeted therapies for BC are focused mainly on these biomarkers. However, development of resistance to targeted drugs is almost unavoidable, emphasizing the importance of biochemical and pharmaceutical advances to improve treatment outcomes. To the best of our knowledge, the present study is the first to show functional crosstalk in vitro between HER2 and epithelial membrane protein 3 (EMP3), a tetraspan membrane protein, in human BC. EMP3 overexpression significantly promoted BC cell proliferation, invasion and migration by Transwell assays via epithelial-mesenchymal transition and transactivated the HER family, resulting in increased ER and PR expression in vitro. Knocking down EMP3 notably suppressed cell proliferation and migration and was accompanied by decreased expression of HER1‑HER3 and p‑SRC proteins. Suppression of EMP3 expression enhanced sensitivity of BC cells to trastuzumab in vitro. Xenograft experiments revealed decreased expression of HER1 and HER2 in stable EMP3‑knockdown cells, resulting in decreased tumor weight and size. In patients with BC, EMP3 overexpression was detected in 72 of 166 cases (43.4%), with 18 of 43 (41.9%) HER2‑amplified BC samples co‑expressing EMP3. Co‑expression of EMP3 and HER2 was positively associated with ER expression (P=0.028) and tended to be associated with nodal metastasis (P=0.085), however this was not significant. Taken together, the present results supported the potential of targeting EMP3 as a novel therapeutic strategy for human BC via co‑expression of HER2 and EMP3.

Bladder cancer is the most common malignant tumor of the urinary system with high morbidity and no clear pathogenesis. The Hippo signaling pathway is an evolutionarily conserved pathway that regulates organ size and maintains tissue homeostasis. Yes‑associated protein 1 (YAP1) is a key effector of this pathway and regulates downstream target genes by binding to transcriptional co‑activators with PDZ binding sequences (TAZ). Several studies have demonstrated that YAP1 is overexpressed in bladder cancer and is involved in adverse outcomes such as bladder cancer occurrence, progression, resistance to cisplatin and the recurrence of tumours. The present review summarized the involvement of YAP1 in bladder cancer disease onset and progression, and the mechanism of YAP1 involvement in bladder cancer treatment. In addition, this study further explored the potential of YAP1 in the diagnosis and treatment of bladder cancer. This study aimed to explore the potential mechanism of YAP1 in the treatment of bladder cancer.