Oncology reports最新文献

{"title":"[Corrigendum] High expression of RELM-α correlates with poor prognosis and promotes angiogenesis in gastric cancer.","authors":"Ping Chen, Deshou Zhao, Weiyi Wang, Yongping Zhang, Yaozong Yuan, Lifu Wang, Yunlin Wu","doi":"10.3892/or.2025.8894","DOIUrl":"https://doi.org/10.3892/or.2025.8894","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, and a corrigendum (doi.org/10.3892/or.2018.6933) that was published in 2018 to account for duplicated data panels in Fig. 6, an interested reader has drawn the authors' attention to the fact that the β‑actin bands featured in Fig. 3B of the above paper were strikingly similar to control data which appeared in Fig. 2D of a paper that had already been published in the journal <i>Oncotarget</i>, which featured one author in common. After having re‑examined their original data files, the authors realized that the β‑actin bands in Fig. 3B of the above paper had been inadvertently assembled incorrectly. The revised version of Fig. 3, now featuring all the correct data for Fig. 3B, including an adjusted version of the histograms in this figure part after having re‑quantified the data, is shown on the next page. Note that the corrections 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 further Corrigendum, and apologize to the readership for any inconvenience caused. [<i>Oncology Reports</i> 34: 77-86, 2015; DOI: 10.3892/or.2015.3943].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Upregulation of interleukin‑17F in colorectal cancer promotes tumor invasion by inducing epi​thelial‑mesenchymal transition.","authors":"Yusheng Chen, Zhou Yang, Dejun Wu, Zhijun Min, Yingjun Quan","doi":"10.3892/or.2025.8885","DOIUrl":"10.3892/or.2025.8885","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' and the Editor's attention that the clone image featured in Fig. 4A for the 'NC' (or 'negative control') data panel on p. 1146 had also been featured as the 'NC' experimental data panel in Fig. 4A of another article entitled 'Interleukin 1β/1RA axis in colorectal cancer regulates tumor invasion, proliferation and apoptosis via autophagy' (DOI: 10.3892/or.2020.7475), which was published by the same research group in the same journal. In this pair of articles, the authors were researching IL‑17F and IL‑1B/1RA, respectively; all experiments were performed on interleukins using the same batch of cells, and it was the authors' intention to have included these data, as they were portrayed, in both articles. However, to avoid any possible confusion, the authors now present alternative data for the 'NC' experiment in Fig. 4A for the above article, and the revised figure is shown on the next page. In addition, the authors have realized that the data panel in Fig. 1C on p. 1144, which was intended to represent the 'Tumor' immunohistochemical experiment (right‑hand panel), was inadvertently chosen incorrectly. The correct data for this panel is shown in the revised version of Fig. 1 opposite. Note that this error did not affect either the results or the conclusions reported in this paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and they apologize to the Editor and to the readership for any inconvenience caused. [Oncology Reports 42: 1141‑1148, 2019; DOI: 10.3892/or.2019.7220].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of quercetin on inhibiting gefitinib‑activated non‑small cell lung cancer‑induced cell pyroptosis in cardiomyocytes via modulating mitochondrial autophagy mediated by the SHP2/ROS/AMPK/XBP‑1/DJ‑1 signaling pathway.","authors":"Jie Zhang, Shanshan Qi, Yanyan Du, Honghong Dai, Ninghua Liu","doi":"10.3892/or.2025.8890","DOIUrl":"https://doi.org/10.3892/or.2025.8890","url":null,"abstract":"&lt;p&gt;&lt;p&gt;It has been reported that treatment of patients with non‑small cell lung cancer (NSCLC) with gefitinib increases the risk of QT interval prolongation. Therefore, the present study aimed to investigate whether quercetin could delay gefitinib‑induced cardiomyocyte apoptosis and its underlying mechanism. A total of 32 nude mice were divided into the sham, NSCLC, NSCLC + gefitinib and NSCLC + gefitinib + quercetin groups. Cardiac fibrosis in mouse heart tissues was assessed by Masson's trichrome staining. Additionally, immunohistochemical staining was performed to detect the expression levels of Src homology‑2 domain‑containing protein tyrosine phosphatase (SHP2), X‑box binding protein 1 (XBP‑1), phosphorylated (p)‑stimulator of interferon genes (STING) and Nod‑like receptor protein 3. Bioinformatics analysis was carried auto to predict the association between quercetin and the SHP2/reactive oxygen species (ROS) axis. Furthermore, the effects of adenosine triphosphate (ATP) + gefitinib, SHP2 silencing and H&lt;sub&gt;2&lt;/sub&gt;O&lt;sub&gt;2&lt;/sub&gt; on ROS levels, as well as on the p‑AMP‑activated protein kinase (AMPK)/XBP‑1/Parkinsonism associated deglycase (DJ‑1) axis, mitochondrial autophagy and apoptosis were assessed via detecting the expression levels of the corresponding proteins in cardiomyocytes by western blot analysis. JC‑1 immunofluorescence was performed to evaluate mitochondrial membrane damage. The results showed that NSCLC could not significantly affect cardiac function. In addition, compared with NSCLC alone, ventricular fibrosis was exacerbated in the NSCLC + gefitinib group. However, treatment with quercetin inhibited gefitinib‑induced ventricular fibrosis, activated the gefitinib‑suppressed SHP2 protein expression and downregulated the gefitinib‑induced XBP‑1 and p‑STING expression. Furthermore, the bioinformatics analysis results predicted that quercetin could interact with SHP2/ROS. The &lt;i&gt;in vitro&lt;/i&gt; experiments demonstrated that the expression levels of the ROS‑related proteins, namely NADPH oxidase 4 and XBP‑1/DJ‑1, and those of the mitochondrial autophagy‑ and apoptosis‑related proteins were enhanced, while those of p‑AMPK, were reduced in cardiomyocytes of the NSCLC + ATP + gefitinib group. However, cell treatment with quercetin inhibited ROS production and the expression levels of XBP‑1/DJ‑1 and apoptosis‑related proteins activated by NSCLC + ATP + gefitinib. By contrast, quercetin activated the expression levels of mitochondrial autophagy‑related proteins and those of p‑AMPK. Furthermore, SHP2 silencing and cell treatment with H&lt;sub&gt;2&lt;/sub&gt;O&lt;sub&gt;2&lt;/sub&gt; could separately inhibit the NSCLC + ATP + gefitinib‑induced expression of mitochondrial autophagy‑related proteins and p‑AMPK, while they could promote ROS production and upregulate XBP‑1/DJ‑1 and apoptosis‑related proteins. In summary, the results of the current study revealed a promising therapeutic approach for addressing cardiac issues caused by gefitinib treatment in patients w","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thermal cycling‑hyperthermia sensitizes non‑small cell lung cancer A549 cells to EGFR tyrosine kinase inhibitor erlotinib.","authors":"Guan-Bo Lin, Wei-Ting Chen, Yu-Yi Kuo, Hsu-Hsiang Liu, You-Ming Chen, Shr-Jeng Leu, Chih-Yu Chao","doi":"10.3892/or.2025.8891","DOIUrl":"https://doi.org/10.3892/or.2025.8891","url":null,"abstract":"<p><p>Molecular targeted therapy has emerged as a mainstream treatment for non‑small cell lung cancer (NSCLC), the most common type of lung cancer and the leading cause of cancer‑related death in both men and women. Erlotinib (Erl), a targeted therapy inhibiting EGFR pathways, has shown notable response rate in NSCLC cells. However, limited efficacy of the treatment has been reported due to resistance among a proportion of patients with NSCLC. Therefore, sensitizers are required to potentiate the efficacy of Erl in NSCLC treatment. The present study proposed a novel thermal therapy, thermal cycling‑hyperthermia (TC‑HT), as a supplement to amplify the effects of Erl. It was demonstrated that TC‑HT reduced the half‑maximal inhibitory concentration of Erl to 0.5 µM and TC‑HT sensitized A549 NSCLC cells to Erl via the downstream EGFR signaling cascades. Furthermore, the combination treatment of Erl and TC‑HT induced G2/M cell cycle arrest and inhibition of cell proliferation and migration. In addition, by slightly raising the temperature of TC‑HT, TC‑HT treatment alone produced antineoplastic effects without damaging the normal IMR‑90 lung cells. The method presented in this study may be applicable to other combination therapies and could potentially act as a starter for anticancer treatments, with fewer side effects.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PFKFB4 promotes endometrial cancer by regulating glycolysis through SRC‑3 phosphorylation.","authors":"Yaling Wu, Jianzhen Zhao, Shuangshuang Zhao, Jianfang Li, Jin Luo, Yingmei Wang","doi":"10.3892/or.2025.8886","DOIUrl":"10.3892/or.2025.8886","url":null,"abstract":"<p><p>The present study aimed to investigate the role of 6‑phosphofructo‑2‑kinase/fructose‑2,6‑biphosphatase 4 (PFKFB4) in endometrial cancer cells and to explore its potential molecular mechanisms. PFKFB4 expression in endometrial cancer tissues was detected by immunohistochemistry. Cell Counting Kit‑8, Transwell assays and flow cytometry were used to detect cell proliferation, invasion and apoptosis in endometrial cancer cells after PFKFB4 knockdown. An enzyme‑linked immunosorbent assay was used to detect the glucose and lactic acid contents. Western blotting was performed to detect the levels of glycolysis‑related enzymes, steroid receptor coactivator‑3 (SRC‑3), and phosphorylated SRC‑3. <i>In vivo</i> experiments were performed to investigate the tumorigenic potential of PFKFB4. PFKFB4 expression was upregulated in endometrial cancer tissues compared with that in normal controls, and its upregulation was positively correlated with the depth of myometrial invasion, lymph node metastasis, surgical pathological stage and vascular invasion. PFKFB4 knockdown significantly inhibited proliferation and invasion, increased apoptosis, and decreased oxygen consumption and lactic acid production in endometrial cancer cells. PFKFB4 knockdown decreased SRC‑3 phosphorylation. After simultaneous PFKFB4 knockdown and SRC‑3 overexpression in cancer cells, oxygen consumption, lactic acid production, and glycolysis‑related protein expression were increased compared with those in control cells. PFKFB4 knockdown inhibited tumor proliferation, apoptosis and the expression of Ki‑67. PFKFB4 may regulate glycolysis in endometrial cancer cells by targeting SRC‑3, thus promoting endometrial cancer progression.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular insights and treatment innovations: Advancing outcomes in acute myeloid leukemia with myelodysplasia‑related changes (Review).","authors":"Hong Qiu, Chaowei Zhang, Xiaochen Ma, Ying Li","doi":"10.3892/or.2025.8887","DOIUrl":"10.3892/or.2025.8887","url":null,"abstract":"<p><p>Acute myeloid leukemia, myelodysplasia‑related (AML‑MR), a challenging and aggressive subtype of AML, is characterized by unique genetic abnormalities and molecular features, which contribute to its poor prognosis compared with other AML subtypes. The present review summarizes the current understanding of AML‑MR pathogenesis, highlighting notable advancements in genetic and cytogenetic insights. Critical mutations, such as those in the tumor antigen p53 and additional sex combs like 1 genes, and their role in disease progression and resistance to treatment, are explored. The review further investigates how clonal evolution and cellular microenvironment alterations drive AML‑MR transformation and impact patient outcomes. Despite the poor outlook typically associated with AML‑MR, developments in treatment approaches offer hope. The present review considers the efficacy of novel therapeutic agents, including CPX‑351, hypomethylating agents and targeted molecular therapies. Additionally, innovations in immunotherapy and allogeneic hematopoietic stem cell transplantation are discussed as promising avenues to improve patient survival rates. The challenges of treating AML‑MR, particularly in elderly and pretreated patients, underline the necessity for individualized treatment strategies that consider both the biological complexity of the disease and the overall health profile of the patient. The present review focuses on the mechanisms of AML‑MR transformation, highlighting factors that may offer a crucial theoretical foundation and pave the way for future applications in precision medicine. Future research directions include exploring novel targeted therapies and combination regimens to mitigate the transformation risks and enhance the quality of life of patients with AML‑MR.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of necroptosis in lung adenocarcinoma by miR‑10b‑5p through modulation of the PKP3/RIPK3/MLKL cascade.","authors":"Ying Hu, Xin Liu, Ziheng Yuan, Jianping He, Run Ma, Yuming Wang, Genfa Yi","doi":"10.3892/or.2025.8889","DOIUrl":"10.3892/or.2025.8889","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Globally, lung adenocarcinoma (LUAD) remains the leading cause of cancer‑related mortality, highlighting the urgent need for innovative therapeutic approaches. Necroptosis has been recognized as a crucial mechanism for inhibiting cancer progression. Research has revealed a significant association between microRNA (miRNA)‑mediated necroptosis and tumor progression. The present study aimed to elucidate the role and underlying mechanisms of miR‑10b‑5p in regulating necroptosis in the context of LUAD. In an investigation of LUAD, miRNA sequencing was conducted on both LUAD and adjacent non‑tumor tissues, followed by the integration of external database information to identify specific target miRNAs. The expression of miR‑10b‑5p was verified in LUAD tissues and corresponding adjacent non‑cancerous tissues using immunohistochemistry. &lt;i&gt;In vitro&lt;/i&gt; experiments, utilizing LUAD cell lines engineered to modulate miR‑10b‑5p levels, assessed its effects on cellular activities and necroptosis. The inhibition of PKP3 by miR‑10b‑5p was determined using a dual luciferase reporter system. Furthermore, alterations in miR‑10b‑5p levels were found to affect PKP3 expression and inhibit the RIPK3/MLKL signaling pathway, as evidenced by western blot analysis in LUAD cell lines. The effect of PKP3 knockdown on cell activity and necroptosis in LUAD cell lines with low miR‑10b‑5p expression levels was assessed using cell function assays. Finally, a nude mouse xenograft model was used to investigate the effect of miR‑10b‑5p on LUAD growth &lt;i&gt;in vivo&lt;/i&gt; and its specific mechanism of action. It has been revealed that miR‑10b‑5p levels are significantly elevated in LUAD specimens. Further investigations demonstrated that an increase in miR‑10b‑5p enhances the proliferation of LUAD cells and suppresses the progression of necroptosis, as evidenced by &lt;i&gt;in vitro&lt;/i&gt; experiments. Through dual luciferase reporter assays, PKP3 was confirmed as a direct target negatively regulated by miR‑10b‑5p, leading to reduced expression levels. Western blot analysis indicated that miR‑10b‑5p inhibits the RIPK3/MLKL pathway activation through downregulation of PKP3, which leads to increased cell proliferation and decreased necroptosis. However, knockdown of PKP3 reversed the inhibitory effect of miR‑10b‑5p inhibitors on cellular activity and inhibited necrosis by suppressing the RIPK3/MLKL signalling pathway. In addition, animal model studies demonstrated that inhibition of miR‑10b‑5p activated the RIPK3/MLKL pathway by promoting PKP3 expression and significantly reduced LUAD growth by promoting necroptosis. In conclusion, our studies have revealed that the miR‑10b‑5p functions as a tumorigenic factor, enhancing various cellular activities in LUAD cells and suppressing necroptosis by specifically targeting PKP3, thereby inhibiting activation of the RIPK3/MLKL pathway. Importantly, interventions using inhibitors that specifically target miR‑10b‑5p have shown significant success in imped","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] The circadian clock gene <i>PER2</i> plays an important role in tumor suppression through regulating tumor‑associated genes in human oral squamous cell carcinoma.","authors":"Xiaoli Su, Dan Chen, Kai Yang, Qin Zhao, Dan Zhao, Xiaoqiang Lv, Yiran Ao","doi":"10.3892/or.2025.8888","DOIUrl":"10.3892/or.2025.8888","url":null,"abstract":"<p><p>Following the publication of this article, a concerned reader drew to the attention of the Editorial Office that certain of the tumor images featured in Fig. 6A on p. 478 bore a striking resemblance to tumor images included in three other papers contributed by the same research group, albeit photographed in some cases in slightly different orientations, where the data were intended to show the results from differently performed experiments. The Editorial Office has conducted a separate investigation of the data in this paper, and concurs with the concerned reader that certain of the tumor images had been re‑used in these papers. Owing to the fact that the contentious data in Fig. 6 of the above article were also already under consideration for publication prior to its submission to <i>Oncology Reports</i>, or had already been published, 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 38: 472‑480, 2017; DOI: 10.3892/or.2017.5653].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of PEG10 in cancer and neurodegenerative disorder (Review).","authors":"Dachao Mou, Shasha Wu, Yanqiong Chen, Yun Wang, Yufang Dai, Min Tang, Xiu Teng, Shijun Bai, Xiufeng Bai","doi":"10.3892/or.2025.8893","DOIUrl":"https://doi.org/10.3892/or.2025.8893","url":null,"abstract":"<p><p>Paternally expressed gene 10 (PEG10) is an imprinting gene. In addition to its known roles in placental development, as well as mouse embryonic stem cell and trophoblast stem cell differentiation, PEG10 has recently been shown to have significance in cancers. High expression of PEG10 is observed in various cancer types and is associated with poor prognosis. Of note, disruption of PEG10 expression leads to increased apoptosis, as well as decreased proliferation, invasion and migration of cancer cells. PEG10 is expected to become a target for cancer and neurodegenerative disorder therapy. This article reviewed the latest progress in the role of PEG10 in cancers.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] (‑)‑β‑hydrastine suppresses the proliferation and invasion of human lung adenocarcinoma cells by inhibiting PAK4 kinase activity.","authors":"Bingyu Guo, Xiaodong Li, Shuai Song, Meng Chen, Maosheng Cheng, Dongmei Zhao, Feng Li","doi":"10.3892/or.2025.8892","DOIUrl":"https://doi.org/10.3892/or.2025.8892","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 4A and Transwell cell migration and invasion assay data in Fig. 6A subsequently appeared in other published articles written by different authors at different research institutes (a pair of which have since been retracted owing to the striking similarity of these data with that featured in previously published articles). Moreover, overlapping data panels were also identified in Fig. 6A, such that these data, which were intended to show the results from differently performed experiments, had apparently been derived from the same original source. Owing to the fact that the contentious data in the above article had apparently subsequently appeared in other unrelated articles, and given the fact that Fig. 6A had clearly been assembled incorrectly, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal on the grounds of a lack of overall confidence in the originality of all the data presented therein. 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: 2246‑2256, 2016; DOI: 10.3892/or.2016.4594].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}