In addition, SEC61G knockdown significantly inhibited kidney cancer cell proliferation, migration and invasion compared with the negative control (NC) group. Furthermore, E‑cadherin expression was significantly upregulated, and N‑cadherin and β‑catenin expression levels were significantly downregulated in SEC61G‑knockdown kidney cancer cells compared with the NC group. In addition, compared with the NC group, SEC61G knockdown significantly promoted cell apoptosis in a caspase‑dependent manner. The aforementioned results suggested that SEC61G might serve as a proto‑oncogene to promote kidney tumor progression. Therefore, the present study provided a novel candidate gene for predicting the prognosis of patients with kidney cancer.Following the publication of the above paper, a concerned reader drew to the Editor's attention that Fig. 5 contained apparent anomalies, including unexpectedly similar-looking cells and repeated patternings of the cells in terms of their layout/arrangement within the data panels. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence regarding the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Molecular Medicine Reports 11 931‑939, 2015; DOI 10.3892/mmr.2014.2819].Ferroptosis is a new form of regulated cell death and closely related to cancer. However, the mechanism underlying the regulation of ferroptosis in lung adenocarcinoma (LUAD) remains unclear. IB, IHC and ELISA were performed to analyze protein expression. RT‑qPCR was used to analyze mRNA expression. Cell viability, 3D cell growth, MDA, the generation of lipid ROS and the Fe2+ concentration were measured to evaluate the responses to the induction of ferroptosis. Measurement of luciferase activity and ChIP were used to analyze the promoter activity regulated by the transcriptional regulator. Co‑IP assays were performed to identify protein‑protein interactions. In the present study, it was revealed that cAMP response element‑binding protein (CREB) was highly expressed in LUAD, and knockdown of CREB inhibited cell viability and growth by promoting apoptosis‑ and ferroptosis‑like cell death, concurrently. It was observed that CREB suppressed lipid peroxidation by binding the promoter region of glutathione peroxidase 4 (GPX4), and this binding could be enhanced by E1A binding protein P300 (EP300). The bZIP domain in CREB and the CBP/p300‑HAT domain in EP300 were essential for CREB‑EP300 binding in LUAD cells. Finally, it was revealed that CREB, GPX4, EP300 and 4‑HNE were closely related to tumor size and stage, and tumors with a higher degree of malignancy were more likely to have a low degree of lipid peroxidation. Therefore, targeting this CREB/EP300/GPX4 axis may provide new strategies for treating LUAD.The present study aimed to analyze the effects and underlying mechanisms of microRNA (miR)‑29‑3p on the proliferation and secretory abilities of prolactinoma cells by targeting insulin‑like growth factor (IGF)‑1/β‑catenin. The relationship between miR‑29a‑3p and the survival of prolactinoma cells was analyzed with the Kaplan‑Meier method in reference to The Cancer Genome Atlas. The expression levels of miR‑29a‑3p and IGF‑1 in MMQ and GH3 cells were detected. A dual‑luciferase reporter gene assay was performed to verify the combination of miR‑29a‑3p and IGF‑1. Cells were transfected with a miR‑29a‑3p mimic and/or IGF‑1 pcDNA3.1 to analyze the effects on the proliferation, apoptosis and secretion of prolactin (PRL) and growth hormone (GH) of prolactinoma cells. read more The effects on β‑catenin in the cytoplasm and nucleus were investigated by western blot analysis. The results showed that miR‑29a‑3p expression was low in MMQ and GH3 cells. Overexpression miR‑29a‑3p inhibited IGF‑1 mRNA and protein expression. miR‑29a‑3p inhibited cell proliferation and PRL and GH expression, and promoted apoptosis by inhibiting IGF‑1. Increasing the expression of miR‑29a‑3p increased β‑catenin levels in the cytoplasm, whereas IGF‑1 promoted β‑catenin activation and entry into the nucleus, and reversed the inhibitory effects of miR‑29a‑3p on β‑catenin. To conclude, miR‑29a‑3p inhibited the proliferation and secretory abilities of prolactinoma cells by inhibiting nuclear translocation of β‑catenin via a molecular mechanism that is inseparable from IGF‑1.Propofol‑based anesthesia has been reported to reduce the recurrence and metastasis of a number of cancer types following surgical resection. However, the effects of propofol in bladder cancer (BC) are yet to be fully elucidated. The aim of the present study was to investigate the functions of propofol in BC and their underlying mechanisms. In the study, the expression of microRNA (miR)‑145‑5p in BC tissues and cell lines was evaluated using reverse transcription‑quantitative PCR, and the effects of propofol on BC cells were determined using cell viability, wound healing and Transwell cell invasion assays, bioinformatics analysis, western blotting, immunohistochemistry and in vivo tumor xenograft models. It was found that propofol significantly suppressed the proliferation, migration and invasion of BC cells in vitro. In addition, propofol induced miR‑145‑5p expression in a time‑dependent manner, and miR‑145‑5p knockdown attenuated the inhibitory effects of propofol on the proliferation, migration and invasion of BC cells. Topoisomerase II α (TOP2A) was a direct target of miR‑145‑5p, and silencing TOP2A reversed the effects of miR‑145‑5p knockdown in propofol‑treated cells. Furthermore, propofol suppressed tumor xenograft growth, which was partially attenuated by miR‑145‑5p knockdown. The present study provided novel insight into the advantages of surgical intervention with propofol anesthesia in patients with BC.