An interested reader drew to our attention that the western blots featured in Figs. 1B and 6C contained strikingly similar protein bands, and repeating patterns of bands, comparing across the lanes of the gels. Furthermore, an image representing the Myc‑YAP colony‑formation assay experiment in Fig. 2C was strikingly similar to the data shown for the Control colony‑formation assay experiment in Fig. 5B. The Editorial office subsequently investigated this matter further, and noted that the western blots shown in Fig. 6A and B likewise contained strikingly similar bands that were purportedly showing the results from different experiments. After having considered the various issues that have been brought to light with this paper, together with an appeal from the authors that a Corrigendum be published, the Editor of Oncology Reports has ruled that the article should be retracted from the publication on account of a lack of overall confidence in the presented data. Note that the authors were not in agreement that the errors reported and identified were sufficient to merit the retraction of the article. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 40 609-620, 2018; DOI 10.3892/or.2018.6486].Breast cancer which is the most common type of diagnosed cancer among women worldwide possesses metastatic potential, multi‑drug resistance, and high mortality. The NF‑κB signaling pathway has been revealed to be abnormally activated in breast cancer cells and closely associated with high metastasis and poor prognosis. In the present study, it was reported that chlorogenic acid (CGA), a potent NF‑κB inhibitor derived from coffee, exerted antitumor activity in breast cancer. MTT and colony formation assays were conducted and it was revealed that CGA inhibited viability and proliferation in breast cancer cells. Additionally, CGA significantly induced apoptosis and suppressed migration and invasion in breast cancer cells. Notably, immunofluorescence analysis confirmed that CGA could efficiently suppress nuclear transcription of NF‑κB p65. In addition, results of western blotting demonstrated that CGA markedly impaired the NF‑κB and EMT signaling pathways.  https://www.selleckchem.com/products/wnt-c59-c59.html  The antitumor effect of CGA was evaluated in a subcutaneous tumor mouse model of 4T1 cells, and the results revealed that CGA markedly retarded tumor growth and prolonged the survival rate of tumor‑bearing mice. Notably, CGA inhibited pulmonary metastasis of 4T1 cells by enhancing the proportion of CD4+ and CD8+ T cells in spleens of mice, which indicated an improvement of antitumor immunity. In conclusion, the present present study demonstrated that CGA improved antitumor immunity, exerting antitumor and anti‑metastatic effects by impairing the NF‑κB/EMT signaling pathway, suggesting that CGA may serve as a potential candidate for therapy of breast cancer.Endometrial cancer (EC) is the most common gynecological cancer, and one of the most important causes of cancer‑related deaths in women worldwide. The long‑term survival rate is lower in advanced‑stage and recurrent EC, therefore it is important to identify new anticancer drugs. Garcinol, a polyisoprenylated benzophenone, is a promising anticancer drug for various cancer types but its effects on EC remain unclear. To investigate the anticancer effects of garcinol on EC, cell proliferation and cell cycle were assessed by real‑time cell proliferation, cell counting, and colony formation assays, flow cytometric analysis, and 5‑ethynyl‑2'‑deoxyuridine (EdU) incorporation assay, in EC Ishikawa (ISH) and HEC‑1B cell lines. Western blotting was used to evaluate the expression of cell cycle‑related protein cyclins, cyclin‑dependent kinase and tumor suppression proteins. Garcinol inhibited ISH and HEC‑1B cell proliferation in a dose‑dependent manner, and induced ISH and HEC‑1B cell cycle arrest at the G1 phase and G2/M phase, respectively, and decreased the S phase and DNA synthesis in these two cell lines. Following garcinol treatment the expression levels of p53 and p21 were increased, while the expression levels of CDK2, CDK4, cyclin D1 and cyclin B1 were gradually decreased in a dose‑dependent manner in both ISH and HEC‑1B cells. In addition, the expression levels of phosphorylated c‑JUN N‑terminal kinase (JNK) and p‑c‑JUN were significantly increased in both types of cells. Collectively, garcinol can induce EC cell cycle arrest and may be a promising candidate for EC chemotherapy.Hepatocellular carcinoma (HCC) is one of the most prevalent types of cancer worldwide. Long non‑coding RNAs (lncRNAs) have been reported to frequently participate in the carcinogenesis and development of various types of cancer, including HCC. However, the molecular mechanisms of lncRNA ST8SIA6‑AS1 in HCC remain poorly understood. The present study performed bioinformatics analysis, in addition to using reverse transcription‑quantitative PCR (RT‑qPCR), nuclear‑cytoplasmic fractionation, RNA immunoprecipitation, and Transwell, wound healing, and dual‑luciferase reporter assays, to determine the biological role and regulatory mechanisms of ST8SIA6‑AS1 in HCC. The results revealed that the expression levels of ST8SIA6‑AS1 were upregulated in HCC tissues and cell lines, which were associated with a poor prognosis. Moreover, the genetic knockdown of ST8SIA6‑AS1 inhibited the hypoxia‑induced HCC cell migration and invasion. Additionally, microRNA (miR)‑338, which exhibited downregulated expression levels in HCC tissues and cell lines, was discovered to bind with ST8SIA6‑AS1. The inhibition of miR‑338 partially reversed the inhibitory effects of ST8SIA6‑AS1‑knockdown on the migration and invasion of HCC cells under hypoxia. Subsequently, methylphosphate capping enzyme (MEPCE) was identified to be targeted and negatively regulated by miR‑338. Notably, the overexpression of MEPCE recovered the inhibitory influence over the migratory and invasive abilities of hypoxia‑treated HCC cells promoted by ST8SIA6‑AS1 inhibition. In conclusion, the findings of the present study suggest that lncRNA ST8SIA6‑AS1 may promote the migration and invasion of hypoxia‑induced HCC cells via the miR‑338/MEPCE axis, indicating a potential diagnostic or therapeutic marker for HCC treatment.