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Microarray data revealed that only Hoxa11 was upregulated in those cells harboring activating PTPN11. Functional studies of Hoxa11 knockdown or overexpression in MLL/AF10(OM‑LZ) cells revealed that Hoxa11 expression levels were associated with survival in vivo and Ara‑C sensitivity/apoptosis in vitro. In addition, Hoxa11 regulated the expression of the apoptosis‑related genes, NF‑κB inhibitor α, transcription factor p65 and transformation‑related protein p53. Furthermore, the results of a meta‑analysis using Heuser's AML dataset supported the finding that chemotherapy responders have higher expression levels of HOXA11. These results indicated that the expression of HOXA11 increased cell apoptosis and predicted an improved response to Ara‑C in AML.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the western blotting data in Fig. 5c were strikingly similar to data appearing in different form in other articles by different authors at different research institutes. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, elsewhere prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 34 1573‑1580, 2015; DOI 10.3892/or.2015.4101].Sepsis‑induced myocardial dysfunction is one of the features of multiple organ dysfunction in sepsis, which is associated with extremely high mortality and is characterized by impaired myocardial compliance. To date, there are few effective treatment options available to cure sepsis. Tannic acid (TA) is reportedly protective during sepsis; however, the underlying mechanisms by which TA protects against septic heart injury remain elusive. The present study investigated the potential effects and underlying mechanisms of TA in alleviating lipopolysaccharide (LPS)‑induced H9C2 cardiomyocyte cell apoptosis. H9C2 cells were treated with LPS (15 µg/ml), TA (10 µM) and TA + LPS; control cells were treated with medium only. Apoptosis was measured using flow cytometry, reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis. Additionally, the levels of cellular reactive oxygen species (ROS), malondialdehyde and nicotinamide adenine dinucleotide phosphate were evaluated. Western blotting and RT‑qPCR wosis. Collectively, the present findings demonstrated that the protective effects of TA against LPS‑induced H9C2 cell apoptosis may be associated with the amelioration of ROS‑mediated ERS. These findings may assist the development of potential novel therapeutic methods to inhibit the progression of myocardial cell injury.Cell‑cell fusion is a dynamic biological phenomenon, which plays an important role in various physiological processes, such as tissue regeneration. Similarly, normal cells, particularly bone marrow‑derived cells (BMDCs), may attempt to fuse with cancer cells to rescue them. The rescue may fail, but the fused cells end up gaining the motility traits of BMDCs and become metastatic due to the resulting genomic instability. In fact, cell‑cell fusion was demonstrated to occur in vivo in cancer and was revealed to promote tumor metastasis. However, its existence and role may be underestimated, and has not been widely acknowledged. In the present review, the milestones in cell fusion research were highlighted, the evidence for cell‑cell fusion in vitro and in vivo in cancer was evaluated, and the current understanding of the molecular mechanisms by which cell‑cell fusion occurs was summarized, to emphasize their important role in tumor metastasis. The summary provided in the present review may promote further study into this process and result in novel discoveries of strategies for future treatment of tumor metastasis.Nasopharyngeal carcinoma (NPC) is a tumor located in the nasopharynx with highly invasive and metastatic properties. Metastasis is a primary cause of mortality in patients with NPC. The terpenoid polyphenol pinosylvin is a known functional compound of the Pinus species that exhibits anti‑inflammatory effects; however, the effect of pinosylvin on human NPC cell migration and invasion is unclear. The present study aimed to investigate the functional role of pinosylvin in NPC cells (NPC‑039, NPC‑BM and RPMI 2650). Gap closure and Transwell assay indicated that pinosylvin at increasing concentrations inhibited migration and invasion of NPC‑039 and NPC‑BM cells. In addition to inhibiting the enzyme activity of MMP‑2, pinosylvin also decreased the protein expression levels of MMP‑2 and MMP‑9. Pinosylvin decreased the expression of vimentin and N‑cadherin and significantly increased the expression of zonula occludens‑1 and E‑cadherin in NPC cells. ZEN-3694 Epigenetic Reader Domain inhibitor Additionally, pinosylvin suppressed the invasion and migration ability of NPC‑039 and NPC‑BM cells by mediating the p38, ERK1/2 and JNK1/2 pathways. The present results revealed that pinosylvin inhibited migration and invasion in NPC cells.Cervical cancer is considered one of the diseases with the highest mortality among women and with limited treatment options. Hydrogen (H2) inhalation has been reported to have a variety of tumor‑suppressive effects, but the exact mechanism remains unclear. In the present study, HeLa cervical cancer cells and HaCaT keratinocytes treated with H2, and a HeLa xenograft mouse model subjected to H2 inhalation were established. TUNEL, Cell Counting Kit‑8 and Ki67 staining assays were used to detect cell apoptosis and proliferation. Oxidative stress was determined according to the levels of reactive oxygen species, malondialdehyde and superoxide dismutase. Tumor growth was recorded every 3 days, and the excised tumors were stained with hematoxylin and eosin. High‑throughput RNA sequencing and subsequent Gene Ontology (GO) enrichment analysis were performed in HeLa‑treated and un‑treated HeLa cells. The expression of hypoxia‑inducible factor (HIF)‑1α and NF‑κB p65 was verified by western blotting, immunohistochemistry and reverse transcription‑quantitative PCR.