Notes

Successful Surgery and Endovascular Multidisciplinary Treatments regarding Mid-aortic Malady with Complicated Atherosclerotic Comorbidities within an More mature Patient.
The results demonstrated that curcumin inhibited BCAT1 expression in Kasumi‑1, KG‑1, HL60, cytarabine‑resistant HL60, and cytarabine‑resistant primary myeloid leukemia cells. Notably, tetrahydrocurcumin, a major metabolite of curcumin, and cytarabine had no inhibitory effect on BCAT1 expression. Furthermore, BCAT1 and mTOR signaling may modulate each other in cytarabine‑resistant HL60 cells. The present results indicated that curcumin may induce apoptosis by inhibiting the BCAT1 and mTOR pathways. Thus, understanding the mechanism underlying curcumin‑induced apoptosis in cytarabine‑resistant cells can support the development of novel drugs for leukemia.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the cell Transwell assay data in the article (featured in Figs. 2C and 4C) were strikingly similar to data appearing in different form in other articles by different authors at different research institutions, which were already under consideration for publication or had already been published elsewhere at the time of the present article's submission [C. Lai et al, 'MicroRNA‑133a inhibits proliferation and invasion, and induces apoptosis in gastric carcinoma cells via targeting fascin actin‑bundling protein 1', Mol Med Rep 12 1473‑1478, 2015; and Y. Shi et al, 'MicroRNA‑204 inhibits proliferation, migration, invasion and epithelial‑mesenchymal transition in osteosarcoma cells via targeting Sirtuin 1', Oncol Rep 34 399‑406, 2015]. Owing to the fact that the contentious data in the above article had already appeared in different form in other articles prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors did not reply to indicate whether or not they agreed with the retraction of the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 13 3349-3355, 2016; DOI 10.3892/mmr.2016.4901].Lung cancer is one of the most lethal diseases and therefore poses a significant threat to human health. The Warburg effect, which is the observation that cancer cells predominately produce energy through glycolysis, even under aerobic conditions, is a hallmark of cancer. 6‑phosphofructo‑2‑kinase/fructose‑2,6‑biphosphatase 2 (PFKFB) is an important regulator of glycolysis. Shikonin is a Traditional Chinese herbal medicine, which has been reported to exert antitumor effects. The present study aimed to investigate the anticancer activity of shikonin in lung cancer. Cell Counting Kit‑8 (CCK‑8) and colony formation assays were used to analyze proliferation in A549 and H446 cells. Wound healing and Transwell assays were used to measure migration and invasion in A549 and H446 cells. Cell apoptosis was analyzed using flow cytometry. Lactate levels, glucose uptake and cellular ATP levels were measured using their corresponding commercial kits. Western blotting was performed to analyze the protein expression levels oft shikonin inhibited the Warburg effect and exerted antitumor activity in lung cancer cells, which was associated with the downregulation of PFKFB2 expression.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Figs. 3C and 5A were strikingly similar to data appearing in different form in another article by different authors, which had already been published elsewhere at the time of the present article's submission. Furthermore, cell Transwell assay data in the article (featured in Fig. 4B) were strikingly similar to data appearing in different form in other articles by different authors, which were either already under consideration for publication or had already been published elsewhere at the time of the present article's. Owing to the fact that the contentious data in the above article were either already under consideration for publication, or had already been published elsewhere, prior to its submission to Molecular Medicine 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 never received any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 14 4422‑4428, 2016; DOI 10.3892/mmr.2016.5769].MicroRNAs (miRs) serve an important role in cell differentiation, proliferation and apoptosis by negatively regulating gene expression at the transcriptional or post‑transcriptional level. EI24 autophagy associated transmembrane protein (EI24) is a tumor suppressor gene that serves an important role in the occurrence and development of digestive system tumors. However, little is known regarding the relationship between EI24 and the prognosis of patients with colorectal cancer (CRC). Our previous study confirmed EI24 as the target molecule of miR‑483, using reporter gene detection. PTC596 clinical trial Thus, the aim of the present study was to elucidate the effect of the abnormal expression of miR‑483 on the malignant phenotype of CRC through a series of cell function experiments and nude mice tumorigenicity experiments, and to determine the expression level of EI24, a downstream target gene of miR‑483, in CRC and its relationship with patient prognosis. In CRC tissues and cells, the expression level of miR‑483 was upregulated, while the expression level of EI24 was downregulated. Cell function tests such as MTT assay, cell cycle assay, colony formation assay, Migration and invasion assays and nude mice tumorigenicity experiments demonstrated that the overexpression of miR‑483 promoted the proliferation, invasion and metastasis of CRC. Moreover, the reverse transcription‑quantitative PCR results indicated that overexpression of miR‑483 inhibited the expression level of EI24. The relationship between the clinical data and immunohistochemical results from 183 patients with CRC and survival was examined. It was found that the expression level of EI24 was positively associated with the prognosis of patients. As a cancer‑promoting factor, miR‑483 enhances the proliferation, migration and invasion of CRC cells by reducing the expression level of EI24.
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