HighlightsExercise can be used as an active intervention for the rehabilitation of various diseases.Exercise therapy could exert positive effects on alleviating the symptoms and improving the physical performance of patients who suffer from these diseases.Exercise prescriptions could provide guidance for patients to engage in suitable physical activities to promote rehabilitation and physical function.

Introduction: Marathon, as a long-distance aerobic exercise, has become a fashionable or popular sport. However, little is known about the holistic metabolic changes occurring within the serum metabolome of athletes after the completion of a marathon. Objectives: The goal of current study was to have an in-depth understanding of the impact of marathon on human metabolomics as well as the relationships among a variety of metabolites. Methods:The 20 studied subjects were all adult males who participated in a marathon. The serum samples of these participants were collected before and after the marathon and the biochemical metabolites in the serum were identified by an untargeted two-dimensional gas chromatography time-of-flight mass spectrometry.Results: All participants completed the marathon within 3 h. Compared to those before exercise, serum urea and creatine kinase, as well as cortisol, elevated significantly (p < 0.05), whereas testosterone decreased significantly (p < 0.01). Metabolomic analysis showed that, compared to those before the competition, metabolites pyruvic acid, glyceric acid, malic acid, cis-aconitic acid, galacturonic acid, methyl fumaric acid, maltotriose, and others increased significantly after the competition (p < 0.05), but glucosamine and O-succinyl-L-homoserine decreased significantly (p < 0.05). Amino acid indexes, such as alanine, L-tyrosine and phenylalanine, increased significantly after exercise compared with those before exercise (p < 0.05), whereas serine, valine and asparagine decreased significantly (p < 0.05). Lipid metabolism indexes, glycerol, glyceric acid, octanoic acid, and quinic acid increased significantly (p < 0.05). Theophylline, xanthine and other indicators of caffeine metabolism increased significantly (p < 0.05). Furthermore, marathon performance, fat percentage, VO 2 max, and hemoglobin were correlated with the serum metabonomic indicators, so were serum testosterone and cortisol.Conclusion: These results illustrate that the metabolism of glucose and lipid of the athletes was enhanced following the marathon match. In addition, the metabolism of glucosamine was decreased and the metabolism of caffeine was increased. Our data provide new insights for marathon performance and nutritional status.

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MicroRNAs (miRs), a class of non-coding RNAs 18-25 nucleotides in length, can lead to mRNA degradation or inhibit protein translation by directly binding to the 3'-untranslational region (UTR) of their target mRNAs. The deregulation of miR-429 has been suggested to be involved in the development and progression of colon cancer. However, the detailed molecular mechanism involved remains to be determined. The aim of the present study was to investigate the role of miR-429 in the regulation of migration and invasion of colon cancer cells using RT-qPCR and western blotting. The results showed that the expression of miR-429 was reduced in colon cancer cell lines, when compared to a normal colon epithelial cell line. Treatment with DNA demethylation agent 5-aza-2'-deoxycytidine and histone deacetylase inhibitor phenylbutyrate (PBA), or transfection with the pre-miR-429 lentivirus plasmid led to the upregulation of miR-429 expression, as well as inhibition of migration and invasion in colon cancer cells. Investigation of the molecular mechanism showed that PAK6 was a novel target of miR-429, and the expression of PAK6 was upregulated in colon cancer tissues and cell lines, and was negatively regulated by miR-429 in colon cancer cells. Moreover, the cofilin signaling acted as a downstream effector of miR-429 in colon cancer cells. In conclusion, the results of the present study suggested that miR-429 inhibits the migration and invasion of colon cancer cells, partly at least, by mediating the expression of PAK6, as well as the activity of cofilin signaling. Therefore, miR-429 is as a potential molecular target for the treatment of colon cancer.