Research Note: Transcriptome analysis reveals differentially expressed genes regulated muscle development in Pekin ducks during dietary threonine deficiency.

To investigate the underlying molecular mechanism of threonine (Thr) regulation on the development of breast muscle in Pekin ducks, 240 male Pekin ducks at 1 d of age were fed a Thr deficiency diet (Thr-D), Thr sufficiency diet (Thr-S), or Thr excess diet (Thr-E) for 21 d. The results showed that Thr-D reduced body weight (BW), average weight gain (ADG), and average feed intake (ADFI), and increased the feed/gain (F/G) in Pekin ducks (P < 0.05), and Thr-E did not affect BW, ADG, ADFI, or F/G (P > 0.05), compared with Thr-S. The diameter and cross-sectional area of the breast muscle fibers in the Thr-S group were larger than those in the Thr-D group (P < 0.05). RNA sequencing revealed 1,300 differential expressed genes (DEGs) between the Thr-D and Thr-S groups, of which 625 were upregulated and 675 were downregulated by Thr-D. KEGG analysis showed that the upregulated genes were enriched in mTOR, FoxO, Wnt, fat digestion and absorption, and other signaling pathways. The downregulated genes were enriched in the MAPK signaling, glycolysis/gluconeogenesis, adipocytokine signaling, and biosynthesis of unsaturated fatty acids signaling pathways. The genes of Wnt family member 3a (Wnt3a), myogenin, myozenin 2, and insulin like growth factor 2 mRNA binding protein were upregulated, and platelet derived growth factor subunit B, PDGF receptor beta and Wnt4 were downregulated by Thr deficiency, which involving in muscle development. Our findings indicated that Thr increased breast fiber size, perhaps because Thr affected the proliferation and differentiation of satellite cells in breast muscle of ducks after hatch. Our results provide novel insights into new understanding of the molecular mechanisms underlying breast muscle development in ducks subjected to dietary Thr.

Analysis of Selenium Levels in Osteosarcoma Patients and the Effects of Se-Methylselenocysteine on Osteosarcoma Cells In Vitro.

The form of selenium appears to be important for preventing cancer in humans. Here, we evaluated selenium levels in the serum and bone tissue samples from osteosarcoma patients using atomic absorption spectrometry. The in vitro effects of Se-methylselenocysteine (Se-MSC) on growth, cell cycle status, and apoptosis of osteosarcoma cells were assessed using the WST-1 assay, Hoechst 33342/propidium iodide staining, and flow cytometry, respectively. In osteosarcoma cases, the mean serum selenium levels in osteosarcoma tissue and normal bone were 0.08 mg/kg and 0.03 mg/kg, respectively (P < 0.05). Serum selenium levels in osteosarcoma and non-osteosarcoma cases were 0.09 mg/L and 0.08 mg/L, respectively (P > 0.05). Se-MSC-treated MG63 cells showed altered cellular morphology, decreased viability in a time- and dose-dependent manner, and an increase in the sub-G1 cell population. Se-MSC also downregulated Bcl-2 expression and upregulated Bax. Se-MSC inhibited the proliferation of the drug-resistant osteosarcoma cell line Saos-2/MTX300 and enhanced the inhibitory effect of pirarubicin on MG63 cells. Our data demonstrate that selenium levels are significantly higher in osteosarcoma tissue than normal bone tissue in osteosarcoma patients. The results also support the anticancer effects of Se-MSC in osteosarcoma. Further development of Se-MSC as an ancillary chemotherapy agent in osteosarcoma is warranted.