Effect of curcumin on the proliferation, apoptosis, migration, and invasion of human melanoma A375 cells.

Malignant melanoma is a melanocytic tumor with a high potential of invasion and metastasis. Curcumin is extracted from Curcuma longa L.; curcumin has anti-tumor efficacy in multiple systemic malignancies. Here, we investigated the effect of curcumin on A375 human melanoma cells. A375 cells were cultivated, passaged, and treated with different concentrations of curcumin. We observed the cellular morphology and determined the migration, invasion, proliferation, and apoptosis of A375 cells in vitro. Our results showed that curcumin induced a significant change in the morphology of A375 cells. Compared to the control group, the groups treated with curcumin showed significantly wider scratches, and the number of A375 cells significantly decreased in the 12.5, 25, and 50 mM curcumin groups (P < 0.05 or < 0.01). The rates of proliferation inhibition in the 5 curcumin groups were 19.38 ± 3.57%, 35.56 ± 4.37%, 63.98 ± 5.95%, 86.38 ± 3.91%, and 95.56 ± 3.15%. The half-maximal inhibitory concentration of curcumin at 48 h was 10.05 mM. The rates of apoptosis in 6.25 and 12.5 mM curcumin groups were significantly higher (P < 0.05), phosphorylation levels of JAK-2 and STAT-3 in 10 and 20 mM curcumin groups were significantly lower (P < 0.05), and Bcl-2 protein expression in 1, 2.5, 5, 10, and 20 curcumin groups was significantly lower (P < 0.05) than that in the control group. In conclusion, curcumin has antiproliferative and proapoptotic activities on A375 cells, the mechanism of which may be related to the inhibition of JAK-2/STAT-3 signaling pathway.

Developmental specificity in skeletal muscle of late-term avian embryos and its potential manipulation.

Unlike the mammalian fetus, development of the avian embryo is independent of the maternal uterus and is potentially vulnerable to physiological and environmental stresses close to hatch. In contrast to the fetus of late gestation in mammals, skeletal muscle in avian embryos during final incubation shows differential developmental characteristics: 1) muscle mobilization (also called atrophy) is selectively enhanced in the type II fibers (pectoral muscle) but not in the type I fibers (biceps femoris and semimembranosus muscle), involving activation of ubiquitin-mediated protein degradation and suppression of S6K1-mediated protein translation; 2) the proliferative activity of satellite cells is decreased in the atrophied muscle of late-term embryos but enhanced at the day of hatch, probably preparing for the postnatal growth. The mobilization of muscle may represent an adaptive response of avian embryos to external (environmental) or internal (physiological) changes, considering there are developmental transitions both in hormones and requirements for glycolytic substrates from middle-term to late-term incubation. Although the exact mechanism triggering muscle fiber atrophy is still unknown, nutritional and endocrine changes may be of importance. The atrophied muscle fiber recovers as soon as feed and water are available to the hatchling. In ovo feeding of late-term embryos has been applied to improve the nutritional status and therein enhances muscle development. Similarly, in ovo exposure to higher temperature or green light during the critical period of muscle development are also demonstrated to be potential strategies to promote pre- and posthatch muscle growth.