This study focused on investigating anticancer effects of tocotrienols and the mechanisms of apoptosis induction by tocotrienols in vivo and in vitro. Dietary delivery of gamma-tocotrienol (gamma-T3) suppressed tumor growth in a syngeneic implantation mouse mammary cancer model

by inhibiting cell proliferation and inducing apoptosis. In cell culture Ispinesib molecular weight studies, gamma-T3 inhibited colony formation of a mouse mammary cancer cell line and human breast cancer cell lines. The anti-proliferative effects of tocotrienols were highly correlated with an increase in apoptosis based on Annexin V assessment. Treatment of human MDA-MB-231 and MCF-7 cells with gamma-T3 induced cleavages of PARP as well as caspase-8, -9, and -3. Additional analyses showed that gamma-T3 activated c-Jun NH(2)-terminal kinase (JNK) and p38 MAPK, and upregulated death find more receptor 5 (DR5) and C/EBP homologous protein (CHOP), an endoplasmic reticulum (ER) stress marker. Silencing either JNK or p38 MAPK reduced the increase in DR5 and CHOP and partially blocked gamma-T3-induced apoptosis. Both DR5 and CHOP upregulation were required

for gamma-T3-induced apoptosis, and DR5 was transcriptionally regulated by CHOP after gamma-T3 treatment. Moreover, gamma-T3 increased the level of other ER-stress markers. Taken together, these results suggest that upregulation of DR5 by gamma-T3 treatment is dependent on

JNK and p38 MAPK activation which is mediated by ER-stress.”
“Background: Maize rough dwarf disease (MRDD) Vorinostat is a devastating viral disease that results in considerable yield losses worldwide. Three major strains of virus cause MRDD, including maize rough dwarf virus in Europe, Mal de Rio Cuarto virus in South America, and rice black-streaked dwarf virus in East Asia. These viral pathogens belong to the genus fijivirus in the family Reoviridae. Resistance against MRDD is a complex trait that involves a number of quantitative trait loci (QTL). The primary approach used to minimize yield losses from these viruses is to breed and deploy resistant maize hybrids.\n\nResults: Of the 50 heterogeneous inbred families (HIFs), 24 showed consistent responses to MRDD across different years and locations, in which 9 were resistant and 15 were susceptible. We performed trait-marker association analysis on the 24 HIFs and found six chromosomal regions which were putatively associated with MRDD resistance. We then conducted QTL analysis and detected a major resistance QTL, qMrdd1, on chromosome 8. By applying recombinant-derived progeny testing to self-pollinated backcrossed families, we fine-mapped the qMrdd1 locus into a 1.2-Mb region flanked by markers M103-4 and M105-3. The qMrdd1 locus acted in a recessive manner to reduce the disease-severity index (DSI) by 24.2-39.3%.