Efficacy of postharvest sodium nitroprusside application to extend storability by regulating physico-chemical quality of pear fruit.

Quality loss in pear fruit during storage reduces its marketability for long run. To increase its storability, the efficacy of postharvest dip treatment donor sodium nitroprusside (SNP) 0.000, 0.001, 0.002 and 0.003 mol L-1 were investigated on pear fruit cv. Patharnakh under storage conditions (low temperature 0-1 °C and relative humidity (90-95%). SNP effectively lowered fruit mass loss, retained colour and higher firmness, suppressed browning and respiration rate and sustained soluble solids content, titratable acidity, total phenol content and ascorbic acid thus conserved the fruit quality for longer period. SNP treatments suppressed the activity of polyphenol oxidase and increased activity of superoxide dismutase enzyme. Additionally, the SNP treated fruit exhibited lesser activities of fruit softening enzymes like pectin methylesterase, polygalacturonase and cellulase. Among all, 0.002 mol L-1 SNP concentration was superior to lengthen storability and sensory quality of pear up to 60 d under cold storage.

Inverse PPARß/δ agonists suppress oncogenic signaling to the ANGPTL4 gene and inhibit cancer cell invasion.

Besides its established functions in intermediary metabolism and developmental processes, the nuclear receptor peroxisome proliferator-activated receptor ß/δ (PPARß/δ) has a less defined role in tumorigenesis. In the present study, we have identified a function for PPARß/δ in cancer cell invasion. We show that two structurally divergent inhibitory ligands for PPARß/δ, the inverse agonists ST247 and DG172, strongly inhibit the serum- and transforming growth factor ß (TGFß)-induced invasion of MDA-MB-231 human breast cancer cells into a three-dimensional matrigel matrix. To elucidate the molecular basis of this finding, we performed chromatin immunoprecipitation sequencing (ChIP-Seq) and microarray analyses, which identified the gene encoding angiopoietin-like 4 (ANGPTL4) as the major transcriptional PPARß/δ target in MDA-MB-231 cells, previously implicated in TGFß-mediated tumor progression and metastatic dissemination. We show that the induction of ANGPTL4 by TGFß and other oncogenic signals is strongly repressed by ST247 and DG172 in a PPARß/δ-dependent fashion, resulting in the inhibition of ANGPTL4 secretion. This effect is attributable to these ligands' ability to induce a dominant transcriptional repressor complex at the site of transcription initiation that blocks preinitiation complex formation through an histone deacetylase-independent, non-canonical mechanism. Repression of ANGPTL4 transcription by inverse PPARß/δ agonists is functionally linked to the inhibition of cancer cell invasion into a three-dimensional matrix, as (i) invasion of MDA-MB-231 cells is critically dependent on ANGPTL4 expression, (ii) recombinant ANGPTL4 stimulates invasion, and (iii) reverses the inhibitory effect of ST247 and DG172. These findings indicate that a PPARß/δ-ANGPTL4 pathway is involved in the regulation of tumor cell invasion and that its pharmacological manipulation by inverse PPARß/δ agonists is feasible.