Piceatannol mediated regulation of deregulated signaling pathways in different cancers: Tumbling of the ninepins of molecular oncology.

With the recent technological advancements, a new golden era of natural products drug discovery has dawned. Increasingly it is being realized that structural modularity of many pharmacologically active products derived natural sources allows a building-block approach which can be exploited for analysis of regulation of deregulated oncogenic protein networks in different cancers. Piceatannol has been shown to effectively modulate JAK/STAT, Wnt/ß-catenin, mTOR pathway in different cancers. In addition, certain hints have emerged which shed light on the regulation of microRNAs by piceatannol in some cancers. Regulation of deregulated oncogenic pathways by Piceatannol is gradually capturing attention and might be helpful in the multi-targeting of deregulated oncogenic networks in cancers.

Regulation of Hippo, TGFß/SMAD, Wnt/ß-Catenin, JAK/STAT, and NOTCH by Long Non-Coding RNAs in Pancreatic Cancer.

Rapidly evolving and ever-increasing knowledge of the molecular pathophysiology of pancreatic cancer has leveraged our understanding altogether to a next level. Compared to the exciting ground-breaking discoveries related to underlying mechanisms of pancreatic cancer onset and progression, however, there had been relatively few advances in the therapeutic options available for the treatment. Since the discovery of the DNA structure as a helix which replicates semi-conservatively to pass the genetic material to the progeny, there has been conceptual refinement and continuous addition of missing pieces to complete the landscape of central dogma. Starting from transcription to translation, modern era has witnessed non-coding RNA discovery and central role of these versatile regulators in onset and progression of pancreatic cancer. Long non-coding RNAs (lncRNAs) have been shown to act as competitive endogenous RNAs through sequestration and competitive binding to myriad of microRNAs in different cancers. In this article, we set spotlight on emerging evidence of regulation of different signaling pathways (Hippo, TGFß/SMAD, Wnt/ß-Catenin, JAK/STAT and NOTCH) by lncRNAs. Conceptual refinements have enabled us to understand how lncRNAs play central role in post-translational modifications of various proteins and how lncRNAs work with epigenetic-associated machinery to transcriptionally regulate gene network in pancreatic cancer.

Mutational screening of GABRG2 gene in Pakistani population of Punjab with generalized tonic clonic seizures and children with childhood absence epilepsy.

BACKGROUND: Epilepsy is a multifaceted and multistep disorder that disrupts the proper functioning of neurons. It is becoming increasingly clear that the responsiveness of neurons depends on the appropriate trafficking of ions across the channels in the membrane of neurons. In line with this notion, impairment among these ion channels due to mutations has gain increasing attention in molecular neuroscience. METHODS: Mutation analysis of the coding exons (exon 3, 5 and 9) was performed by sequencing GABRG2 to identify any complex biological entities among two different types of epilepsies. RESULTS: Sequencing of the candidate gene "GABRG2" revealed a single polymorphic site in exon 3 in the children with absence epilepsy and generalized tonic clonic seizures. However, this single nucleotide alteration was more common in the patients with childhood absence epilepsy patients compared to the generalized cases. CONCLUSION: A silent mutation was identified at locus 27,909 C > T in 30.66% of the total screened or analyzed cases. However, no single nucleotide polymorphism was identified in exon 5 of GABRG2 in a Pakistani population, in contrast to a study of Chinese patients with childhood absence epilepsy.