galangin and Neoplasms

Galangin, a non-toxic phytochemical is known to possess several therapeutic applications. Mounting evidences have demonstrated that galangin a naturally available flavonoid exerts anticancer effects via several mechanisms. The phytocompound induces apoptosis and renders antiangiogenic property. Additionally, galangin has demonstrated significate results in combating various cancer types when administered in combination with other phytocompounds or with gold nanoparticles (GNPs). The present article is a critical review of galangin for its treatment on different types of cancer and its usability as an alternative cancer therapeutics.

Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Flavonoids; Gold; Humans; Metal Nanoparticles; Neoplasms; Phytotherapy

Topics: Animals; Antineoplastic Agents; Enzyme Inhibitors; Gene Regulatory Networks; Humans; Neoplasms; Protein Structure, Secondary; Sarcoplasmic Reticulum Calcium-Transporting ATPases

Flavonoids are polyphenolic compounds that are present in plants. They have been shown to possess a variety of biological activities at non-toxic concentrations in organisms. Galangin, a member of the flavonol class of flavonoid, is present in high concentrations in medicinal plants (e.g. Alpinia officinarum) and propolis, a natural beehive product. Results from in vitro and in vivo studies indicate that galangin with anti-oxidative and free radical scavenging activities is capable of modulating enzyme activities and suppressing the genotoxicity of chemicals. These activities will be discussed in this review. Based on our review, galangin may be a promising candidate for cancer chemoprevention.

Topics: Alkylating Agents; Animals; Anticarcinogenic Agents; Antimutagenic Agents; Antioxidants; Carcinogens; Cell Division; Cyclooxygenase 2; DNA Adducts; Flavonoids; Humans; In Vitro Techniques; Isoenzymes; Membrane Proteins; Neoplasms; Polycyclic Aromatic Hydrocarbons; Prostaglandin-Endoperoxide Synthases; Radiation-Protective Agents; Structure-Activity Relationship

In vertebrates, the glucuronidation of small lipophilic agents is catalyzed by the endoplasmic reticulum UDP-glucuronosyltransferases (UGTs). This metabolic pathway leads to the formation of water-soluble metabolites originating from normal dietary processes, cellular catabolism, or exposure to drugs and xenobiotics. This classic detoxification process, which led to the discovery nearly 50 years ago of the cosubstrate UDP-glucuronic acid (19), is now known to be carried out by 15 human UGTs. Characterization of the individual gene products using cDNA expression experiments has led to the identification of over 350 individual compounds that serve as substrates for this superfamily of proteins. This data, coupled with the introduction of sophisticated RNA detection techniques designed to elucidate patterns of gene expression of the UGT superfamily in human liver and extrahepatic tissues of the gastrointestinal tract, has aided in understanding the contribution of glucuronidation toward epithelial first-pass metabolism. In addition, characterization of the UGT1A locus and genetic studies directed at understanding the role of bilirubin glucuronidation and the biochemical basis of the clinical symptoms found in unconjugated hyperbilirubinemia have uncovered the structural gene polymorphisms associated with Crigler-Najjar's and Gilbert's syndrome. The role of the UGTs in metabolism and different disease states in humans is the topic of this review.

Topics: Autoimmunity; Chromosome Mapping; Glucuronides; Glucuronosyltransferase; Humans; Hyperbilirubinemia; Neoplasms; Steroids; Terminology as Topic

Smad3 linker phosphorylation is a candidate target for several kinases that play important roles in cancer cell initiation, proliferation and progression. Also, Smad3 is an essential intracellular mediator of TGF-β1-induced transcriptional responses during carcinogenesis. Therefore, it is highly advantageous to identify and develop inhibitors targeting Smad3 linker phosphorylation for the treatment of cancers. Galangin (3,5,7-trihydroxyflavone) has been known to be an active flavonoid showing a cytotoxic effect on several cancer cells. However, the mechanism of action of galangin in various cancers remains unclear, and there has been no report concerning regulation of Smad3 phosphorylation by galangin. In the present study, we show that galangin significantly induced apoptosis and inhibited cell proliferation in the presence of TGF-β1 in both human prostate and pancreatic cancer cell lines. Particularly, galangin effectively inhibits phosphorylation of the Thr-179 site at Smad3 linker region through suppression of CDK4 phosphorylation. Thus, galangin can be a promising candidate as a selective inhibitor to suppress phosphorylation of Smad3 linker region.

Topics: Antineoplastic Agents; Apoptosis; Binding Sites; Cell Line, Tumor; Cell Proliferation; Flavonoids; Humans; Neoplasms; Phosphorylation; Protein Binding; Smad3 Protein; Threonine; Transforming Growth Factor beta1; Treatment Outcome