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      • Molecular Mechanisms of Casticin Action: an Update on its Antitumor Functions

        Rasul, Azhar,Zhao, Bin-Ji,Liu, Jun,Liu, Bao,Sun, Jia-Xin,Li, Jiang,Li, Xiao-Meng Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.21

        Casticin (3', 5-dihydroxy-3, 4', 6, 7-tetramethoxyflavone) is an active compound isolated from roots, stems, leaves, fruits and seeds of a variety of plants. It is well known for its pharmacological properties and has been utilized as an anti-hyperprolactinemia, anti-tumor, anti-inflammatory, neuroprotetective, analgesic and immunomodulatory agent. Recently, the anticancer activity of casticin has been extensively investigated. The resulkts showed that it exerts protective potential by targeting apoptosis, considered important for cancer therapies. In this article, our aim was to review the pharmacological and therapeutic applications of casticin with specific emphasis on its anticancer functions and related molecular mechanisms. Chemotherapeutic effects are dependent on multiple molecular pathways, which may provide a new perspective of casticin as a candidate anti-neoplastic drug. This review suggests that additional studies and preclinical trials are required to determine specific intracellular sites of action and derivative targets in order to fully understand the mechanisms of its antitumor activity and validate this compound as a medicinal agent for the prevention and treatment of various cancers.

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        Isoalantolactone, a sesquiterpene lactone, induces apoptosis in SGC-7901 cells via mitochondrial and phosphatidylinositol 3-kinase/Akt signaling pathways

        Azhar Rasul,Muhammad Khan,Bo Yu,Muhammad Ali,Yang Jing Bo,Hong Yang,Tonghui Ma 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.10

        Isoalantolactone, a sesquiterpene lactone, possessesanti-fungal as well as cytotoxic properties. In thisstudy, the effects of Isoalantolactone on cell viability, cellcycle, and apoptosis were investigated in human gastricadenocarcinoma SGC-7901 cells. The results demonstratedthat Isoalantolactone induced morphological changes anddecreased cell viability. Subsequently, we found that Isoalantolactoneinduced G2/M and S phase arrest, which wasassociated with a decrease in the expression level of cyclinB1. Apoptosis triggered by Isoalantolactone was visualizedusing propidium iodide (PI) and Annexin V-FITC/PIstaining. Isoalantolactone-induced apoptosis of SGC-7901cells was associated with the dissipation of mitochondrialmembrane potential (DWm) that was due to the down-regulationof Bcl-2 and up-regulation of Bax that led to thecleavage of caspase-3. Additionally, it was found thatIsoalantolactone was involved in the inhibition of phosphorylationof PI3K/Akt. Isoalantolactone-induced cytotoxicityand apoptosis of SGC-7901 cells involvemitochondria-caspase and PI3K/Akt dependent pathways,which gives the rationale for in vivo studies on the utilizationof Isoalantolactone as a potential cancer therapeuticcompound.

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