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Algae extracts and methyl jasmonate anti-cancer activities in prostate cancer: choreographers of ‘the dance macabre’

DOI: 10.1186/1475-2867-12-50

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Abstract:

Scientists worldwide are making efforts to design targeted therapies that can kill cancer cells without harming normal cells. Such therapies primarily rely on understanding of how and by what mean cancer cells differ from normal non-transformed cells. It is comprehensible that cancer cells do not resemble normal cells in terms of morphology and behavior. Confluence of information suggests that bioactive components extracted from algae, as well as methyl jasmonate (a natural compound belongs to the jasmonates family of plant stress hormones), seem to have anti-cancer activities through multiple mechanisms of action, including inhibition of cancer-cell growth and of invasion and metastasis, and through the promotion of apoptosis of cancerous cells. Considerable emerging evidence supports the inhibitory actions of bioactive components of algae and methyl jasmonate on prostate cancer. The purpose of this mini-review is to bring to limelight the findings from recent research regarding the potential effects and mechanisms of action of bioactive components of algae and methyl jasmonate on cancer. Finally, we highlight the research efforts that need to be made to facilitate the optimal development of algae derived bioactive ingredients.Cell death pathway is subdivided into two categories namely extrinsic pathway and intrinsic pathway and former is initiated by binding of the extracellular ligands, TNF (tumour necrosis factor-) or FAS (apoptosis antigen-1) ligand (FASL), to death receptors TNFR1 (TNF-receptor1) and FAS. The resulting heteromeric complex activates procaspase 8, that mediates apoptosis through caspase 3 or alternatively another pathway intrinsic pathway is opted that initiates via cleavage of BID to tBID (truncated BID). FAS-mediated death occurs through a FADD-mediated activation of procaspase 8. Membrane permeabilization is an important step in intrinsic pathway and is mediated by BH3-only proteins, which sequester and restore the activity of BAX. It is nota

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