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Áö¹æ ¡í Áö¹æÀÇ ÇÕ¼º ¡í Ethylene

Áö¹æÀÇ ÇÕ¼º Ethylene -->Poly ethylene

Áö¹æÀÇ ÇÕ¼º
- ¿¡Æ¿·» : Æú¸®¿¡Æ¿·», ½Ä¹°È£¸£¸ó
- Áö¹æ»êÀÇ ÇÕ¼º , ÃàÀû, Áö¹æ´ë»ç : ºÐÇØ
- Áö¹æ»êÀÇ Á¾·ù
- À̼ÒÇÁ·¹³ëÀ̵å ÇÕ¼º
- HCA, ±¸¿¬»ê --> Acetyl Coa

    



 

 

One of the most important and most common features of cancer cells is the dramatic reprogramming of their metabolic pathways (1). Because of the high proliferation rate of cancer cells, demand for energy and macromolecules is increased. To cope with these elevated requirements, cancer cells undergo major modifications in their metabolic pathways. One of the most important metabolic hallmarks of cancer cells is increased de novo lipid synthesis (2). Lipid synthesis pathways may include the fatty acid synthesis pathway as well as the mevalonate pathway, which leads to the synthesis of cholesterol and isoprenoids.
Various types of tumors display enhanced endogenous fatty acid biosynthesis, irrespective of levels of extracellular lipids (3). Most normal cells, even those with comparatively high proliferation rates, preferentially use dietary and/or exogenous lipids for synthesis of new structural lipids (2, 3). Some normal tissues also have a very active fatty acid synthesis pathway, such as adipocytes, hepatocytes, hormone-sensitive cells (4), and fetal lung tissue (5); however, in general, de novo fatty acid synthesis is suppressed in most normal cells. The upregulated fatty acid synthesis in cancer cells fuels membrane biogenesis in rapidly proliferating cancer cells and renders membrane lipid more saturated (6), thereby affecting fundamental cellular processes, including signal transduction, gene expression, ciliogenesis, and therapy response (6). The upregulated fatty acid synthesis in tumor cells is reflected by a substantial increase in expression and activity of various enzymes involved in the fatty acid synthesis pathway (3).
Several research groups have also associated the mevalonate pathway with cancer cell growth and transformation (7, 8). The first and rate-limiting step in this pathway is the formation of mevalonate by the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR). Inhibition of HMGCR in normal cells triggers a robust homeostatic feedback response that ensures the cells upregulate and restore the mevalonate pathway (9). However, a number of tumors have been reported to have either deficient feedback control of HMGCR or increased HMGCR expression and activity (10).
ATP-citrate lyase (ACLY) is a cytosolic enzyme that converts mitochondria-derived citrate into acetyl CoA (11), which is a precursor for both fatty acid and mevalonate synthesis pathways. ACLY is reported to be upregulated in cancer cells, and its inhibition suppresses proliferation of certain types of tumor cells (12–14). This review focuses on current understanding of the role of ACLY in mediating tumor growth and its importance as a therapeutic target for cancer.

 

 


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ATP citrate lyase is the primary enzyme responsible for the synthesis of cytosolic acetyl-CoA in many tissues. The enzyme is a tetramer of apparently identical subunits. The product, acetyl-CoA, in animals serves several important biosynthetic pathways, including lipogenesis and cholesterogenesis.[4] It is activated by insulin.[5] In plants, ATP citrate lyase generates the acetyl-CoA for cytosolically-synthesized metabolites. (Acetyl-CoA is not transported across subcellular membranes of plants.) These include: elongated fatty acids (used in seed oils, membrane phospholipids, the ceramide moiety of sphingolipids, cuticle, cutin, and suberin); flavonoids; malonic acid; acetylated phenolics, alkaloids, isoprenoids, anthocyanins, and sugars; and, mevalonate-derived isoprenoids (e.g., sesquiterpenes, sterols, brassinosteroids); malonyl and acyl-derivatives (d-amino acids, malonylated flavonoids, acylated, prenylated and malonated proteins).[3] De novo fatty acid biosynthesis in plants is plastidic, thus ATP citrate lyase is not important for this pathway.

citrate + ATP + CoA ¡æ oxaloacetate + Acetyl-CoA + ADP + Pi