Blog
About

38
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      De novo fatty-acid synthesis and related pathways as molecular targets for cancer therapy

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Enhanced lipid biosynthesis is a characteristic feature of cancer. Deregulated lipogenesis plays an important role in tumour cell survival. These observations suggest that enzymes in the lipid synthesis pathway would be rational therapeutic targets for cancer. To this end, we review the enzymes in de novo fatty-acid synthesis and related pathways.

          Related collections

          Most cited references 34

          • Record: found
          • Abstract: not found
          • Article: not found

          On the origin of cancer cells.

           O WARBURG (1956)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found

            Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis.

            There is a renewed interest in the ultimate role of fatty acid synthase (FASN)--a key lipogenic enzyme catalysing the terminal steps in the de novo biogenesis of fatty acids--in cancer pathogenesis. Tumour-associated FASN, by conferring growth and survival advantages rather than functioning as an anabolic energy-storage pathway, appears to necessarily accompany the natural history of most human cancers. A recent identification of cross-talk between FASN and well-established cancer-controlling networks begins to delineate the oncogenic nature of FASN-driven lipogenesis. FASN, a nearly-universal druggable target in many human carcinomas and their precursor lesions, offers new therapeutic opportunities for metabolically treating and preventing cancer.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found

              ATP citrate lyase inhibition can suppress tumor cell growth.

              Many tumors display a high rate of glucose utilization, as evidenced by 18-F-2-deoxyglucose PET imaging. One potential advantage of catabolizing glucose through glycolysis at a rate that exceeds bioenergetic need is that the growing cell can redirect the excess glycolytic end product pyruvate toward lipid synthesis. Such de novo lipid synthesis is necessary for membrane production and lipid-based posttranslational modification of proteins. A key enzyme linking glucose metabolism to lipid synthesis is ATP citrate lyase (ACL), which catalyzes the conversion of citrate to cytosolic acetyl-CoA. ACL inhibition by RNAi or the chemical inhibitor SB-204990 limits in vitro proliferation and survival of tumor cells displaying aerobic glycolysis. The same treatments also reduce in vivo tumor growth and induce differentiation.
                Bookmark

                Author and article information

                Affiliations
                [1 ]simpleDivision of Molecular Biotherapy, Cancer Chemotherapy Centre, Japanese Foundation for Cancer Research, 3-10-6 Ariake, Koto-ku Tokyo 135-8550, Japan
                [2 ]simpleDirector's Room, Cancer Chemotherapy Centre, Japanese Foundation for Cancer Research, 3-10-6 Ariake, Koto-ku Tokyo 135-8550, Japan
                Author notes
                [* ]Author for correspondence: tmashima@ 123456jfcr.or.jp
                [3]

                Takashi Tsuruo would have been the corresponding author had he lived to see the paper's publication

                Journal
                Br J Cancer
                British Journal of Cancer
                Nature Publishing Group
                0007-0920
                1532-1827
                07 April 2009
                28 April 2009
                05 May 2009
                : 100
                : 9
                : 1369-1372
                2694429
                6605007
                10.1038/sj.bjc.6605007
                19352381
                Copyright 2009, Cancer Research UK
                Categories
                Minireview

                Oncology & Radiotherapy

                lipid metabolism, fatty-acid synthase, acyl-coa synthetase

                Comments

                Comment on this article