Cytochalasin E, a member of the cytochalasin group, is an inhibitor of actin polymerization in blood platelets. It inhibits angiogenesis and tumor growth. Unlike cytochalasin A and cytochalasin B, it does not inhibit glucose transport. Cytochalasin E, however, was noted to decrease glucose absorption in mice around the intestinal tissues by increasing the Km needed for glucose to reach the Vmax, which meant that a higher concentration of glucose was required in its presence to attain Vmax. Since Vmax remained the same according to another study, it is evident that CE is indeed a competitive inhibitor at the intestinal receptor sites for glucose.[2]
Because of its antiangiogenic effect, cytochalasin E is a potential drug for age-related macular degeneration, a kind of blindness caused by an abnormal proliferation of blood vessels in the eye.[3]
Cytochalasin E was found to be a potent and selective inhibitor of bovine capillary endothelial (BCE) cell proliferation. Cytochalasin E differs from other cytochalasin molecules by having an epoxide, which is required for specificity and potency. Cytochalasin E is a potent antiangiogenic agent that may be useful for treatments of cancer and other pathologic angiogenesis.[4] Cytochalasin E was also found to inhibit autophagy, a process vital in recycling dysfunctional cells and cellular components. Cancer cells thus favor autophagy due to its role in countering metabolic stresses induced by anti-cancer drugs such as bortezomib in order to regenerate healthier cancer cells for continued proliferation and growth. In a study, it was confirmed that when CE was used, fusion of autophagosomes with lysozyme was inhibited and so cell death due to bortezomib, a proteasome inhibitor, was amplified as unnecessary proteins would continue to build up inside cancer cells unable to be further recycled through autophagy, leading to apoptosis.[5]
ReferencesEdit
^Cytochalasin E from Aspergillus clavatus at Sigma-Aldrich
^Glinsukon, T.; Kongsuktrakoon, B.; Toskulkao, C.; Sophasan, S. (1983-03-01). "Cytochalasin E: inhibition of intestinal glucose absorption in the mouse". Toxicology Letters. 15 (4): 341–348. doi:10.1016/0378-4274(83)90154-6. ISSN 0378-4274. PMID 6836602.
^. 2006-05-19. Archived from the original on 19 May 2006. Retrieved 2022-05-12.
^Udagawa, T.; Yuan, J.; Panigrahy, D.; Chang, Y. H.; Shah, J.; D'Amato, R. J. (2000-08-01). "Cytochalasin E, an epoxide containing Aspergillus-derived fungal metabolite, inhibits angiogenesis and tumor growth". The Journal of Pharmacology and Experimental Therapeutics. 294 (2): 421–427. ISSN 0022-3565. PMID 10900214.
^Takanezawa, Yasukazu; Nakamura, Ryosuke; Kojima, Yuka; Sone, Yuka; Uraguchi, Shimpei; Kiyono, Masako (2018-04-06). "Cytochalasin E increased the sensitivity of human lung cancer A549 cells to bortezomib via inhibition of autophagy". Biochemical and Biophysical Research Communications. 498 (3): 603–608. doi:10.1016/j.bbrc.2018.03.029. ISSN 1090-2104. PMID 29524420.
cytochalasin, member, cytochalasin, group, inhibitor, actin, polymerization, blood, platelets, inhibits, angiogenesis, tumor, growth, unlike, cytochalasin, cytochalasin, does, inhibit, glucose, transport, however, noted, decrease, glucose, absorption, mice, ar. Cytochalasin E a member of the cytochalasin group is an inhibitor of actin polymerization in blood platelets It inhibits angiogenesis and tumor growth Unlike cytochalasin A and cytochalasin B it does not inhibit glucose transport Cytochalasin E however was noted to decrease glucose absorption in mice around the intestinal tissues by increasing the Km needed for glucose to reach the Vmax which meant that a higher concentration of glucose was required in its presence to attain Vmax Since Vmax remained the same according to another study it is evident that CE is indeed a competitive inhibitor at the intestinal receptor sites for glucose 2 Cytochalasin E 1 NamesPreferred IUPAC name 4E 6R 8S 10E 11aS 11bS 12aR 13S 13aS 14S 14 Benzyl 6 hydroxy 6 8 12a 13 tetramethyl 9 11a 11b 12a 13 13a 14 15 octahydro 2H 1 3 dioxacyclotridecino 4 5 d oxireno 2 3 f isoindole 2 7 16 6H 8H trioneIdentifiersCAS Number 36011 19 5 Y3D model JSmol Interactive image3DMet L06226ChEBI CHEBI 68201ChEMBL ChEMBL494856ChemSpider 4572350 NECHA InfoCard 100 048 018EC Number 252 835 7KEGG C19953PubChem CID 5458385CompTox Dashboard EPA DTXSID60894866InChI InChI 1S C28H33NO7 c1 16 9 8 12 19 23 27 4 35 23 17 2 21 20 15 18 10 6 5 7 11 18 29 24 31 28 19 21 36 25 32 34 14 13 26 3 33 22 16 30 h5 8 10 14 16 17 19 21 23 33H 9 15H2 1 4H3 H 29 31 b12 8 14 13 t16 17 19 20 21 23 26 27 28 m0 s1 NKey LAJXCUNOQSHRJO ZYGJITOWSA N NInChI 1 C28H33NO7 c1 16 9 8 12 19 23 27 4 35 23 17 2 21 20 15 18 10 6 5 7 11 18 29 24 31 28 19 21 36 25 32 34 14 13 26 3 33 22 16 30 h5 8 10 14 16 17 19 21 23 33H 9 15H2 1 4H3 H 29 31 b12 8 14 13 t16 17 19 20 21 23 26 27 28 m0 s1Key LAJXCUNOQSHRJO ZYGJITOWBMSMILES C C H 1C C C C H 2 C H 3 C O3 C H C H 4 C 2 C O N C H 4CC5 CC CC C5 OC O O C C C C1 O C O C CPropertiesChemical formula C 28H 33N O 7Molar mass 495 572 g mol 1Density 1 309 g mlHazardsOccupational safety and health OHS OSH Main hazards ToxicGHS labelling PictogramsSignal word DangerHazard statements H300 H310 H330 H361Precautionary statements P201 P202 P260 P262 P264 P270 P271 P280 P281 P284 P301 P310 P302 P350 P304 P340 P308 P313 P310 P320 P321 P322 P330 P361 P363 P403 P233 P405 P501Except where otherwise noted data are given for materials in their standard state at 25 C 77 F 100 kPa N verify what is Y N Infobox references Because of its antiangiogenic effect cytochalasin E is a potential drug for age related macular degeneration a kind of blindness caused by an abnormal proliferation of blood vessels in the eye 3 Cytochalasin E was found to be a potent and selective inhibitor of bovine capillary endothelial BCE cell proliferation Cytochalasin E differs from other cytochalasin molecules by having an epoxide which is required for specificity and potency Cytochalasin E is a potent antiangiogenic agent that may be useful for treatments of cancer and other pathologic angiogenesis 4 Cytochalasin E was also found to inhibit autophagy a process vital in recycling dysfunctional cells and cellular components Cancer cells thus favor autophagy due to its role in countering metabolic stresses induced by anti cancer drugs such as bortezomib in order to regenerate healthier cancer cells for continued proliferation and growth In a study it was confirmed that when CE was used fusion of autophagosomes with lysozyme was inhibited and so cell death due to bortezomib a proteasome inhibitor was amplified as unnecessary proteins would continue to build up inside cancer cells unable to be further recycled through autophagy leading to apoptosis 5 References Edit Cytochalasin E from Aspergillus clavatus at Sigma Aldrich Glinsukon T Kongsuktrakoon B Toskulkao C Sophasan S 1983 03 01 Cytochalasin E inhibition of intestinal glucose absorption in the mouse Toxicology Letters 15 4 341 348 doi 10 1016 0378 4274 83 90154 6 ISSN 0378 4274 PMID 6836602 Cytochalasin E 2006 05 19 Archived from the original on 19 May 2006 Retrieved 2022 05 12 Udagawa T Yuan J Panigrahy D Chang Y H Shah J D Amato R J 2000 08 01 Cytochalasin E an epoxide containing Aspergillus derived fungal metabolite inhibits angiogenesis and tumor growth The Journal of Pharmacology and Experimental Therapeutics 294 2 421 427 ISSN 0022 3565 PMID 10900214 Takanezawa Yasukazu Nakamura Ryosuke Kojima Yuka Sone Yuka Uraguchi Shimpei Kiyono Masako 2018 04 06 Cytochalasin E increased the sensitivity of human lung cancer A549 cells to bortezomib via inhibition of autophagy Biochemical and Biophysical Research Communications 498 3 603 608 doi 10 1016 j bbrc 2018 03 029 ISSN 1090 2104 PMID 29524420 External pages EditCytochalasin E from Fermentek Cytochalasin E from Cayman Chemical Retrieved from https en wikipedia org w index php title Cytochalasin E amp oldid 1151517921, wikipedia, wiki, book, books, library,
