ZNF300 knockdown inhibits forced megakaryocytic differentiation by phorbol and erythrocytic differentiation by arabinofuranosyl cytidine in K562 cells.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read Online Read More Add to Saved list
  • Additional Information
    • Source:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • Publication Information:
      Original Publication: San Francisco, CA : Public Library of Science
    • Subject Terms:
      Cell Differentiation/*drug effects ; Cytarabine/*pharmacology ; Erythrocytes/*pathology ; Megakaryocytes/*pathology ; RNA, Small Interfering/*genetics ; Repressor Proteins/*antagonists & inhibitors ; Tetradecanoylphorbol Acetate/*pharmacology; Antimetabolites, Antineoplastic/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Carcinogens/pharmacology ; Cell Proliferation/drug effects ; Erythrocytes/drug effects ; Erythrocytes/metabolism ; Flow Cytometry ; Humans ; K562 Cells ; Megakaryocytes/drug effects ; Megakaryocytes/metabolism ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
    • Abstract:
      Previously, we reported that ZNF300 might play a role in leukemogenesis. In this study, we further investigated the function of ZNF300 in K562 cells undergoing differentiation. We found that ZNF300 upregulation in K562 cells coincided with megakaryocytic differentiation induced by phorbol-12-myristate-13-acetate (PMA) or erythrocytic differentiation induced by cytosine arabinoside (Ara-C), respectively. To further test whether ZNF300 upregulation promoted differentiation, we knocked down ZNF300 and found that ZNF300 knockdown effectively abolished PMA-induced megakaryocytic differentiation, evidenced by decreased CD61 expression. Furthermore, Ara-C-induced erythrocytic differentiation was also suppressed in ZNF300 knockdown cells with decreased γ-globin expression and CD235a expression. These observations suggest that ZNF300 may be a critical factor controlling distinct aspects of K562 cells. Indeed, ZNF300 knockdown led to increased cell proliferation. Consistently, ZNF300 knockdown cells exhibited an increased percentage of cells at S phase accompanied by decreased percentage of cells at G0/G1 and G2/M phase. Increased cell proliferation was further supported by the increased expression of cell proliferation marker PCNA and the decreased expression of cell cycle regulator p15 and p27. In addition, MAPK/ERK signaling was significantly suppressed by ZNF300 knockdown. These findings suggest a potential mechanism by which ZNF300 knockdown may impair megakaryocytic and erythrocytic differentiation.
    • References:
      Cancer Res. 2009 Jun 1;69(11):4665-73. (PMID: 19487285)
      Leuk Res. 1979;3(6):363-70. (PMID: 95026)
      Leuk Res. 2010 Dec;34(12):1636-46. (PMID: 20471086)
      J Clin Invest. 1984 Sep;74(3):821-7. (PMID: 6590568)
      Leuk Res. 1989;13(8):683-8. (PMID: 2796376)
      FEBS Lett. 1995 Aug 7;369(2-3):153-7. (PMID: 7649249)
      Mol Cell Biol. 1999 Jun;19(6):4366-78. (PMID: 10330177)
      J Biol Chem. 1999 Jun 4;274(23):16412-22. (PMID: 10347202)
      DNA Cell Biol. 1999 May;18(5):381-96. (PMID: 10360839)
      Genes Cells. 2005 Feb;10(2):97-106. (PMID: 15676021)
      Clin Cancer Res. 2006 Jan 1;12(1):5-10. (PMID: 16397017)
      Mol Cell Biol. 2006 Nov;26(22):8623-38. (PMID: 16954381)
      Bioinformatics. 2006 Dec 1;22(23):2841-5. (PMID: 17032681)
      PLoS Genet. 2007 Jun;3(6):e89. (PMID: 17542650)
      Cell Res. 2007 Sep;17(9):804-14. (PMID: 17768398)
      Cell Mol Life Sci. 2007 Dec;64(23):3105-18. (PMID: 17922230)
      Nat Protoc. 2008;3(6):1101-8. (PMID: 18546601)
      Cell Mol Biol Lett. 2008;13(3):391-403. (PMID: 18350257)
      Ann Hematol. 2008 Oct;87(10):777-95. (PMID: 18516602)
      Carcinogenesis. 2008 Nov;29(11):2096-105. (PMID: 18765415)
      J Cell Biochem. 2009 Jun 1;107(3):548-56. (PMID: 19350553)
      J Biol Chem. 2000 Dec 22;275(51):40463-70. (PMID: 11013263)
      Genes Dev. 2001 Feb 15;15(4):428-43. (PMID: 11230151)
      Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
      Genes Dev. 2002 Apr 15;16(8):919-32. (PMID: 11959841)
      Genome Biol. 2003;4(10):231. (PMID: 14519192)
      Biochim Biophys Acta. 2004 Jan 20;1676(2):203-9. (PMID: 14746915)
      Nat Biotechnol. 2004 Jun;22(6):707-16. (PMID: 15146197)
      Proc Natl Acad Sci U S A. 1975 Jan;72(1):98-102. (PMID: 164031)
      Front Biosci (Landmark Ed). 2011;16:422-39. (PMID: 21196179)
      PLoS One. 2012;7(1):e29518. (PMID: 22235304)
      J Cell Mol Med. 2012 May;16(5):1134-45. (PMID: 21777376)
      J Biol Chem. 2012 Dec 14;287(51):42856-66. (PMID: 23091055)
      Cell Mol Life Sci. 2013 Oct;70(20):3947-58. (PMID: 23665872)
      Cell. 2014 Aug 14;158(4):849-60. (PMID: 25126789)
      J Cell Mol Med. 2009 Nov-Dec;13(11-12):4551-9. (PMID: 19017354)
    • Accession Number:
      0 (Antimetabolites, Antineoplastic)
      0 (Carcinogens)
      0 (RNA, Messenger)
      0 (RNA, Small Interfering)
      0 (Repressor Proteins)
      0 (ZNF300 protein, human)
      04079A1RDZ (Cytarabine)
      NI40JAQ945 (Tetradecanoylphorbol Acetate)
    • Publication Date:
      Date Created: 20141209 Date Completed: 20160112 Latest Revision: 20181113
    • Publication Date:
      20240829
    • Accession Number:
      PMC4259388
    • Accession Number:
      10.1371/journal.pone.0114768
    • Accession Number:
      25485965