1 Ocak 2002 Dergi makalesi Açık Erişim

Guzey, M; Kitada, S; Reed, JC

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/96283</identifier>
  <creators>
    <creator>
      <creatorName>Guzey, M</creatorName>
      <givenName>M</givenName>
      <familyName>Guzey</familyName>
    </creator>
    <creator>
      <creatorName>Kitada, S</creatorName>
      <givenName>S</givenName>
      <familyName>Kitada</familyName>
    </creator>
    <creator>
      <creatorName>Reed, JC</creatorName>
      <givenName>JC</givenName>
      <familyName>Reed</familyName>
    </creator>
  </creators>
  <titles>
    <title>Apoptosis Induction By 1 Alpha,25-Dihydroxyvitamin D-3 In Prostate Cancer</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2002</publicationYear>
  <dates>
    <date dateType="Issued">2002-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/96283</alternateIdentifier>
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    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsVersionOf">10.81043/aperta.96282</relatedIdentifier>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.81043/aperta.96283</relatedIdentifier>
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  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
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  <descriptions>
    <description descriptionType="Abstract">Calcitriol [1alpha,25-dihydroxyvitamin D-3] is the natural ligand of the vitamin D receptor (VDR). Using cultured prostate cancer (PC) cell lines, LN-CaP and ALVA-31, we studied the effects of 1alpha,25(OH)(2)-Vitamin D-3 (VD3) on expression of several apoptosis-regulating proteins including: (a) Bcl-2 family proteins (Bcl-2, Bcl-X-L, Mcl-1 Bax, and Bak); (b) the heat shock protein 70-binding protein BAG1L; and (c) IAP family proteins (XIAP, cIAP1, and cIAP2). VD3 induced decreases in levels of antiapoptotic proteins Bcl-2, Bcl-X-L, and Mcl-1, BAG1L, XIAP, cIAP1, and cIAP2 (without altering proapoptotic Bax and Bak) in association with increases in apoptosis. In contrast to VDR-expressing LN-CaP and ALVA-31 cells, VDR-deficient prostate cancer line Du-145 demonstrated no changes in apoptosis protein expression after treatment with VD3. In sensitive PC cell lines, VD3 activates downstream effector protease, caspase-3, and upstream initiator protease caspase-9, the apical protease in the mitochondrial ("intrinsic") pathway for apoptosis, but not caspase-8, an initiator caspase linked to an alternative ("extrinsic") apoptosis pathway triggered by cytokine receptors. VD3 induced declines in antiapoptotic proteins and also stimulated cytochrome c release from mitochondria by a caspase-independent mechanism. Moreover, apoptosis induction by VD3 was suppressed by over-expressing Bcl-2, a known blocker of cytochrome c release, whereas the caspase-8 suppressor CrmA afforded little protection. Thus, VD3 is capable of inhibiting expression of multiple antiapoptotic proteins in VDR-expressing prostate cancer cells, leading to activation of the mitochondrial pathway for apoptosis.</description>
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