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Involvement of nuclear factor-kappa B, Bax and Bcl-2 in induction of cell cycle arrest and apoptosis by apigenin in human prostate carcinoma cells.

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  • المؤلفون: Gupta S;Gupta S; Afaq F; Mukhtar H
  • المصدر:
    Oncogene [Oncogene] 2002 May 23; Vol. 21 (23), pp. 3727-38.
  • نوع النشر :
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • اللغة:
    English
  • معلومة اضافية
    • المصدر:
      Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8711562 Publication Model: Print Cited Medium: Print ISSN: 0950-9232 (Print) Linking ISSN: 09509232 NLM ISO Abbreviation: Oncogene Subsets: MEDLINE
    • بيانات النشر:
      Publication: <2002->: Basingstoke : Nature Publishing Group
      Original Publication: Basingstoke, Hampshire, UK : Scientific & Medical Division, MacMillan Press, c1987-
    • الموضوع:
      Apoptosis/*drug effects ; Cell Cycle/*drug effects ; Flavonoids/*pharmacology ; NF-kappa B/*metabolism ; Prostatic Neoplasms/*pathology ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism; Antineoplastic Agents/pharmacology ; Apigenin ; Blotting, Western ; Cell Cycle Proteins/metabolism ; Cell Division/drug effects ; Cell Survival/drug effects ; Down-Regulation ; Flow Cytometry ; Humans ; Male ; Prostate-Specific Antigen/metabolism ; Prostatic Neoplasms/metabolism ; Retinoblastoma Protein/metabolism ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/metabolism ; bcl-2-Associated X Protein
    • نبذة مختصرة :
      Apigenin, a common dietary flavonoid abundantly present in fruits and vegetables, may have the potential for prevention and therapy for prostate cancer. Here, we report for the first time that apigenin inhibits the growth of androgen-responsive human prostate carcinoma LNCaP cells and provide molecular understanding of this effect. The cell growth inhibition achieved by apigenin treatment resulted in a significant decrease in AR protein expression along with a decrease in intracellular and secreted forms of PSA. These effects were also observed in DHT-stimulated cells. Further, apigenin treatment of LNCaP cells resulted in G1 arrest in cell cycle progression which was associated with a marked decrease in the protein expression of cyclin D1, D2 and E and their activating partner cdk2, 4 and 6 with concomitant induction of WAF1/p21 and KIP1/p27. The induction of WAF1/p21 appears to be transcriptionally upregulated and is p53 dependent. In addition, apigenin inhibited the hyperphosphorylation of the pRb protein in these cells. Apigenin treatment also resulted in induction of apoptosis as determined by DNA fragmentation, PARP cleavage, fluorescence microscopy and flow cytometry. These effects were found to correlate with a shift in Bax/Bcl-2 ratio more towards apoptosis. Apigenin treatment also resulted in down-modulation of the constitutive expression of NF-kappaB/p65. Taken together, these findings suggest that apigenin has strong potential for development as an agent for prevention against prostate cancer.
    • Grant Information:
      R01CA 78809 United States CA NCI NIH HHS
    • الرقم المعرف:
      0 (Antineoplastic Agents)
      0 (BAX protein, human)
      0 (Cell Cycle Proteins)
      0 (Flavonoids)
      0 (NF-kappa B)
      0 (Proto-Oncogene Proteins)
      0 (Proto-Oncogene Proteins c-bcl-2)
      0 (Retinoblastoma Protein)
      0 (Tumor Suppressor Protein p53)
      0 (bcl-2-Associated X Protein)
      7V515PI7F6 (Apigenin)
      EC 3.4.21.77 (Prostate-Specific Antigen)
    • الموضوع:
      Date Created: 20020529 Date Completed: 20020614 Latest Revision: 20220331
    • الموضوع:
      20221213
    • الرقم المعرف:
      10.1038/sj.onc.1205474
    • الرقم المعرف:
      12032841