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Sökning: WFRF:(Pan ZJ)

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  • Huang, H, et al. (författare)
  • Flow cytometric analysis of BHRF1 expression prohibiting apoptosis induced by radiation
  • 1999
  • Ingår i: The Annals of otology, rhinology, and laryngology. - : SAGE Publications. - 0003-4894 .- 1943-572X. ; 108:5, s. 481-484
  • Tidskriftsartikel (refereegranskat)abstract
    • The Epstein-Barr virus gene BHRF1 has homology with proto-oncogene bcl-2, which can protect cells from apoptosis. In order to investigate the effect of BHRF1 expression on the anti-apoptotic ability of nasopharyngeal carcinoma (NPC) cells after irradiation, a high—BHRF1 expression vector was constructed and transfected into the NPC cell line CNE2. Then, the alteration of proliferation and apoptosis in the cells was tested by flow cytometry after cobalt 60 irradiation. The results showed that BHRF1 expression could increase G1 delay and decrease the cell percentage in S phase before irradiation, and reduce the apoptotic rate of CNE2 cells and increase the cell percentage in S phase after irradiation. The results suggest that BHRF1 expression is able to alter the cell cycle and protect CNE2 cells from apoptosis induced by radiation.
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  • Xia, HG, et al. (författare)
  • Degradation of HK2 by chaperone-mediated autophagy promotes metabolic catastrophe and cell death
  • 2015
  • Ingår i: The Journal of cell biology. - : Rockefeller University Press. - 1540-8140 .- 0021-9525. ; 210:5, s. 705-716
  • Tidskriftsartikel (refereegranskat)abstract
    • Hexokinase II (HK2), a key enzyme involved in glucose metabolism, is regulated by growth factor signaling and is required for initiation and maintenance of tumors. Here we show that metabolic stress triggered by perturbation of receptor tyrosine kinase FLT3 in non–acute myeloid leukemia cells sensitizes cancer cells to autophagy inhibition and leads to excessive activation of chaperone-mediated autophagy (CMA). Our data demonstrate that FLT3 is an important sensor of cellular nutritional state and elucidate the role and molecular mechanism of CMA in metabolic regulation and mediating cancer cell death. Importantly, our proteome analysis revealed that HK2 is a CMA substrate and that its degradation by CMA is regulated by glucose availability. We reveal a new mechanism by which excessive activation of CMA may be exploited pharmacologically to eliminate cancer cells by inhibiting both FLT3 and autophagy. Our study delineates a novel pharmacological strategy to promote the degradation of HK2 in cancer cells.
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  • Resultat 1-11 av 11

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