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Sökning: WFRF:(Vakifahmetoglu Norberg H.)

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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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  • Centeno, D, et al. (författare)
  • The nutritional supplement taurine activates p53-dependent and independent tumor suppressor mechanisms in various cellular models of ovarian cancer
  • 2023
  • Ingår i: bioRxiv : the preprint server for biology. - : Cold Spring Harbor Laboratory.
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Loss of treatment-induced ovarian carcinoma (OC) growth suppression poses a major clinical challenge because it leads to disease recurrence. Therefore, new and well-tolerated approaches to maintain OC suppression after standard-of-care treatment are needed. We have profiled ascites as OC tumor microenvironments (TMs) to search for potential components that would exert growth suppression on OC cell cultures. Our investigations revealed that low levels of taurine, a non-proteogenic sulfonic amino acid, were present within OC ascites. Taurine supplementation, beyond levels found in ascites, induced growth suppression without causing cytotoxicity in multiple OC cell cultures, including patient-derived chemotherapy-resistant spheroid and organoid cultures. Suppression of proliferation by taurine was associated with the inhibition of glycolysis, mitochondrial function, and the activation of p21 and TIGAR, theTP53-dependent and independent tumor suppression regulatory pathways. Expression of p21 or TIGAR in various OC cells, in part, mimicked taurine-induced inhibition of OC cell proliferation. Our data support the potential therapeutic value of taurine supplementation in OC after chemotherapy.
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  • Resultat 1-10 av 25

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