Therapeutic starvation and autophagy in prostate cancer: A new paradigm for targeting metabolism in cancer therapy

Autophagy is a starvation induced cellular process of self‐digestion that allows cells to degrade cytoplasmic contents. The understanding of autophagy, as either a mechanism of resistance to therapies that induce metabolic stress, or as a means to cell death, is rapidly expanding and supportive of a new paradigm of therapeutic starvation.

[1]  N. Savaraj,et al.  Hypoxia increases tumor cell sensitivity to glycolytic inhibitors: a strategy for solid tumor therapy (Model C). , 2002, Biochemical pharmacology.

[2]  D. Petrylak Future directions in the treatment of androgen-independent prostate cancer. , 2005, Urology.

[3]  C. Thompson,et al.  The Roles of Therapy-Induced Autophagy and Necrosis in Cancer Treatment , 2007, Clinical Cancer Research.

[4]  Rebecca L Aft,et al.  Enhancing targeted radiotherapy by copper(II)diacetyl- bis(N4-methylthiosemicarbazone) using 2-deoxy-D-glucose. , 2003, Cancer research.

[5]  S. Weinhouse,et al.  The Warburg hypothesis fifty years later , 2004, Zeitschrift für Krebsforschung und Klinische Onkologie.

[6]  R. Deberardinis,et al.  The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. , 2008, Cell metabolism.

[7]  R. DiPaola,et al.  Targeting apoptosis in prostate cancer. , 2001, Hematology/oncology clinics of North America.

[8]  E. White,et al.  Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis. , 2007, Genes & development.

[9]  Robin Mathew,et al.  Role of autophagy in cancer , 2007, Nature Reviews Cancer.

[10]  Kevin Bray,et al.  Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. , 2006, Cancer cell.

[11]  A. Lane,et al.  Under normoxia, 2-deoxy-d-glucose elicits cell death in select tumor types not by inhibition of glycolysis but by interfering with N-linked glycosylation , 2007, Molecular Cancer Therapeutics.

[12]  G. Evan,et al.  Autophagy inhibition enhances therapy-induced apoptosis in a Myc-induced model of lymphoma. , 2007, The Journal of clinical investigation.

[13]  E. White,et al.  Epothilone induced cytotoxicity is dependent on p53 status in prostate cells , 2004, The Prostate.

[14]  E. White,et al.  Metabolic catastrophe as a means to cancer cell death , 2007, Journal of Cell Science.

[15]  D L Pincus,et al.  Cloning and genomic organization of beclin 1, a candidate tumor suppressor gene on chromosome 17q21. , 1999, Genomics.

[16]  David J. Foran,et al.  A prototype for unsupervised analysis of tissue microarrays for cancer research and diagnostics , 2004, IEEE Transactions on Information Technology in Biomedicine.

[17]  E. White,et al.  A novel proteomic coculture model of prostate cancer cell growth , 2004, Proteomics.

[18]  A. López-Rivas,et al.  Inhibition of Glucose Metabolism Sensitizes Tumor Cells to Death Receptor-triggered Apoptosis through Enhancement of Death-inducing Signaling Complex Formation and Apical Procaspase-8 Processing* , 2003, The Journal of Biological Chemistry.