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Metastasis is promoted by a bioenergetic switch: New targets for progressive renal cell cancer
International journal of cancer, 2008-06, Vol.122 (11), p.2422-2428
Langbein, Sigrun
Frederiks, Wilma M.
zur Hausen, Axel
Popa, Juljane
Lehmann, Jan
Weiss, Christel
Alken, Peter
Coy, Johannes F.
2008
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Langbein, Sigrun
Frederiks, Wilma M.
zur Hausen, Axel
Popa, Juljane
Lehmann, Jan
Weiss, Christel
Alken, Peter
Coy, Johannes F.
Titel
Metastasis is promoted by a bioenergetic switch: New targets for progressive renal cell cancer
Ist Teil von
International journal of cancer, 2008-06, Vol.122 (11), p.2422-2428
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2008
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
Targeted therapies have demonstrated clinical benefit with limited impact on long‐term disease specific survival in the treatment of renal cell cancer (RCC). New opportunities for the treatment of tumors that are resistant or have relapsed, are needed. Increased anaerobic glucose fermentation to lactate (aerobic glycolysis), leading to oxygen‐ and mitochondria‐independent ATP generation is a hallmark of aggressive cancer growth. This metabolic shift results in increased lactate production via cycling through the pentose phosphate pathway (PPP), and plays an important role in tumor immune escape, progression and resistance to immune‐, radiation‐ and chemo‐therapy. This study explored the activity and impact of the oxidative and nonoxidative branches of the PPP on RCC to evaluate new therapeutic options. Activity was determined in the oxidative branch by glucose‐6‐phosphate‐dehydrogenase (G6PD) activity, and in the nonoxidative branch by the total transketolase activity and the specific expression of the transketolase‐like‐1 (TKTL1) protein. Transketolase and G6PD activity were intensely elevated in tumor tissues. Transketolase, but not G6PD activity, was more elevated in metastasizing tumors and TKTL1 protein was significantly overexpressed in progressing tumors (p = 0.03). Lethal tumors, where surrogate parameters such as grading and staging had failed to predict progression, showed intensive TKTL1 protein expression. RCC was found to have activated oxidative and nonoxidative glucose metabolism through the PPP, displaying a bioenergetic shift toward nonoxidative glucose fermentation in progressing tumors. The coexistence of cancer cells with differentially regulated energy supplies provides new insights in carcinogenesis and novel anticancer targets. © 2008 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0020-7136
eISSN: 1097-0215
DOI: 10.1002/ijc.23403
Titel-ID: cdi_proquest_miscellaneous_19312113
Format
–
Schlagworte
Adult
,
Aged
,
Biological and medical sciences
,
Biomarkers, Tumor - metabolism
,
Carcinoma, Renal Cell - enzymology
,
Carcinoma, Renal Cell - metabolism
,
Carcinoma, Renal Cell - secondary
,
Female
,
Gene Expression Regulation, Enzymologic
,
Gene Expression Regulation, Neoplastic
,
Glucosephosphate Dehydrogenase - metabolism
,
glucose‐6‐phosphate‐dehydrogenase
,
Humans
,
Immunohistochemistry
,
Kidney Neoplasms - enzymology
,
Kidney Neoplasms - metabolism
,
Kidney Neoplasms - pathology
,
Kidneys
,
Male
,
Medical sciences
,
Middle Aged
,
Nephrology. Urinary tract diseases
,
pentose phosphate pathway
,
renal cell carcinoma
,
Transketolase - metabolism
,
transketolase‐like‐1 enzyme
,
Tumors
,
Tumors of the urinary system
,
Warburg effect
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