6533b82ffe1ef96bd1295b9d

RESEARCH PRODUCT

Glucose metabolism of malignant cells is not regulated by transketolase-like (TKTL)-1.

Arnulf MayerPeter VaupelAngelika Von Wallbrunn

subject

Cancer ResearchBlotting WesternClone (cell biology)TransketolaseBiologyIsozymeGene Expression Regulation EnzymologicMiceCell Line TumorNeoplasmsAnimalsHumansNuclear proteinTumor hypoxiaOncogeneLeiomyomaAntibodies MonoclonalCell cycleGene Expression Regulation NeoplasticGlucoseOncologyBiochemistryMonoclonalUterine NeoplasmsCancer researchFemaleTransketolaseHeLa Cells

description

An isoenzyme of transketolase, transketolase-like (TKTL)-1, has been hypothesized to play a pivotal role in the pathophysiology of malignant tumors. Available data are based on the detection of the putative TKTL-1 protein with one particular mouse monoclonal anti-TKTL-1 antibody, clone JFC12T10. In this study it was demonstrated that a) JFC12T10 detects multiple unspecific bands in Western blots, b) a 75-kDa band hitherto referred to as TKTL-1 corresponds to a nuclear protein and c) immunohistochemical detection of TKTL-1 in benign leiomyomas yields an expression pattern identical to that found in a variety of malignant tumors. In RT-PCR assays, using three different primer pairs for transketolase, TKTL-1 and yet another isogene of transketolase, TKTL-2, a relevant expression of TKTL-1 was not detectable in any of the 6 malignant tumor cell lines investigated (MCF-7, A549, HeLa, HT1080, M21 and TF-1). Expression levels of TKTL-1 were rather similar to those found for TKTL-2, although the latter has never been implicated in malignant disease. On the basis of these data, nutritional recommendations based on a hypothetically TKTL-1 controlled metabolism of tumor cells must be regarded as lacking scientific evidence.

10.3892/ijo_00000674https://pubmed.ncbi.nlm.nih.gov/20596653