Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells

Abstract We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and transketolase-like-2 (TKTL2) transcripts were not upregulated. We inhibited the expression of TKTL1 by RNAi in HepG2 cells. It was found that...

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Published inCancer letters Vol. 253; no. 1; pp. 108 - 114
Main Authors Zhang, Song, Yang, Ju-Hong, Guo, Chang-Kai, Cai, Peng-cheng
Format Journal Article
LanguageEnglish
Published Ireland Elsevier Ireland Ltd 08.08.2007
Elsevier Limited
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Abstract Abstract We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and transketolase-like-2 (TKTL2) transcripts were not upregulated. We inhibited the expression of TKTL1 by RNAi in HepG2 cells. It was found that total transketolase activity was dramatically downregulated and the proliferation of cancer cells was significantly inhibited in HepG2 cells. These results indicate that TKTL1 gene influences total transketolase activity and cell proliferation in human hepatoma cells, suggesting that TKTL1 gene plays an important role on glycometabolism in tumors and it might become a novel target for tumor gene therapy.
AbstractList Abstract We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and transketolase-like-2 (TKTL2) transcripts were not upregulated. We inhibited the expression of TKTL1 by RNAi in HepG2 cells. It was found that total transketolase activity was dramatically downregulated and the proliferation of cancer cells was significantly inhibited in HepG2 cells. These results indicate that TKTL1 gene influences total transketolase activity and cell proliferation in human hepatoma cells, suggesting that TKTL1 gene plays an important role on glycometabolism in tumors and it might become a novel target for tumor gene therapy.
We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and transketolase-like-2 (TKTL2) transcripts were not upregulated. We inhibited the expression of TKTL1 by RNAi in HepG2 cells. It was found that total transketolase activity was dramatically downregulated and the proliferation of cancer cells was significantly inhibited in HepG2 cells. These results indicate that TKTL1 gene influences total transketolase activity and cell proliferation in human hepatoma cells, suggesting that TKTL1 gene plays an important role on glycometabolism in tumors and it might become a novel target for tumor gene therapy.
Author Zhang, Song
Guo, Chang-Kai
Yang, Ju-Hong
Cai, Peng-cheng
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Issue 1
Keywords Small interfering RNA (siRNA)
Tansketolase activity
Transketolase
HepG2 cell line
Transketolase-like-1 (TKTL1)
Language English
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Snippet Abstract We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and...
We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and...
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SubjectTerms Cancer
Carcinoma, Hepatocellular - genetics
Cell Cycle
Cell growth
Cell Line, Tumor
Cell Proliferation
Cloning
Enzymes
Gene Silencing
Genes
Hematology, Oncology and Palliative Medicine
HepG2 cell line
Humans
Metabolism
Metabolites
Plasmids
Proteins
RNA Interference
Small interfering RNA (siRNA)
Software packages
Tansketolase activity
Transfection
Transketolase
Transketolase - genetics
Transketolase - metabolism
Transketolase-like-1 (TKTL1)
Tumorigenesis
Tumors
Title Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells
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https://dx.doi.org/10.1016/j.canlet.2007.01.010
https://www.ncbi.nlm.nih.gov/pubmed/17321041
https://www.proquest.com/docview/1505457759
https://search.proquest.com/docview/19868667
https://search.proquest.com/docview/70609441
Volume 253
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