RESVERATROL INHIBITS EXPRESSION OF CANCER-SPECIFIC PENTOSE PHOSPHATE PATHWAY ENZYME TKTL1

Authors

  • Bhupender Kumar National Centre of Applied Human Genetics, School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

DOI:

https://doi.org/10.22159/ajpcr.2018.v11i6.25021

Keywords:

Resveratrol, Transketolase-like 1, HeLa, Pentose phosphate pathway

Abstract

Objective: The objective of this study was to identify cancer-specific metabolic enzyme Transketolase-like 1 (TKTL1) from pentose phosphate pathway as target of resveratrol, a naturally occurring nutraceutical.

Methods: Methylthiazolyldiphenyl-tetrazolium bromide assay and trypan blue assay were used for the estimation of growth and proliferation. Reactive oxygen species (ROS) was estimated using 2'-7'-Dichlorodihydrofluorescein diacetate while reduced glutathione (GSH) was estimated using commercially available kit. Promoter activity, reverse transcription polymerase chain reaction, and western blotting were used for expression analysis.

Results: Resveratrol treatment in HeLa cells inhibited proliferation, promoted ROS, and reduced intracellular GSH levels. In TKTL1 promoter activity assay, we found that resveratrol treatment directly inhibited promoter activity of TKTL1. Resveratrol inhibited both mRNA and protein expression of TKTL1 in a dose-dependent manner.

Conclusion: This is the first report where we show that resveratrol inhibits cancer-specific isoform TKTL1 as one of its targets to elicit its anticancer activity.

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Author Biography

Bhupender Kumar, National Centre of Applied Human Genetics, School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

Assistant Professor,

Dept. of Biochemistry, Institute of Home Economics

University of Delhi,

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Published

07-06-2018

How to Cite

Kumar, B. “RESVERATROL INHIBITS EXPRESSION OF CANCER-SPECIFIC PENTOSE PHOSPHATE PATHWAY ENZYME TKTL1”. Asian Journal of Pharmaceutical and Clinical Research, vol. 11, no. 6, June 2018, pp. 332-5, doi:10.22159/ajpcr.2018.v11i6.25021.

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Section

Original Article(s)