The pentose phosphate pathway as a potential target for cancer therapy

Eunae Sandra Cho, Yong Hoon Cha, Hyun Sil Kim, Nam Hee Kim, Jong In Yook

Research output: Contribution to journalReview articlepeer-review

88 Citations (Scopus)

Abstract

During cancer progression, cancer cells are repeatedly exposed to metabolic stress conditions in a resource-limited environment which they must escape. Increasing evidence indicates the importance of nicotinamide adenine dinucleotide phosphate (NADPH) homeostasis in the survival of cancer cells under metabolic stress conditions, such as metabolic resource limitation and therapeutic intervention. NADPH is essential for scavenging of reactive oxygen species (ROS) mainly derived from oxidative phosphorylation required for ATP generation. Thus, metabolic reprogramming of NADPH homeostasis is an important step in cancer progression as well as in combinational therapeutic approaches. In mammalian, the pentose phosphate pathway (PPP) and one-carbon metabolism are major sources of NADPH production. In this review, we focus on the importance of glucose flux control towards PPP regulated by oncogenic pathways and the potential therein for metabolic targeting as a cancer therapy. We also summarize the role of Snail (Snai1), an important regulator of the epithelial mesenchymal transition (EMT), in controlling glucose flux towards PPP and thus potentiating cancer cell survival under oxidative and metabolic stress.

Original languageEnglish
Pages (from-to)29-38
Number of pages10
JournalBiomolecules and Therapeutics
Volume26
Issue number1
DOIs
Publication statusPublished - 2018 Jan

Bibliographical note

Funding Information:
We thank E. Tunkle for preparation of the manuscript. This work was supported by grants from the National Research Foundation of Korea (NRF-2016R1E1A1A01942724, NRF-2017R1A2B3002241, NRF-2017R1C1B1012464, NRF-2017M3A9G2074773) funded by the Korea government (MSIP) and a grant from the National Research Foundation of Korea (NRF-2014R1A6A3A04055110) funded by the Korea government (MOE).

Funding Information:
This work was supported by grants from the National Research Foundation of Korea NRF (NRF-2016R1E1A1A01942724, NRF-2017R1A2B3002241, NRF-2017R1C1B1012464, NRF-2017M3A9G2074773) funded by the Korea government (MSIP) and a grant from the National Research Foundation of Korea NRF (NRF-2014R1A6A3A04055110) funded by the Korea government (MOE).

Publisher Copyright:
© 2018 The Korean Society of Applied Pharmacology.

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Pharmacology
  • Drug Discovery

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