Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme

By A. Wolf, S. Agnihotri, J. Micallef, J. Mukherjee, N. Sabha, R. Cairns, C. Hawkins, A. Guha. Journal of Experimental Medicine, 2011

770 citations recorded by the source corpus.

In glioblastoma multiforme, the most common adult primary brain tumor, the glycolytic enzyme hexokinase 2 facilitates growth and therapeutic resistance.

Subfields: Cancer Research, Genetics, Neurology

View Paper: https://www.semanticscholar.org/paper/4a82c0d9d5d72aebf3c50d516da6e7bfcb96b245

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Navdeep S. Chandel
2. M. V. Vander Heiden
3. David M. Sabatini
4. Sophia Y. Lunt
5. J. Cantor
6. N. Hay
7. Ralph J. Deberardinis
8. C. V. Dang

In Genetics

1. David M. Sabatini
2. M. V. Vander Heiden
3. Sophia Y. Lunt
4. Navdeep S. Chandel

In Neurology

1. M. V. Vander Heiden
2. Navdeep S. Chandel

Citations in the corpus

• Mesenchymal glioma stem cells are maintained by activated glycolytic metabolism involving aldehyde dehydrogenase 1A3 (2013, background): “, glycolysis) in cancer cells play critical roles in rendering malignancy and poor responses to therapies of malignant gliomas (21).”
• Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, background): “Previous studies have demonstrated the ability of RNAi-mediated HK2 silencing to inhibit tumor growth in a xenograft model of glioblastoma (Wolf et al., 2011).”
• Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Perhaps the elevated expression of HK2 in some tumors is indicative of this particular HK imparting some additional functional role necessary in the context of these malignancies.”
• Aerobic glycolysis: meeting the metabolic requirements of cell proliferation. (2011, positive): “However, cancer cells frequently overexpress HK II (Mathupala et al 2006), and at least some glioblastoma cells are specifically dependent on HK II over other isoforms of the enzyme (Wolf et al 2011).”