Hypoxia-induced IL-32β increases glycolysis in breast cancer cells

Highlights • Hypoxia-induced ROS increase IL-32β expression. • IL-32β enhances glycolytic pathway through increase of LDH activity under hypoxic conditions. • Inhibition of hypoxia-induced IL-32β impairs tumor cell growth. • IL-32β increases Src activity via protecting the dephosphorylation of Src b...

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Veröffentlicht in:	Cancer letters 2015-01, Vol.356 (2), p.800-808
Hauptverfasser:	Park, Jeong Su, Lee, Sunyi, Jeong, Ae Lee, Han, Sora, Ka, Hye In, Lim, Jong-Seok, Lee, Myung Sok, Yoon, Do-Young, Lee, Jeong-Hyung, Yang, Young
Format:	Artikel
Sprache:	eng
Schlagworte:	Blotting, Western Breast Neoplasms - drug therapy Breast Neoplasms - enzymology Breast Neoplasms - pathology Energy Metabolism Female Glycolysis Hematology, Oncology and Palliative Medicine Humans Hypoxia Immunoenzyme Techniques Immunoprecipitation Interleukin-32 Interleukins - antagonists & inhibitors Interleukins - genetics Interleukins - metabolism Membrane Potential, Mitochondrial Mitochondria - metabolism Mitochondrial biogenesis Oxidative Phosphorylation OXPHOS RNA, Small Interfering - genetics src-Family Kinases - metabolism Tumor Cells, Cultured
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Zusammenfassung:	Highlights • Hypoxia-induced ROS increase IL-32β expression. • IL-32β enhances glycolytic pathway through increase of LDH activity under hypoxic conditions. • Inhibition of hypoxia-induced IL-32β impairs tumor cell growth. • IL-32β increases Src activity via protecting the dephosphorylation of Src by PP2A.
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2014.10.030