Leptin enhances the invasive ability of glioma stem-like cells depending on leptin receptor expression

Guosheng Han; Wenyuan Zhao; Laixing Wang; Zhijian Yue; Rui Zhao; Yanan Li; Xiaoping Zhou; Xiaowu Hu; Jianmin Liu

doi:10.1016/j.brainres.2013.10.027

Leptin enhances the invasive ability of glioma stem-like cells depending on leptin receptor expression

Brain Res. 2014 Jan 16:1543:1-8. doi: 10.1016/j.brainres.2013.10.027. Epub 2013 Oct 23.

Authors

Guosheng Han¹, Wenyuan Zhao¹, Laixing Wang¹, Zhijian Yue¹, Rui Zhao¹, Yanan Li¹, Xiaoping Zhou¹, Xiaowu Hu¹, Jianmin Liu²

Affiliations

¹ Department of Neurosurgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
² Department of Neurosurgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. Electronic address: liujianmin2011@hotmail.com.

PMID: 24161825
DOI: 10.1016/j.brainres.2013.10.027

Abstract

Glioma stem-like cells have been demonstrated to have highly invasive activity, which is the major cause of glioma recurrence after therapy. Leptin plays a role in glioma invasion, however, whether and how leptin contributes to the biological properties of glioma stem-like cells, such as invasion, remains to be explored. In the current study, we aimed to explore the role of leptin during glioma stem-like cells invasion as well as the signaling pathway. We found that glioma stem-like cells exhibited high invasive potential, especially in the presence of leptin, Ob-R coexpressed with CD133 in glioma stem-like cells was showed to be responsible for leptin mediated invasion of glioma stem-like cells. Our results indicated that leptin served as a key intermediary linking the accumulation of excess adipokine to the invasion of glioma stem-like cells, which may be a novel therapeutic target for suppressing tumor invasion and recurrence.

Keywords: Glioma stem-like cells; Invasion; Leptin; Leptin receptor.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

AC133 Antigen
Antigens, CD / metabolism
Brain Neoplasms / metabolism
Brain Neoplasms / pathology*
Cell Movement / drug effects
Chromones / pharmacology
Colony-Forming Units Assay
Enzyme Inhibitors / pharmacology
Gene Expression Regulation, Neoplastic / drug effects*
Glioma / metabolism
Glioma / pathology*
Glycoproteins / metabolism
Humans
Leptin / pharmacology*
Matrix Metalloproteinase 9 / genetics
Matrix Metalloproteinase 9 / metabolism
Morpholines / pharmacology
Neoplasm Invasiveness / pathology
Neoplasm Invasiveness / physiopathology
Neoplastic Stem Cells / drug effects*
Organic Chemicals / pharmacology
Peptides / metabolism
RNA, Small Interfering / pharmacology
Receptors, Leptin / genetics
Receptors, Leptin / metabolism*
STAT3 Transcription Factor / genetics
STAT3 Transcription Factor / metabolism
Signal Transduction / drug effects
Tumor Cells, Cultured

Substances

AC133 Antigen
Antigens, CD
Chromones
Enzyme Inhibitors
Glycoproteins
Leptin
Morpholines
Organic Chemicals
PD 98058
PROM1 protein, human
Peptides
RNA, Small Interfering
Receptors, Leptin
STAT3 Transcription Factor
STAT3 protein, human
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
Matrix Metalloproteinase 9