Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Apr 8;19(4):1115.
doi: 10.3390/ijms19041115.

Migration/Invasion of Malignant Gliomas and Implications for Therapeutic Treatment

Ching-Ann Liu  1   2 , Chia-Yu Chang  3   4 , Kuo-Wei Hsueh  5   6 , Hong-Lin Su  7 , Tzyy-Wen Chiou  8 , Shinn-Zong Lin  9   10 , Horng-Jyh Harn  11   12
Affiliations
Review

Migration/Invasion of Malignant Gliomas and Implications for Therapeutic Treatment

Ching-Ann Liu et al. Int J Mol Sci. .

Abstract

Malignant tumors of the central nervous system (CNS) are among cancers with the poorest prognosis, indicated by their association with tumors of high-level morbidity and mortality. Gliomas, the most common primary CNS tumors that arise from neuroglial stem or progenitor cells, have estimated annual incidence of 6.6 per 100,000 individuals in the USA, and 3.5 per 100,000 individuals in Taiwan. Tumor invasion and metastasis are the major contributors to the deaths in cancer patients. Therapeutic goals including cancer stem cells (CSC), phenotypic shifts, EZH2/AXL/TGF-β axis activation, miRNAs and exosomes are relevant to GBM metastasis to develop novel targeted therapeutics for GBM and other brain cancers. Herein, we highlight tumor metastasis in our understanding of gliomas, and illustrate novel exosome therapeutic approaches in glioma, thereby paving the way towards innovative therapies in neuro-oncology.

Keywords: AXL/EZH2; cancer stem cells; epithelial-mesenchymal transition (EMT); exosomes; glioma; invasion/metastasis; microRNA; phenotypic shift.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
HA-CD44 triggers PI3K/Rho signaling for cytoskeletal re-pattering. Blue arrow (→): Promotion or activation; Red Y bar (⊥): Inhibition.
Figure 2
Figure 2
PI3K/Akt/mTOR (PAM) signaling network and effector functions associated with metastasis.
Figure 3
Figure 3
The schematic mechanism of BP treatment and Gas6 activation in GBM cells.
Figure 4
Figure 4
miRNAs regulate GBM invasion and progression through EMT. Solid arrows, activation; dotted arrows, putative activation; solid Y bar, inhibition; dotted Y bar, putative inhibition.
Figure 5
Figure 5
Roles of exosomes in cancer.
Figure 6
Figure 6
Exosomes as anti-cancer drug delivery vehicles.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Goodenberger M.L., Jenkins R.B. Genetics of adult glioma. Cancer Genet. 2012;205:613–621. doi: 10.1016/j.cancergen.2012.10.009. - DOI - PubMed
    1. Ostrom Q.T., Gittleman H., Fulop J., Liu M., Blanda R., Kromer C., Wolinsky Y., Kruchko C., Barnholtz-Sloan J.S. CBTRUS Statistical Report: Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2008–2012. Neuro Oncol. 2015;17(Suppl. 4):iv1–iv62. doi: 10.1093/neuonc/nov189. - DOI - PMC - PubMed
    1. Behin A., Hoang-Xuan K., Carpentier A.F., Delattre J.Y. Primary brain tumours in adults. Lancet. 2003;361:323–331. doi: 10.1016/S0140-6736(03)12328-8. - DOI - PubMed
    1. Louis D.N., Ohgaki H., Wiestler O.D., Cavenee W.K., Burger P.C., Jouvet A., Scheithauer B.W., Kleihues P. The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol. 2007;114:97–109. doi: 10.1007/s00401-007-0243-4. - DOI - PMC - PubMed
    1. Guan X., Vengoechea J., Zheng S., Sloan A.E., Chen Y., Brat D.J., O’Neill B.P., de Groot J., Yust-Katz S., Yung W.K., et al. Molecular subtypes of glioblastoma are relevant to lower grade glioma. PLoS ONE. 2014;9:e91216. doi: 10.1371/journal.pone.0091216. - DOI - PMC - PubMed

MeSH terms

Substances

LinkOut - more resources