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
. 2014 Feb 10;6(1):376-95.
doi: 10.3390/cancers6010376.

STAT3 Activation in Glioblastoma: Biochemical and Therapeutic Implications

Affiliations

STAT3 Activation in Glioblastoma: Biochemical and Therapeutic Implications

Jennifer E Kim et al. Cancers (Basel). .

Abstract

Signal transducer and activator of transcription 3 (STAT3) is a potent regulator of gliomagenesis through its induction of angiogenesis, host immunosuppression, and tumor invasion. Gain of function mutations result in constitutive activation of STAT3 in glioma cells, making STAT3 an attractive target for inhibition in cancer therapy. Nevertheless, some studies show that STAT3 also participates in terminal differentiation and apoptosis of various cell lines and in glioma with phosphatase and tensin homolog (PTEN)-deficient genetic backgrounds. In light of these findings, the utility of STAT3 as a prognostic indicator and as a target of drug therapies will be contingent on a more nuanced understanding of its pro- and anti-tumorigenic effects.

PubMed Disclaimer

Figures

Figure 1
Figure 1
STAT3 as convergence point in the oncogenic pathway.

Similar articles

Cited by

References

    1. Ostrom Q.T., Gittleman H., Farah P., Ondracek A., Chen Y., Wolinsky Y., Stroup N.E., Kruchko C., Barnholtz-Sloan J.S. CBTRUS statistical report: Primary brain and central nervous system tumors diagnosed in the united states in 2006–2010. Neuro-oncology. 2013;15:ii1–ii56. - PMC - PubMed
    1. Stewart L.A. Chemotherapy in adult high-grade glioma: A systematic review and meta-analysis of individual patient data from 12 randomised trials. Lancet. 2002;359:1011–1018. doi: 10.1016/S0140-6736(02)08091-1. - DOI - PubMed
    1. Rich J.N., Reardon D.A., Peery T., Dowell J.M., Quinn J.A., Penne K.L., Wikstrand C.J., van Duyn L.B., Dancey J.E., McLendon R.E., et al. Phase II trial of gefitinib in recurrent glioblastoma. J. Clin. Oncol. 2004;22:133–142. - PubMed
    1. Taylor T.E., Furnari F.B., Cavenee W.K. Targeting EGFR for treatment of glioblastoma: Molecular basis to overcome resistance. Curr. Cancer Drug Targets. 2012;12:197–209. doi: 10.2174/156800912799277557. - DOI - PMC - PubMed
    1. Mellinghoff I.K., Wang M.Y., Vivanco I., Haas-Kogan D.A., Zhu S., Dia E.Q., Lu K.V., Yoshimoto K., Huang J.H., Chute D.J., et al. Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors. N. Engl. J. Med. 2005;353:2012–2024. doi: 10.1056/NEJMoa051918. - DOI - PubMed