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ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis.

Yuk Kien Chong1, Edwin Sandanaraj1, Lynnette W H Koh1

  • 1Department of Research (YKC, ES, LWHK, MT, MSYT, GRHK, TBT, GGYL, KLL, CT), Department of Neuroradiology (MN), and Department of Neurosurgery (IN, WHN, BTA), National Neuroscience Institute, Singapore; Department of Physiology (YKC, KLL, BTA) and Department of Biochemistry (OLK), Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Singapore Institute for Clinical Sciences (ES, JDH, BTA) and Institute of Molecular and Cell Biology (NST), Agency for Science, Technology and Research (A*STAR), Singapore; School of Biological Sciences, Nanyang Technological University, Singapore (ES, LWHK, MSYT, NST); Division of Medical Sciences, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore (OLK, CT); Duke-National University of Singapore Graduate Medical School, Singapore (IN, WHN, KLL, CT, BTA).

Journal of the National Cancer Institute
|November 9, 2015
PubMed
Summary
This summary is machine-generated.

High ST3GAL1 expression drives glioblastoma invasiveness and self-renewal. Inhibiting ST3GAL1 improves survival in mouse models and correlates with better patient prognosis, highlighting its role in tumor growth.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genomics

Background:

  • Cell surface sialylation is linked to cancer cell invasiveness.
  • Glioblastoma is a highly infiltrative and malignant brain tumor.
  • The ST3GAL1 sialyltransferase gene is amplified in some glioblastomas, with its role in tumor cell self-renewal being previously unstudied.

Purpose of the Study:

  • To investigate the role of ST3GAL1 in glioblastoma cell self-renewal and invasiveness.
  • To determine the prognostic significance of ST3GAL1 in glioma patients.
  • To elucidate the molecular mechanisms underlying ST3GAL1-mediated glioblastoma growth.

Main Methods:

  • Patient glioma cell self-renewal was assessed using clonogenic, viability, and invasiveness assays.
  • ST3GAL1 expression was analyzed in clinical databases (REMBRANDT, Gravendeel).
  • TGFβ signaling, FoxM1 regulation, and downstream transcriptomic pathways were investigated in ST3GAL1 knockdown models and xenografts.

Main Results:

  • High ST3GAL1 expression identified an invasive subpopulation with self-renewal capacity, and its loss prolonged survival in a mouse model.
  • The ST3GAL1 transcriptomic program significantly stratified patient survival, correlating with higher tumor grade and volume, independent of age and histology.
  • ST3GAL1 knockdown enriched for mitotic cell cycle processes, with FoxM1 identified as a key mediator of ST3Gal1 signaling via the (APC/C)-Cdh1 complex.

Conclusions:

  • The ST3GAL1-associated transcriptomic program indicates a poor prognosis in glioma patients, particularly in mesenchymal subtypes.
  • ST3Gal1-regulated self-renewal traits are critical for glioblastoma multiforme growth.
  • ST3GAL1 represents a potential therapeutic target for glioblastoma.