Open Access

Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells

  • Authors:
    • Chengjin Ai
    • Yu Zhou
    • Kunming Pu
    • Yi Yang
    • Yingying Zhou
  • View Affiliations

  • Published online on: May 27, 2022     https://doi.org/10.3892/ol.2022.13351
  • Article Number: 230
  • Copyright: © Ai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Neurite outgrowth inhibitor A (Nogo‑A), a member of the reticulon 4 family, is an axon regeneration inhibitor that is negatively associated with the malignancy of oligodendroglial tumors. It has been suggested that the Nogo‑A/Nogo Receptor (NgR) pathway plays a promoting effect in regulating cancer stem‑like cells (CSCs) derived from glioblastoma, indicating that Nogo‑A could exert different roles in CSCs than those in parental cancer cells. In the present study, CSCs were generated from the human Uppsala 87 malignant glioma (U87MG) cell line. These U87MG‑CSCs were characterized by the upregulation of CD44 and CD133, which are two markers of stemness. The expression levels of Nogo‑A and the differentiation of U87MG‑CSCs were investigated. In addition, the proliferation, invasion and colony formation U87MG‑CSCs were examined. Using culture in serum‑containing medium, U87MG‑CSCs were differentiated into neuron‑like cells specifically expressing MAP2, β‑III‑tubulin and nestin. Nogo‑A was upregulated in U87MG‑CSCs compared with parental cells. Knockdown of Nogo‑A and inhibition of the Nogo‑A/NgR signaling pathway in U87MG‑CSCs markedly decreased cell viability, cell cycle entry, invasion and tumor formation, indicating that Nogo‑A could regulate U87MG‑CSC function. Moreover, Nogo‑A was involved in intracellular ATP synthesis and scavenging of accumulated reactive oxygen species. Nogo‑A/NgR pathway exerted protective effects against hypoxia‑induced non‑apoptotic and apoptotic cell death. These results suggest that Nogo‑A plays an important role in regulating U87MG‑CSCs via the Nogo‑A/NgR signaling pathway. Nogo‑A may also different roles in U87MG‑CSCs compared with their parental cells.

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July-2022
Volume 24 Issue 1

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Copy and paste a formatted citation
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Spandidos Publications style
Ai C, Zhou Y, Pu K, Yang Y and Zhou Y: Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells. Oncol Lett 24: 230, 2022
APA
Ai, C., Zhou, Y., Pu, K., Yang, Y., & Zhou, Y. (2022). Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells. Oncology Letters, 24, 230. https://doi.org/10.3892/ol.2022.13351
MLA
Ai, C., Zhou, Y., Pu, K., Yang, Y., Zhou, Y."Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells". Oncology Letters 24.1 (2022): 230.
Chicago
Ai, C., Zhou, Y., Pu, K., Yang, Y., Zhou, Y."Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells". Oncology Letters 24, no. 1 (2022): 230. https://doi.org/10.3892/ol.2022.13351