The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype
Open accessAbstract
The tyrosine kinase c-Met promotes the formation and malignant progression of multiple cancers. It is well known that c-Met hyperactivation increases tumorigenicity and tumor cell resistance to DNA damaging agents, properties associated with tumor-initiating stem cells. However, a link between c-Met signaling and the formation and/or maintenance of neoplastic stem cells has not been previously identified. Here, we show that c-Met is activated and functional in glioblastoma (GBM) neurospheres enriched for glioblastoma tumor-initiating stem cells and that c-Met expression/function correlates with stem cell marker expression and the neoplastic stem cell phenotype in glioblastoma neurospheres and clinical glioblastoma specimens. c-Met activation was found to induce the expression of reprogramming transcription factors (RFs) known to support embryonic stem cells and induce differentiated cells to form pluripotent stem (iPS) cells, and c-Met activation counteracted the effects of forced differentiation in glioblastoma neurospheres. Expression of the reprogramming transcription factor Nanog by glioblastoma cells is shown to mediate the ability of c-Met to induce the stem cell characteristics of neurosphere formation and neurosphere cell self-renewal. These findings show that c-Met enhances the population of glioblastoma stem cells (GBM SCs) via a mechanism requiring Nanog and potentially other c-Met–responsive reprogramming transcription factors.
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Cites
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Glioma stem cells promote radioresistance by preferential activation of the DNA damage response
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Met, metastasis, motility and more
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Isolation and Characterization of Tumorigenic, Stem-like Neural Precursors from Human Glioblastoma
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Suppression of induced pluripotent stem cell generation by the p53–p21 pathway
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Linking the p53 tumour suppressor pathway to somatic cell reprogramming
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SSEA-1 Is an Enrichment Marker for Tumor-Initiating Cells in Human Glioblastoma
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Cited by
Cancer Research Communications
(2021) · doi:10.1158/1078-0432 · Cited by 1,532
Molecular targeted therapy of glioblastoma
Le Rhun, E., Preusser, M., Roth, P., Reardon, D. A., van den Bent, M., Wen, P., Reifenberger, G., & Weller, M. (2019) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2019.101896 · Cited by 688
Overcoming therapeutic resistance in glioblastoma: the way forward
Osuka, S., & Van Meir, E. G. (2017) · Journal of Clinical Investigation · doi:10.1172/jci89587 · Cited by 511
Glioblastoma targeted therapy: updated approaches from recent biological insights
Touat, M., Idbaih, A., Sanson, M., & Ligon, K. L. (2017) · Annals of Oncology · doi:10.1093/annonc/mdx106 · Cited by 441
Bao, Z.-S., Chen, H.-M., Yang, M.-Y., Zhang, C.-B., Yu, K., Ye, W.-L., Hu, B.-Q., Yan, W., Zhang, W., Akers, J., et al. (2014) · Genome Research · doi:10.1101/gr.165126.113 · Cited by 409
Metadata
- Authors
- Li, Y., Li, A., Glas, M., Lal, B., Ying, M., Sang, Y., Xia, S., Trageser, D., Guerrero-Cázares, H., Eberhart, C. G., Quiñones-Hinojosa, A., Scheffler, B., & Laterra, J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2011-05-31
- Volume
- 108
- Issue
- 24
- Pages
- 9951-9956
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1992301683
- Cited by
- 266
- References
- 33
- FWCI
- 12.27
- Type
- journal article
- Language
- en
- Open access
- green
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- Li, Y., Li, A., Glas, M., Lal, B., Ying, M., Sang, Y., Xia, S., Trageser, D., Guerrero-Cázares, H., Eberhart, C. G., Quiñones-Hinojosa, A., Scheffler, B., & Laterra, J. (2011). c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1016912108
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