The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways
Open accessAbstract
Hepatocyte growth factor (HGF) is a ligand of the receptor tyrosine kinase encoded by the c-Met protooncogene. HGF/Met signaling has multifunctional effects on various cell types. We sought to determine the role of HGF/Met in apoptosis and identify signal transducers involved in this process. In experiments with human SK-LMS-1 leiomyosarcoma cells, we show that the Akt kinase is activated by HGF in a time- and dose-dependent manner by phosphatidylinositol 3-kinase (PI3-kinase). Akt is also activated by active tumorigenic forms of Met, i.e., ligand-independent Tpr-Met, a truncated and constitutively dimerized form of Met, and a mutationally activated version of Met corresponding to that found in human hereditary papillary renal carcinoma. In NIH 3T3 cells transfected with wild-type Met, HGF inhibits apoptosis induced by serum starvation and UV irradiation. HGF-induced survival correlates with Akt activity and is inhibited by the specific PI3-kinase inhibitor LY294002, indicating that HGF inhibits cell death through the PI3-kinase/Akt signal transduction pathway. Furthermore, transiently transfected Tpr-Met activates Akt (both Akt1 and Akt2) and protects cells from apoptosis. Mitogen-activated protein kinase (MAPK) also is activated by HGF and rescues cells from apoptosis, although the cytoprotective effect is less marked than for PI3-kinase/Akt. Blocking MAPK with the specific MAPK kinase inhibitor PD098059 impairs the ability of HGF to promote cell survival. Similar results were obtained with NIH 3T3 cells expressing the fusion protein Trk-Met and stimulated with nerve growth factor, the Trk ligand. These results demonstrate that HGF/Met is capable of protecting cells from apoptosis by using both PI3-kinase/Akt and, to a lesser extent, MAPK pathways.
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Cites
Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis
Xia, Z., Dickens, M., Raingeaud, J., Davis, R. J., & Greenberg, M. E. (1995) · Science · doi:10.1126/science.270.5240.1326 · Cited by 5,287
Regulation of Cell Death Protease Caspase-9 by Phosphorylation
Cardone, M. H., Roy, N., Stennicke, H. R., Salvesen, G. S., Franke, T. F., Stanbridge, E., Frisch, S., & Reed, J. C. (1998) · Science · doi:10.1126/science.282.5392.1318 · Cited by 2,481
Regulation of neuronal survival by the serine-threonine protein kinase Akt
Dudek, H., Datta, S. R., Franke, T. F., Birnbaum, M. J., Yao, R., Cooper, G. M., Segal, R. A., Kaplan, D. R., & Greenberg, M. E. (1997) · Science · doi:10.1126/science.275.5300.661 · Cited by 2,436
NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase
Nidai Ozes, O., Mayo, L. D., Gustin, J. A., Pfeffer, S. R., Pfeffer, L. M., & Donner, D. B. (1999) · Nature · doi:10.1038/43466 · Cited by 1,832
Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase Akt
Peso, L. D., González-Garcı́a, M., Page, C., Herrera, R., & Nuñez, G. (1997) · Science · doi:10.1126/science.278.5338.687 · Cited by 1,797
Suppression of ceramide-mediated programmed cell death by sphingosine-1-phosphate
Cuvillier, O., Pirianov, G., Kleuser, B., Vanek, P. G., Coso, O. A., Gutkind, J. S., & Spiegel, S. (1996) · Nature · doi:10.1038/381800a0 · Cited by 1,529
Schmidt, L., Duh, F.-M., Chen, F., Kishida, T., Glenn, G., Choyke, P., Scherer, S. W., Zhuang, Z., Lubensky, I., Dean, M., et al. (1997) · Nature Genetics · doi:10.1038/ng0597-68 · Cited by 1,524
NF-κB is a target of AKT in anti-apoptotic PDGF signalling
Romashkova, J. A., & Makarov, S. S. (1999) · Nature · doi:10.1038/43474 · Cited by 1,517
Scatter factor/hepatocyte growth factor is essential for liver development
Schmidt, C., Bladt, F., Goedecke, S., Brinkmann, V., Zschiesche, W., Sharpe, M., Gherardi, E., & Birchmeler, C. (1995) · Nature · doi:10.1038/373699a0 · Cited by 1,394
Essential role for the c-met receptor in the migration of myogenic precursor cells into the limb bud
Bladt, F., Riethmacher, D., Isenmann, S., Aguzzi, A., & Birchmeier, C. (1995) · Nature · doi:10.1038/376768a0 · Cited by 1,284
Cited by
Huh, C.-G., Factor, V. M., Sánchez, A., Uchida, K., Conner, E. A., & Thorgeirsson, S. S. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0306068101 · Cited by 750
Liver Regeneration after Partial Hepatectomy
Michalopoulos, G. K. (2010) · The American Journal of Pathology · doi:10.2353/ajpath.2010.090675 · Cited by 713
Novel Therapeutic Inhibitors of the c-Met Signaling Pathway in Cancer
Eder, J. P., Vande Woude, G. F., Boerner, S. A., & LoRusso, P. M. (2009) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-1306 · Cited by 522
The prognostic significance of phosphatidylinositol 3-kinase pathway activation in human gliomas
Chakravarti, A., Zhai, G., Suzuki, Y., Sarkesh, S., Black, P. M., Muzikansky, A., & Loeffler, J. S. (2004) · Journal of Clinical Oncology · doi:10.1200/jco.2004.07.193 · Cited by 377
Ultraviolet radiation and cutaneous malignant melanoma
Jhappan, C., Noonan, F. P., & Merlino, G. (2003) · Oncogene · doi:10.1038/sj.onc.1206450 · Cited by 283
Metadata
- Authors
- Xiao, G.-H.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2000-12-26
- Volume
- 98
- Issue
- 1
- Pages
- 247-252
- ISSN
- 0027-8424 (ISSN-L)
- OpenAlex
- W2139440398
- Cited by
- 417
- References
- 37
- FWCI
- 12.56
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways. https://app.cochat.ai/papers/10.1073/pnas.011532898
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- Xiao, G.-H. (2001). Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.011532898
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