Stem Cell Mobilization
Regenerative medicine focuses on the potential use of stem cells in the cure of diverse diseases. A typical stem cell therapy would consist of
delivering stem cells directly to the injured tissue. However an option could be the stimulation of endogenous stem cells both in the injured
tissue as well as in remote tissues that serve as reservoirs for adult stem cells (e.g. bone marrow). Likely, stem cell mobilization from
reservoirs to damage sites may improve healing.
My lab is studying endogenous stem cell mobilization with emphasis on factors contributing to stem/progenitor cell release.
Additionally, we are also studying a subpopulation of tumor cells having stem cell characteristics. These tumor cells
are known as "cancer stem cells" or "tumor initiating cells". Research suggest that cancer stem cells can be released from the tumor into
circulation and participate in metastasis. We are interested in characterizing the conditions needed in cancer stem cell release. On the
other hand, the study of circulating cancer stem cells could be a useful diagnostic tool.
More information on the Soto Lab
1997-1998 Alexander von Humboldt Research Fellowship
Williams VM, Filippova M, Soto U, Duerksen-Hughes PJ. (2011) HPV-DNA integration and carcinogenesis: putative roles for inflammation and
oxidative stress. Future Virol. 6:45-57.
Lao VV, Herring JL, Kim C H, Darwanto A, Soto U and Sowers L (2009) Incorporation of 5-Chlorocytosine into mammalian DNA results in
heritable gene silencing and altered cytosine methylation patterns. Carcinogenesis 30:886-893.
Mc Lean L, Soto U, Agama K, Francis J, Jimenez R, Pommier Y, Sowers L and Brantley E. (2008) Aminoflavone induces oxidative DNA damage
and oxidative species-mediated apoptosis in breast cancer cells. Int.J.Cancer 122:1665-1674.
van Riggelen J, Buchwalter G, Soto U, De-Castro Arce J, Zur Hausen H, Wasylyk B and Rösl F.( 2005) Loss of Net as repressor leads to
constitutive increased c-fos transcription in cervical cancer cells. J. Biol. Chem. 280:3286-3294.
De Castro-Arce, J., Soto, U., van Riggelen, J., Schwarz, E., zur Hausen, H. and Rösl, F. (2004) Ectopic expression of non-liganded
RAR-beta abrogates AP-1 activity by selective degradation of c-Jun in cervical carcinoma cells. J Biol Chem. 279: 45408-45416.
Finzer, P., Krueger, A., Stöhr, M., Brenner, D., Soto, U., Kuntzen, C., Krammer, P.H. and Rösl, F. (2004) HDAC-inhibitors trigger
type II apoptosis in HPV-positive cells via induction of the E2F-p73 pathway. Oncogene 23:4807-17.
Hergenhahn, M., Soto, U., Weninger, A., Polack, A., Hsu, C-H., Cheng, A-L. and Rösl, F. (2002) The chemopreventive compound curcumin
is an efficient inhibitor of Epstein-Barr virus BZLF-1 transcription in Raji DR-Luc cells. Mol. Car. 33:137-145.
Soto, U., Denk, C., Finzer, P., Hutter, K.J., zur Hausen, H. and Rösl, F. (2000) Genetic complementation to non-tumorigenicity in
cervical carcinoma cells correlates with alterations in AP-1 composition. Int. J. Cancer 86: 811-817.
Soto, U., Das, B.C., Lengert, M., Finzer, P., zur Hausen, H. and Rösl, F. (1999) Conversion of HPV 18 positive non-tumorigenic
HeLa-fibroblast hybrids to invasive growth involves loss of TNF-? mediated repression of viral transcription and modification of the
AP-1 transcription complex. Oncogene 18: 3187-3198.