Research Interest

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.

I am member of the University of  California Riverside (UCR) - Stem Cell Center and of the Inland Empire Stem Cell Consortium.

Selected Publications

1.   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.

2.   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.

3.   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.

4.   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.

5.   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.

6.   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.

7.   Finzer, P., Ventz, R., Kuntzen, C., Seibert, N., Soto, U. and Rösl, F. (2002) Growth arrest of HPV-positive cells after histone deacetylase inhibition is independent of E6/E7 oncogene expression. Virology 304: 265-273

8.   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.

9.   Bachmann, A., Hanke, B., Zawatzky, R., Soto, U., van Riggelen, J., zur Hausen, H. and Rösl F. (2001) Disturbance of tumor necrosis factor alpha-mediated beta interferon signalling in cervical carcinoma cells. J. Virol. 76:280-291.

10.  Finzer, P., Kuntzen, C., Soto, U., zur Hausen, H. and Rösl, F. (2001) Inhibitors of histone deacetylase arrest cell cycle and induce apoptosis in cervical carcinoma cells circumventing human papillomavirus oncogene expression. Oncogene 20:4768-4776.

11. Finzer, P., Soto, U., Delius, H., Patzelt, A., Coy, J.F., Pustka, A.,  zur Hausen, H. and Rösl, F. (2000) Differential transcriptional regulation of the monocyte-chemoattractant protein-1 (MCP-1) gene in tumorigenic and non-tumorigenic HPV 18 positive cells: The role of the chromatin structure and AP-1 composition. Oncogene 19: 3235-3244.

12. 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.

13. 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-α mediated repression of viral transcription and modification of the AP-1 transcription complex. Oncogene 18: 3187-3198.