Hernan Roca

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. ncbi request reprint Cooperative interactions between RUNX2 and homeodomain protein-binding sites are critical for the osteoblast-specific expression of the bone sialoprotein gene
    Hernan Roca
    Department of Periodontics, Prevention, and Geriatrics and Center for Craniofacial Regeneration, School of Dentistry, University of Michigan, Ann Arbor 48109 1078, USA
    J Biol Chem 280:30845-55. 2005
  2. pmc IL-4 induces proliferation in prostate cancer PC3 cells under nutrient-depletion stress through the activation of the JNK-pathway and survivin up-regulation
    Hernan Roca
    Department of Urology, Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Cell Biochem 113:1569-80. 2012
  3. pmc CCL2 is a negative regulator of AMP-activated protein kinase to sustain mTOR complex-1 activation, survivin expression, and cell survival in human prostate cancer PC3 cells
    Hernan Roca
    Department of Urology, University of Michigan, Ann Arbor, MI 48109, USA
    Neoplasia 11:1309-17. 2009
  4. pmc CCL2 protects prostate cancer PC3 cells from autophagic death via phosphatidylinositol 3-kinase/AKT-dependent survivin up-regulation
    Hernan Roca
    Department of Urology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109, USA
    J Biol Chem 283:25057-73. 2008
  5. ncbi request reprint CCL2, survivin and autophagy: new links with implications in human cancer
    Hernan Roca
    Department of Urology, Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan 48109, USA
    Autophagy 4:969-71. 2008
  6. pmc CCL2 and interleukin-6 promote survival of human CD11b+ peripheral blood mononuclear cells and induce M2-type macrophage polarization
    Hernan Roca
    Department of Urology, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Biol Chem 284:34342-54. 2009
  7. pmc Transcriptional regulation of osteoblasts
    Renny T Franceschi
    School of Dentistry, University of Michigan, Ann Arbor, Mich 48109 1078, USA
    Cells Tissues Organs 189:144-52. 2009
  8. pmc Identification and functional characterization of ERK/MAPK phosphorylation sites in the Runx2 transcription factor
    Chunxi Ge
    Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, Michigan 48109 1078, USA
    J Biol Chem 284:32533-43. 2009
  9. pmc The chemokine CCL2 increases prostate tumor growth and bone metastasis through macrophage and osteoclast recruitment
    Kosuke Mizutani
    Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, MI 48109 5946, USA
    Neoplasia 11:1235-42. 2009
  10. pmc Chemical transfection of dye-conjugated microRNA precursors for microRNA functional analysis of M2 macrophages
    Yee Seng Ng
    Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109 5946, USA
    J Cell Biochem 113:1714-23. 2012

Collaborators

Detail Information

Publications16

  1. ncbi request reprint Cooperative interactions between RUNX2 and homeodomain protein-binding sites are critical for the osteoblast-specific expression of the bone sialoprotein gene
    Hernan Roca
    Department of Periodontics, Prevention, and Geriatrics and Center for Craniofacial Regeneration, School of Dentistry, University of Michigan, Ann Arbor 48109 1078, USA
    J Biol Chem 280:30845-55. 2005
    ..Taken together, our data show that RUNX2 is a direct regulator of Bsp in osteoblasts and that it functions in cooperation with DLX5 or a related factor to activate osteoblast-specific gene expression...
  2. pmc IL-4 induces proliferation in prostate cancer PC3 cells under nutrient-depletion stress through the activation of the JNK-pathway and survivin up-regulation
    Hernan Roca
    Department of Urology, Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Cell Biochem 113:1569-80. 2012
    ..Overall, these findings suggest that in a tumor microenvironment under stress conditions, IL-4 triggers a simultaneous activation of the JNK-pathway and the up-regulation of survivin turning on a cancer proliferation mechanism...
  3. pmc CCL2 is a negative regulator of AMP-activated protein kinase to sustain mTOR complex-1 activation, survivin expression, and cell survival in human prostate cancer PC3 cells
    Hernan Roca
    Department of Urology, University of Michigan, Ann Arbor, MI 48109, USA
    Neoplasia 11:1309-17. 2009
    ..Altogether, these findings suggest that CCL2 hyperactivates mTORC1 through simultaneous regulation of both AMPK and Akt pathways and reveals a new network that promotes prostate cancer: CCL2-AMPK-mTORC1-survivin...
  4. pmc CCL2 protects prostate cancer PC3 cells from autophagic death via phosphatidylinositol 3-kinase/AKT-dependent survivin up-regulation
    Hernan Roca
    Department of Urology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109, USA
    J Biol Chem 283:25057-73. 2008
    ..Altogether, these findings indicate that CCL2 protects prostate cancer PC3 cells from autophagic death via the phosphatidylinositol 3-kinase/Akt/survivin pathway and reveal survivin as a critical molecule in this survival mechanism...
  5. ncbi request reprint CCL2, survivin and autophagy: new links with implications in human cancer
    Hernan Roca
    Department of Urology, Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan 48109, USA
    Autophagy 4:969-71. 2008
    ..How these life or death decisions are regulated remains unclear. Here we discuss the function of survivin in the control of autophagy and the interaction between CCL2, survivin and autophagy in the complex program of tumor progression...
  6. pmc CCL2 and interleukin-6 promote survival of human CD11b+ peripheral blood mononuclear cells and induce M2-type macrophage polarization
    Hernan Roca
    Department of Urology, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Biol Chem 284:34342-54. 2009
    ....
  7. pmc Transcriptional regulation of osteoblasts
    Renny T Franceschi
    School of Dentistry, University of Michigan, Ann Arbor, Mich 48109 1078, USA
    Cells Tissues Organs 189:144-52. 2009
    ..These studies allow us to begin understanding the complex mechanisms necessary to fine-tune bone formation as mesenchymal progenitors progress down the osteoblast lineage...
  8. pmc Identification and functional characterization of ERK/MAPK phosphorylation sites in the Runx2 transcription factor
    Chunxi Ge
    Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, Michigan 48109 1078, USA
    J Biol Chem 284:32533-43. 2009
    ....
  9. pmc The chemokine CCL2 increases prostate tumor growth and bone metastasis through macrophage and osteoclast recruitment
    Kosuke Mizutani
    Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, MI 48109 5946, USA
    Neoplasia 11:1235-42. 2009
    ..These findings suggest that CCL2 increases tumor growth and bone metastasis through recruitment of macrophages and OCs to the tumor site...
  10. pmc Chemical transfection of dye-conjugated microRNA precursors for microRNA functional analysis of M2 macrophages
    Yee Seng Ng
    Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109 5946, USA
    J Cell Biochem 113:1714-23. 2012
    ..Among the most common methods of transfection, the chemical transfection of dye-conjugated miRNA precursors was determined to be the best-suited approach for the functional analysis of M2 macrophages...
  11. pmc Transcription factors OVOL1 and OVOL2 induce the mesenchymal to epithelial transition in human cancer
    Hernan Roca
    Department of Urology, University of Michigan School of Medicine, Ann Arbor, Michigan, United States of America
    PLoS ONE 8:e76773. 2013
    ..The role of OVOL-TFs as inducers of MET is further supported by expression analyses in 917 cancer cell lines, suggesting their role as crucial regulators of epithelial-mesenchymal cell plasticity in cancer...
  12. ncbi request reprint Possible mechanism of CCL2-induced Akt activation in prostate cancer cells
    Kosuke Mizutani
    Departments of Internal Medicine and Urology, University of Michigan School of Medicine, 7308 CCC 1500 E Medical Center Drive, Ann Arbor, MI 48109 5946, USA
    Anticancer Res 29:3109-13. 2009
    ..The results suggest that CCL2-induced Akt phosphorylation is mediated by the Galphai complex and adenylyl cyclase. This is the first study that demonstrates a direct involvement of adenylyl cyclase in CCL2-induced Akt phosphorylation...
  13. ncbi request reprint Transcriptional regulation of osteoblasts
    Renny T Franceschi
    Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI 48109 1078, USA
    Ann N Y Acad Sci 1116:196-207. 2007
    ..These studies allow us to begin understanding the complex mechanisms necessary to fine-tune bone formation in response to extracellular stimuli including ECM interactions, mechanical loads, and hormonal stimulation...
  14. pmc Analysis of transcription factor interactions in osteoblasts using competitive chromatin immunoprecipitation
    Hernan Roca
    Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI, USA
    Nucleic Acids Res 36:1723-30. 2008
    ....
  15. pmc BMP signaling is required for RUNX2-dependent induction of the osteoblast phenotype
    Mattabhorn Phimphilai
    Department of Biological Chemistry, University of Michigan School of Medicine, Ann Arbor, Michigan 48109 1078, USA
    J Bone Miner Res 21:637-46. 2006
    ..BMP blocking agents were used to show that RUNX2-dependent osteoblast differentiation and transactivation activity both require BMP signaling and, further, that RUNX2 enhances the responsiveness of cells to BMPs...
  16. pmc A bioinformatics approach reveals novel interactions of the OVOL transcription factors in the regulation of epithelial - mesenchymal cell reprogramming and cancer progression
    Hernan Roca
    Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA
    BMC Syst Biol 8:29. 2014
    ..We now test this hypothesis by developing a model, OVOL Induced MET (OI-MET), and sub-model (OI-MET-TF), to characterize differential gene expression in MET common to prostate cancer (PC) and breast cancer (BC)...