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Last Name
Institution

FENG YANG

TitleAssistant Professor
InstitutionBaylor College of Medicine
DepartmentDepartment of Molecular & Cellular Biology
AddressMolecular & Cellular Biology Department
One Baylor Plaza
Houston TX 77030
Email

 Biography 
 awards and honors
2007 - 2008Exploration-Hypothesis Development Award
2009 - 2012New Investigator Award
2009 - 2010Concept Award
2013 - 2016Individual Investigator Research Award
2013 - 2016Idea Development Award
2013 - 2016Idea Development Award

 Overview 
 overview
The research in my laboratory focuses on the following four major areas.

(1) MAPK4 in regulating key signaling pathways in human cancers. MAPK4 is an atypical MAPK that were not well studied. Unlike other “typical” MAPK such as p38a/b/g, Erk1/2, JNK1/2/3, etc., MAPK4 lacks the highly conserved TXY activation motif that can be phosphorylated by MAPKK, the dual Ser/Thr and Tyr kinase. Instead, MAPK4 carries the SEG motif that lacks a key Tyr (Y) residue for phosphorylation by MAPKK. Hence, there is no identified MAPKK for MAPK4. PAKs were shown to phosphorylate MAPK4/Erk4 and MAPK6/Erk3 (another atypical MAPK). However, the biological significance of PAKs in MAPK4 activation remains to be determined. Currently, the roles of MAPK4 in human cancers are unknown. We discovered that MAPK4 regulates several key signaling pathways that are essential for cancer progression as well as the development of therapy-resistance. We are now carrying out in-depth studies to reveal the molecular mechanisms underlying MAPK4 regulation of human cancers, focusing on prostate cancer.

(2) Tumor microenvironment regulation of prostate cancer. Tumor microenvironment, including stromal cells, has been documented to play key roles in regulating human cancers. Our study revealed that prostate stromal cells profoundly regulate prostate cancer biology, including inducing androgen-dependent and androgen-independent AR activation. We are now investigating the detailed molecular mechanisms underlying this tumor stroma-induced AR activation in prostate cancer cells in the absence of significant amount of androgen. This may provide a direct mechanism for relapse of the lethal castration-resistant prostate cancer after androgen-deprivation therapy.

(3) Development of a novel transgenic model for prostate cancer. c-Myc is the most significantly amplified oncogene in human prostate cancer. Dr. Sawyer’s group has developed the Hi-MYC model using an enhanced probasin promoter to drive c-Myc expression in prostate epithelia. These mice developed invasive prostate carcinomas that shared molecular features with human prostate cancers. This study, along with others, provided crucial data supporting key roles of c-Myc oncogenic pathway in prostate tumorigenesis. However, since probasin promoter activity is crucially dependent on androgen, the prostate tumors lose c-Myc oncogene expression upon castration in such MYC models. Therefore, the tumor regression in these androgen-depleted MYC mice represents the mixed effects of both artificial direct effects from loss of oncogene expression and potential real effects from tumor cellular responses to castration. These greatly limit the abilities to use such models to concisely study androgen signaling, castration-responses, and castration-resistance of prostate cancer. Accordingly, we have developed a novel transgenic model that allows maintained expression of c-Myc oncogene along with luciferase (for real-time in vivo bioluminescence imaging) in prostate after castration. We are performing detailed characterization of this model and using it to study therapy-resistance such as castration-resistance and chemoresistance of prostate cancers.

(4) FGFR1 signaling in prostate cancer and breast cancer. We are also investigating the biological functions of FGFR1 in prostate cancer and breast cancer, focusing on its role in promoting tumor progression and metastasis.

 keywords
Prostate Cancer, Mouse model, Therapy resistance, Tumor microenvironment


 Bibliographic 
 selected publications
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
List All   |   Timeline
  1. Yang F, Chen Y, Shen T, Guo D, Dakhova O, Ittmann MM, Creighton CJ, Zhang Y, Dang TD, Rowley DR. Stromal TGF-ß signaling induces AR activation in prostate cancer. Oncotarget. 2014 Oct 14.
    View in: PubMed
  2. Kim W, Barron DA, San Martin R, Chan KS, Tran LL, Yang F, Ressler SJ, Rowley DR. RUNX1 is essential for mesenchymal stem cell proliferation and myofibroblast differentiation. Proc Natl Acad Sci U S A. 2014 Oct 13.
    View in: PubMed
  3. Strand DW, Liang YY, Yang F, Barron DA, Ressler SJ, Schauer IG, Feng XH, Rowley DR. TGF-ß induction of FGF-2 expression in stromal cells requires integrated smad3 and MAPK pathways. Am J Clin Exp Urol. 2014; 2(3):239-48.
    View in: PubMed
  4. Ressler SJ, Dang TD, Wu SM, Tse DY, Gilbert BE, Vyakarnam A, Yang F, Schauer IG, Barron DA, Rowley DR. WFDC1 Is a Key Modulator of Inflammatory and Wound Repair Responses. Am J Pathol. 2014 Sep 16.
    View in: PubMed
  5. Yang F, Zhang Y, Ressler SJ, Ittmann MM, Ayala GE, Dang TD, Wang F, Rowley DR. FGFR1 is essential for prostate cancer progression and metastasis. Cancer Res. 2013 Jun 15; 73(12):3716-24.
    View in: PubMed
  6. Barron DA, Strand DW, Ressler SJ, Dang TD, Hayward SW, Yang F, Ayala GE, Ittmann M, Rowley DR. TGF-ß1 induces an age-dependent inflammation of nerve ganglia and fibroplasia in the prostate gland stroma of a novel transgenic mouse. PLoS One. 2010; 5(10):e13751.
    View in: PubMed
  7. Alvarez R, Reading J, King DF, Hayes M, Easterbrook P, Farzaneh F, Ressler S, Yang F, Rowley D, Vyakarnam A. WFDC1/ps20 is a novel innate immunomodulatory signature protein of human immunodeficiency virus (HIV)-permissive CD4+ CD45RO+ memory T cells that promotes infection by upregulating CD54 integrin expression and is elevated in HIV type 1 infection. J Virol. 2008 Jan; 82(1):471-86.
    View in: PubMed
  8. Yang F, Strand DW, Rowley DR. Fibroblast growth factor-2 mediates transforming growth factor-beta action in prostate cancer reactive stroma. Oncogene. 2008 Jan 17; 27(4):450-9.
    View in: PubMed
  9. Yang F, Tuxhorn JA, Ressler SJ, McAlhany SJ, Dang TD, Rowley DR. Stromal expression of connective tissue growth factor promotes angiogenesis and prostate cancer tumorigenesis. Cancer Res. 2005 Oct 1; 65(19):8887-95.
    View in: PubMed
  10. McAlhany SJ, Ressler SJ, Larsen M, Tuxhorn JA, Yang F, Dang TD, Rowley DR. Promotion of angiogenesis by ps20 in the differential reactive stroma prostate cancer xenograft model. Cancer Res. 2003 Sep 15; 63(18):5859-65.
    View in: PubMed
  11. Li Y, Li H, Yang F, Smith-Gill SJ, Mariuzza RA. X-ray snapshots of the maturation of an antibody response to a protein antigen. Nat Struct Biol. 2003 Jun; 10(6):482-8.
    View in: PubMed
  12. Tuxhorn JA, McAlhany SJ, Yang F, Dang TD, Rowley DR. Inhibition of transforming growth factor-beta activity decreases angiogenesis in a human prostate cancer-reactive stroma xenograft model. Cancer Res. 2002 Nov 1; 62(21):6021-5.
    View in: PubMed
  13. Yang F, Cheng Y, Peng J, Zhou J, Jing G. Probing the conformational state of a truncated staphylococcal nuclease R using time of flight mass spectrometry with limited proteolysis. Eur J Biochem. 2001 Aug; 268(15):4227-32.
    View in: PubMed
  14. Yang F, Jing GZ, Zhou JM, Zheng YZ. Free luciferase may acquire a more favorable conformation than ribosome-associated luciferase for its activity expression. FEBS Lett. 1997 Nov 17; 417(3):329-32.
    View in: PubMed
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