The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases

 Wenliang Li, Ph.D.

Wenliang Li, Ph.D.

Assistant Professor, Texas Therapeutics Institute


Dr. Wenliang Li’s research is to study novel molecular mechanisms of cancer metastasis with the goal of identifying new biomarkers and drug targets for the development of better therapeutics for human cancers.

Dr. Li obtained his Ph.D. in Genetics from Case Western Reserve University in 2004. His dissertation work was conducted in Dr. Bryan Williams’ lab at Cleveland Clinic Foundation, where he constructed a large cancer specific microarray and used it to identify gene expression patterns that were associated with genetics and prognostics of human Wilms tumors. He then joined Dr. Ed Harlow’s lab at Harvard Medical School for his postdoctoral training, where he provided critical contributions in a series of collaborative studies in identifying kinases controlling survival and proliferation of human normal and tumor cells. In 12/2010, Dr. Li joined the Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston.

Cancer metastasis, the spread of tumor to other parts of patient’s body, is responsible for over 90% of cancer death. However, it is still poorly understood and the current approaches to prevent or treat human metastatic diseases are mostly unsuccessful. Through genomics, RNAi and cDNA functional screens, Dr. Li’s lab has identified some critical but previously unknown regulators for cancer metastasis. Signaling pathways and molecular mechanisms of these genes are under investigation with molecular, cellular, biochemical, genomic and proteomic approaches, as well as with mouse models and patient samples. These studies will yield new insights in cancer metastasis and may facilitate the development of new cancer therapeutics and biomarkers.

Another exciting research program in Dr. Li's lab is involved in identifying and studying novel regulators of epithelial-mesenchymal transition (EMT) and stem cell phenotypes. Epithelial-mesenchymal transition (EMT), a developmental process, is believed to play a key role in cancer metastasis, drug resistance, organ fibrosis and stem cell-like phenotypes. Kinases play central roles in many aspects of signaling transduction, cell physiology and diseases. They are also one of the most important gene families for cancer drug development. Our literature search indicated that the majority of >700 kinases in human genome are still poorly studied. Dr. Li’s lab is employing unbiased functional screens against hundreds of human kinases to identify novel regulators for EMT and linking them to stem cell-like phenotypes and cancer metastasis. Investigation of the molecular mechanisms of these kinases will have a significant impact in expanding our knowledge in the crossroad of exciting and critical areas, such as development, stem cell, drug resistance and metastasis. These kinases may also become new biomarkers and cancer drug targets for the development of novel therapeutics for human cancer.

Bullet points of research projects:

  • Mechanisms of action for novel regulators of cancer metastasis.
  • New pathways and mechanisms of EMT/MET.
  • Acquired resistance to cancer therapeutics.


  • Rising STARS Award, University of Texas System, 2010
  • AACR-Aflac Scholar-In-Training Award, 2009
  • Excellence in Graduate Research Award, Cleveland Clinic Foundation, 2004

Publications in peer reviewed journals:

  1. Li L, Li W*. Epithelial-mesenchymal transition in human cancer: comprehensive reprogramming of metabolism, epigenetics and differentiation. Pharmacology & Therapeutics (in press) (Invited Review). *corresponding author
  2. Li L, Liu C, Amato RJ, Chang JT, Du G, Li W*. CDKL2 promotes epithelial- mesenchymal transition and breast cancer progression. Oncotarget 2014 Nov 5;5(21):10840-53. *corresponding author
  3. Li W*, Ai N, Wang S, Bhattacharya N, Vrbanac V, Collins M, Signoretti S, Hu Y, Boyce FM, Gravdal K, Halvorsen OJ, Nalwoga H, Akslen LA, Harlow E*, Watnick RS. GRK3 is essential for metastatic cells and promotes prostate tumor progression. Proceedings of the National Academy of Sciences USA (PNAS) 2014 Jan 28;111(4):1521-6.*corresponding author
  4. Baldwin A, Grueneberg DA, Hellner K, Sawyer J, Grace M, Li W, Harlow E, Münger K. V. Synthetic lethal interactions between p53 and the protein kinases SGK2 and PAK3. Proceedings of the National Academy of Sciences USA (PNAS). 2010 Jul 13;107(28):12463-8.
  5. Grueneberg DA*, Li W*, Davies JE and Harlow, E. IV. shRNA screens identify kinase requirements in human cells: differential kinase requirements in cervical and renal human tumor cell lines. Proceedings of the National Academy of Sciences USA (PNAS). 2008 Oct 28;105(43):16490-5. * these authors contributed equally (co-first author)
  6. Bommi-Reddy A, Almeciga I, Sawyer J, Geisen C, Li W, Harlow E, Kaelin WG Jr, rueneberg DA. III. Altered Kinase Requirements in VHL-/- Renal Carcinoma Cells Detected in a Pilot Synthetic Lethal Screen. Proceedings of the National Academy of Sciences USA (PNAS). 2008 Oct 28;105(43):16484-9.
  7. Baldwin A, Li W, Grace M, Harlow E, Münger K and Grueneberg DA. II. Genetic Interaction Screens Identify Alterations in Kinase Requirements Following HPV16 E7 Expression in Cancer Cells. Proceedings of the National Academy of Sciences USA (PNAS). 2008 Oct 28;105(43):16478-83.
  8. Grueneberg DA*, Degot S*, Pearlberg J*, Li W*, Davies JE*, Baldwin A*, Endege W, Doench J, Sawyer J, Hu Y, Boyce F, Xian J, Munger K, Harlow E. I. Comparing Kinase requirements across Various Cell types. Proceedings of the National Academy of Sciences USA (PNAS). 2008 Oct 28;105(43):16472-7. * these authors contributed equally (co-first author)
    Note: These 4 PNAS papers in 2008 were selected as one of Signaling Breakthroughs of 2008 by the annual Editorial Guide of Science Signaling.
  9. Sengupta S, Kim KS, Berk MP, Escobar P, Li W, Lindner DJ, Williams BRG, Xu Y. Lysophosphatidic acid down regulates tissue inhibitor of metalloproteinases (TIMPs), which are negatively involved in LPA-induced cell invasion. Oncogene. 2007 May 3;26(20):2894-901.
  10. Graham K, Li W, Williams B, Fraizer G. VEGF is differentially expressed in WT1-and DDS-LNCaP cells. Gene Expression. 2006;13(1):1-14.
  11. Pearlberg J, Degot S, Endege W, Park J, Davies J, Gelfand E, Sawyer J, Conery A, Doench J, Li W, Gonzalez L, Boyce FM, Brizuela L, Labaer J, Grueneberg D, Harlow E. Screens using RNAi and cDNA expression as surrogates for genetics in mammalian tissue culture cells. Cold Spring Harb Symp Quant Biol. 2005;70:449-59.
  12. Li W, Kessler P, Yeger H, Alami J, Reeve AE, Heathcott R, Skeen J, Williams BRG. A gene expression signature for relapse in primary Wilms tumor. Cancer Research. 2005 Apr 1; 65(7):2592-601.
  13. Li W, Kessler P, Williams BRG. Transcript profiling of Wilms tumors reveals systematic connections to kidney morphogenesis and a gene expression pattern associated with unfavorable histology.Oncogene. 2005 Jan 13; 24(3):457-68.
  14. Stanhope-Baker P, Kessler P, Li W, Williams BRG. The WT1 target gene Podocalyxin is transcriptionally repressed by p53. J Biol Chem. 2004 Aug 6;279(32):33575-85.

Wenliang Li, Ph.D.

Assistant Professor
The Brown Foundation Institute of Molecular Medicine
The University of Texas Health Science Center at Houston
Texas Therapeutics Institute, SRB 537C
1825 Pressler Street
Houston, TX 77030