Shile Huang, Ph.D.

Associate Professor


Contact Information:

Email:shuan1@lsuhsc.edu
Office Phone: 318-675-7759
Laboratory Phone: 318-675-7793 or 318-675-8399
Office Fax: 318-675-5180

Education/Training:

B.S. (D.V.M.), 1984, Anhui Agricultural University, Hefei, China
M.S., 1987, Nanjing Agricultural University, Nanjing, China
Ph.D., 1997, University of Salzburg, Salzburg, Austria

Major Research Interests: 

Dr. Huang's major research interests include cell signaling and tumorigenesis.

The laboratory is primarily interested in studying mTOR signaling in tumorigenesis and metastasis. mTOR functions as two complexes, mTORC1 and mTORC2, and regulates cell proliferation, growth (cell size), and survival. Recently, we have demonstrated that mTOR also regulates cell motility. Disruption of mTORC1 or mTORC2 by silencing the expression of raptor or rictor down-regulates cell motility, implicating critical roles of mTORC1 and mTORC2 in this cellular process. We are focusing on identifying the molecular mechanisms by which mTORC1 and mTORC2 regulate cell motility. In addition, the laboratory is investigating anticancer mechanisms of small molecules such as curcumin, cryptotanshinone, artemisinin, and ciclopirox olamine. Curcumin, cryptotanshinone, and artemisinin are natural products isolated from the plants Curcuma longa, Salvia miltiorrhiza, and Artemisia annua, respectively, whereas ciclopirox olamine is an off-patent synthetic fungicide. Notably, curcumin, artesunate (a water-soluble artemisinin derivative), and ciclopirox olamine are undergoing initial clinical trials as novel anticancer agents. However, the anticancer mechanisms of these compounds remain to be elucidated. Our recent studies indicate that they may execute their anticancer activities by inhibiting cell proliferation, inducing cell death, suppressing cell motility, or inhibiting angiogenesis/lymphangiogenesis. We are elucidating the molecular mechanisms underlying these effects.

Representative Publications:

  1. SKLB188 inhibits the growth of head and neck squamous cell carcinoma by suppressing EGFR signalling.
  2. Ciclopirox activates ATR-Chk1 signaling pathway leading to Cdc25A protein degradation.
  3. Dihydroartemisinin inhibits the mammalian target of rapamycin-mediated signaling pathways in tumor cells.
  4. Curcumin disrupts the Mammalian target of rapamycin-raptor complex.
  5. Rapamycin inhibits F-actin reorganization and phosphorylation of focal adhesion proteins.

All Publications: PubMed