Michael Wendt

Michael Wendt Profile Picture

Associate Professor
Ph.D., Medical College of Wisconsin (2007)

Contact Info:

(765) 494-0860
Lab website: wendtlab.com

Training Group(s):
Cancer Biology

Active Mentor - currently hosting PULSe students for laboratory rotations and recruiting PULSe students into the laboratory; serves on preliminary exam committees

Current Research Interests:

Research in the Wendt lab focuses on pharmacological targeting of molecular players involved in the metastatic outgrowth of breast cancer. Systemic dissemination is an extremely early event in breast cancer progression, therefore we primarily focus on developing strategies that are specifically designed to target secondary tumors. We take two major approaches to this challenge: 1.Through metastatic progression breast cancer cells under epithelial-mesenchymal transition (EMT) and reverse process of mesenchymal-epithelial transition (MET). An overriding hypothesis in the lab is that through the processes of EMT:MET the secondary epithelial state that characterizes the metastatic tumor is fundamentally unique from the epithelial status of the primary tumors. We believe these differences hold the keys to developing therapeutics capable to pharmacologically treating metastatic lesions. 2.Subsequent to dissemination, a large fraction of tumor cells enter into an asymptomatic state of dormancy. The ability of normal organs to resist secondary tumor formation is the body’s last defense against metastatic disease progression. The environmental factors (drugs, alcohol, diet, etc…) capable of “awaking” disseminated cells are poorly characterized. Understanding these factors is required if we hope to design therapeutics capable of maintaining systemic tumor dormancy. We use a combination of molecular, biochemical, cell biological and whole animal studies to evaluate the impact of anticancer therapies on EMT and metastatic progression. Specifically, we utilize a variety of 3D and multicellular colculture models to evaluate growth factor signaling, pharmacological response to anti-cancer drugs, and as a platform for genetic and compound screening assays. In addition to these in vitro approaches we have developed novel in vivo mouse models of metastasis and drug resistance. We utilize these models in combination with bioluminesent imaging as a robust approach to locate and quantify metastatic progression.

Selected Publications:

  1. Shinde A, Hardy SD, Kim D, Salehin Akhand S, Jolly MK, Wang W, Anderson JC, Khodadadi RB, Brown WS, George JT , Liu S, Wan J, Levine H, Willey CD, Krusemark CJ, Geahlen RL, Wendt MK. Spleen tyrosine kinase-mediated autophagy is required for epithelial-mesenchymal plasticity and breast cancer metastasis. Cancer Research, 2019 Apr 15;79(8):1831-1843. Comment on article: Lulling the Cancer Cell into an Eternal Sleep. Cancer Research. 2019 Apr 15;79(8):1756-1757
  2. Ali R, Brown W, Purdy SC, Davisson VJ, Wendt MK. Biased signalling downstream of epidermal growth factor receptor regulates proliferative versus apoptotic response to ligand. Cell Death and Disease; 9: 976 (2018).
  3. Shinde A, Alpsoy A, Abdullah A, Schaber J, Solorio L, Wendt MK. Autocrine fibronectin inhibits breast cancer metastasis. Molecular Cancer Research, 2018 Oct;16(10):1579-1589. Epub 2018 Jun 22
  4. Shinde A, Wilmanski T, Chen H, Teegarden D, Wendt MK. Pyruvate carboxylase supports the pulmonary tropism of metastatic breast cancer. Breast Cancer Research. 2018. 20:76.
  5. Hardy S, Shinde A, Wang WH, Wendt MK†, Geahlen R†. Regulation of epithelial-mesenchymal transition and metastasis by TGF-beta, P-bodies, and autophagy. Oncotarget, DOI:10.18632/oncotarget.21871. Epub Oct 17 2017
  6. Brown WS, Akhand SS, Wendt MK. FGFR signaling maintains a drug persistent state following induction of epithelial-mesenchymal transition. Oncotarget. DOI: 10.18632/oncotarget.13117. Epub Nov 4 2016.
  7. Brown WS, Tan L, Smith A, Gray NS, Wendt MK. Covalent targeting of fibroblast growth factor receptor inhibits metastatic breast cancer. Molecular Cancer Therapeutics. Sep;15(9):2096-106. Epub July 1 2016.
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