Michelle C. Mendoza, PhD
- Cancer Biology
- Cell Signaling
- Cell Migration
- Actin Cytoskeleton Dynamics
- Departments: Oncological Sciences - Assistant Professor
Academic Office Information
Huntsman Cancer Hospital
1950 Circle of Hope, Room: 5344
Salt Lake City, UT 84112
My research in the Department of Oncological Sciences and Huntsman Cancer Institute is aimed at understanding the mechanical and chemical signals that control cell migration and cancer dissemination. We want to understand how oncogenic mutations in tumor cells cause changes in the extracellular matrix environment, and how cancer cells adapt to their altered signaling and environment to elicit the physical process of movement. Current work focuses on the RAS/ERK pathway, a key driver of progression and resistance in solid tumors. We study how the pathway signals, at the molecular level and with spatio-temporal precision, in model epithelial cells and organotypic cultures. Our fundamental findings on cell migration and cancer invasion support molecular targeting efforts to block invasion and improve long-term care.
Cancer spread, or metastasis, involves improper cell movement. My research focuses on determining - at the mechanistic level - how a cell normally regulates the processes of cell movement and how this goes awry during cancer dissemination.
Biography: Dr. Mendoza received her B.S. (Highest Honors) in Animal Bioscience from Pennsylvania State University in University Park, Pennsylvania in 2000. She conducted her graduate work at the University of California, San Diego with Dr. Richard A. Firtel, studying signal transduction and cell migration using the model organism Dictyostelium. She received her PhD in Biomedical Science from UCSD in 2005. She carried out postdoctoral training with cancer cell signaling expert Dr. John Blenis (funding from Susan G. Komen) and computer vision pioneer Dr. Gaudenz Danuser (K01 funding from the NCI) in the Department of Cell Biology at Harvard Medical School. She studied the molecular signals that control the actin cytoskeleton during cell movement. In 2013, Dr. Mendoza started her independent research program at the University of California, San Francisco, in the Department of Cell and Tissue Biology. In 2015, Dr. Mendoza moved her lab to join the faculty of the Department of Oncological Sciences, within the University of Utah, School of Medicine and the Huntsman Cancer Institute. She is currently Assistant Professor in Oncological Sciences. She is a member of the Cell Response and Regulation Program and the Upper Aerodigestive Tract DOT.
Research: The Mendoza lab strives to understand the molecular signals that control cell movement, with an emphasis on the RAS/ERK pathway and cancer. The lab utilizes biochemistry and quantitative imaging to address: 1) cytoskeletal dynamics during motility: How do signaling pathways contribute to the coordinated assembly and disassembly of actin and adhesion complexes during cell migration, and how is this spatiotemporal coordination altered in cancer when the signals are hyperactivated? 2) cell invasion: Does RAS/ERK signaling enable the morphological changes necessary for cell invasion through 3D collagen environments? 3) cancer progression: Are cell division and survival signals, such as oncogenic activation of RAS and RAF, important for cancer dissemination and progression and what are the key, targetable, effectors?
Current Administrative Positions: Member, University of Utah and Satellite Huntsman Cancer Institute Microscopy Cores. Member, Huntsman Cancer Institute Cancer Training and Innovation Committee.
Teaching: Dr. Mendoza teaches in the Cell Biology core course for the first year Molecular Biology graduate students and in the Department of Oncological Sciences Cancer Biology and Cancer Training 360 courses. She is mentoring 2 PhD students and 2 postdoctoral fellows.
Service: Dr. Mendoza is an ad hoc reviewer for multiple peer-reviewed scientific journals, including Science Signaling, the Journal of Cell Biology, and Oncogene.
|Postdoctoral Fellowship||Harvard Medical School
Department of Cell Biology
|Doctoral Training||University of California, San Diego
|Undergraduate||Pennsylvania State University
- Samson SC, Elliott A, Mueller BD, Kim Y, Carney KR, Bergman JP, Blenis J, Mendoza MC (2019). p90 ribosomal S6 kinase (RSK) phosphorylates myosin phosphatase and thereby controls edge dynamics during cell migration. J Biol Chem, 294(28), 10846-10862.
- Kircher DA, Trombetti KA, Silvis MR, Parkman GL, Fischer GM, Angel SN, Stehn CM, Strain SC, Grossmann AH, Duffy KL, Boucher KM, McMahon M, Davies MA, Mendoza MC, VanBrocklin MW, Holmen SL (2019). AKT1E17K Activates Focal Adhesion Kinase and Promotes Melanoma Brain Metastasis. (Epub ahead of print) Mol Cancer Res.
- Er EE, Mendoza MC, Mackey AM, Rameh LE, Blenis J (2013). AKT facilitates EGFR trafficking and degradation by phosphorylating and activating PIKfyve. Sci Signal, 6(279), ra45.
- Mendoza MC, Besson S, Danuser G (2012). Quantitative fluorescent speckle microscopy (QFSM) to measure actin dynamics. Curr Protoc Cytom, Chapter 2, Unit2.18.
- Zhang W, Mendoza MC, Pei X, Ilter D, Mahoney SJ, Zhang Y, Ma D, Blenis J, Wang Y (2012). Down-regulation of CMTM8 induces epithelial-to-mesenchymal transition-like changes via c-MET/extracellular signal-regulated kinase (ERK) signaling. J Biol Chem, 287(15), 11850-8.
- Mendoza MC, Er EE, Blenis J (2011). The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation. Trends Biochem Sci, 36(6), 320-8.
- Mendoza MC, Er EE, Zhang W, Ballif BA, Elliott HL, Danuser G, Blenis J (2011). ERK-MAPK drives lamellipodia protrusion by activating the WAVE2 regulatory complex. Mol Cell, 41(6), 661-71.
- Mendoza MC, Er EE, Blenis J (2010). ERK-MAP Kinase signaling in the cytoplasm. 661, 185-203.
- Abe Y, Yoon SO, Kubota K, Mendoza MC, Gygi SP, Blenis J (2009). p90 ribosomal S6 kinase and p70 ribosomal S6 kinase link phosphorylation of the eukaryotic chaperonin containing TCP-1 to growth factor, insulin, and nutrient signaling. J Biol Chem, 284(22), 14939-48.
- Mendoza MC (2013). Phosphoregulation of the WAVE regulatory complex and signal integration. [Review]. Semin Cell Dev Biol, 24(4), 272-9.
- Mendoza MC, Er EE, Blenis J (2011). The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation. [Review]. Trends Biochem Sci, 36(6), 320-8.