Update Your ProfileAcademic Title:
Assistant Professor
Primary Appointment:
Pharmacology & Physiology
Location:
BRB 10-029
Phone (Primary):
410-706-3331
Education and Training
I completed my undergraduate work at Franklin and Marshall College in 1995, obtained my M.S. in 1999 and my Ph.D. in 2004 from University of Maryland Baltimore. I began my postdoctoral training in the laboratory of Dr. Kurtis Bachman where I learned powerful genetic techniques to develop a novel in vitro isogenic cell system for examining PTEN deficiency on cell signaling. I continued my postdoctoral training in the laboratory of Dr. Stuart Martin where I examined the role of PTEN loss in the formation of microtentacles (McTNs) and the ability of cancer cells to metastasize. Currently, I am an Assistant Professor in the Pharmacology Department at the University of Maryland School of Medicine and a member of the University of Maryland Greenebaum NCI Comprehensive Cancer Center. My research focuses on elucidating aberrant cell signaling and cytoskeletal regulation in migratory metastatic cells and circulating tumor cells (CTCs). My goal is to improve the understanding of how biochemical signals and environmental cues modulate cytoskeletal alterations to provide new insight for future development of pharmacologic approaches for inhibiting metastasis by chemically targeting cytoskeletal structures that regulate cell stiffness and deformability.
Highlighted Publications
- Mull, M.L., Pratt, S.J.P., Thompson, K.N., Annis, D.A., Gad, A.A., Lee, R.M., Chang, K.T., Stemberger, M.B., Ju, J.A., Gilchrist, D.E., Boyman, L., Lederer, W.J., Vitolo, M.I.* and Martin*, S.S. (2025) Disruption of P2Y2 signaling promotes breast tumor cell dissemination by reducing ATP-dependent calcium elevation and actin localization to cell junctions. (*co-corresponding author) Int J Mol Sci. May 1;26(9):4286. PMC12071985
- Ju, J.A., Thompson, K.N., Annis, D.A., Mull, M.L., Gilchrist, D.E., Moriarty, A., Chang, K.T., Stemberger, M.B., Noto, M.J., Vitolo, M.I.* and Martin, S.S.* (2025) Tubulin-based microtentacles aid in heterotypic neutrophil-tumor cell clustering in breast cancer. (*co-corresponding author) Sci. Feb;12(6):e2409260. PMC11809343
- Chang, K.T., Thompson, K.N., Pratt, S.J.P., Ju, J.A., Lee, R.M., Mathias, T.J., Mull, M.L., Annis, D.A., Ory, E.C., Stemberger, M.B., Vitolo, M.I.* and Martin, S.S.* (2023) Elevation of Cytoplasmic Calcium Suppresses Microtentacle Formation and Function in Breast Tumor Cells. (*co-corresponding author) Cancers. Jan 31;15(3):884. PMC9913253
- Mathias T.J., Ju J.A., Lee R.M., Thompson K.N., Mull, M.L., Annis, D.A., Chang, K.T., Ory, E.C., Stemberger, M.B., Hotta, T., Ohi, R., Vitolo, M.I., Moutin, M. and Martin, S.S. (2022) Tubulin Carboxypeptidase Activity Promotes Focal Gelatin Degradation in Breast Tumor Cells and Induces Apoptosis in Breast Epithelial Cells That Is Overcome by Oncogenic Signaling. Cancers (Basel). Mar 28;14(7):1707. PMC8996877
- Thompson, K.N., Ju, J.A., Ory, E.C., Lee, R.M., Pratt, S.J.P., Mathias, T.J., Lee, C.J., Goloubeva, O.G., Bailey, P.C., Charkrabarti, K.R., Jewell, C.M., Vitolo, M.I.*, and Martin, S.S * (2022) Microtubule disruption reduces metastasis more effectively than primary tumor growth. (*co-corresponding author) Breast Cancer Res. Feb 14;24(1):13. PMC8842877
Research Interests
My research focuses on deciphering how microtubule (MT) posttranslational modifications (PTMs), particularly glutamylation, drive the metastatic progression of breast cancer. While MT-targeting chemotherapeutics like taxanes have achieved some clinical success, their utility remains limited by toxicity, modest efficacy, and the evolution of drug resistance. A growing body of evidence demonstrates that specific MT PTMs—such as detyrosination and acetylation—promote cancer aggressiveness, yet the precise contribution of MT glutamylation, wherein one or more glutamate residues are enzymatically added to tubulin, remains largely unexplored.
Recent findings show that MT glutamylation is upregulated in patient tumors alongside biomechanical stiffening of the tumor microenvironment, a hallmark of advanced and invasive disease. Our laboratory’s functional data further reveal that enhancing MT glutamylation, especially through the upregulation of the tubulin glutamylase TTLL11, increases breast cancer cell migration, invasion, microtentacle formation, and spontaneous lung metastasis in mouse models, without affecting proliferation.
Our ongoing work aims to: elucidate how MT glutamylation regulates migration and invasion using advanced live-cell imaging and machine learning; define its role in circulating tumor cell behaviors and metastatic seeding; and mechanistically dissect how TTLL11-driven glutamylation is coupled to glutamine metabolism. By focusing on the subset of glutamylated MTs that specifically support metastasis, my research seeks to develop more precise and tolerable strategies to impede cancer dissemination, with the ultimate goal of closing the critical gap between our understanding of MT biology and the need for effective anti-metastatic therapies.
Grants and Contracts
NCI Mentored Scientist Research Award (K01 NCI/NIH, 4/13-3/18)
PTEN loss increases efficiency of breast tumor metastasis
American Cancer Society Research Scholar Grant (7/18-6/22)
Targeting cytoskeletal aberrations to prevent breast cancer metastasis