Thomas M Bodenstine, Ph.D.

Associate Professor
Downers Grove, IL

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My laboratory focuses on the connections between cancer cell metabolism and regulation of gap junction communication. Gap junctions are regulated plasma membrane channels mediated by the connexin family of proteins. During early stages of cancer progression, gap junction communication is frequently lost due to decreased expression of connexin proteins or changes to subcellular transport. Loss of gap junction activity has been causatively linked to numerous cancer cell functions. However, this communication is dynamically regulated in cancer cells and can also be increased, particularly during the process of metastasis. This affects qualities including cellular invasion and adaptation to secondary metastatic sites. Additionally, changes to cancer cell energy utilization drive metabolic adaptability and induce therapeutic resistance. The goals of our laboratory are to understand the connections between metabolic pathways and regulation of connexin proteins which affect gap junction activity in the context of cancer.

Associate Professor

Downers Grove, IL

College of Pharmacy
Downers Grove Campus
College of Graduate Studies - IL
College of Health Sciences - IL

Biochemistry and Molecular Genetics

Biomedical Sciences (M.A.)
Biomedical Sciences (M.B.S.)
Dental Medicine
Master of Science in Precision Medicine
Osteopathic Medicine
Physical Therapy
Physician Assistant Studies
Post-Graduate Certificate in Precision Medicine


University of Alabama at Birmingham | 2010 | Ph.D.
Pennsylvania State University | 2004 | B.S.

Courses Taught

BIOCD 1556: Biochemistry I, Pharmacy

BIOCD 0551: Human Biochemistry, Physician Assistant

BIOCD 1553: Cell and Tissue Structure and Function, Physical Therapy (Course Director)

PM 501: Introduction to Genetics and Genomics, Precision Medicine

PM 502: Genomics of Rare and Complex Diseases, Precision Medicine

BIOCD 0511/0561/1557: Biochemistry I/II, Pharmacy, Biomedical Sciences

IBSSD 1520: Molecular, Cellular and Tissue Structure and Function, Dental

BIOCD 1501: Human Clinical Biochemistry and Metabolism, Medical

BIOCD 0521/0571: Biochemistry II, Biomedical Sciences

BIOCD 0530/0580/0581: Human Genetics, Physician Assistant, Biomedical Sciences

IBSSD 1535: Gastrointestinal System, Dental

BIOCD 1590: Biochemistry for Optometry Students, Optometry


Gap junctions are regulated intercellular pores formed by the connexin family of proteins that allow for passage of ions, signaling molecules and nutrients between epithelial cells. Proper regulation of gap junction communication contributes to cellular homeostasis and tissue function.

During cancer development, the normal roles of connexins are often dysregulated. Expression of connexin genes may be lost or connexin protein function may be altered. Collectively, these changes can affect how cancer cells function and respond to therapy. Interestingly, gap junction communication can be restored within metastatic tumor cells by modulation of signaling pathways without the need for exogenous expression of connexin genes.

The focus of my laboratory aims to understand the pathway alterations that lead to changes in connexin function during breast cancer progression, and how this information may be used from a therapeutic standpoint.


Research Manuscripts

Jones JC, Miceli AM, Chaudhry MM, Kaunitz CS, Jai MA, Pancho RN, Lazzar A, Taylor BS, Bodempudi V, Jain PP, Hanjra S, Urban AE, Zanotti B, Kohlmeir EK, Bodenstine TM. Glucose-limiting conditions induce an invasive population of MDA-MB-231 breast cancer cells with increased connexin 43 expression and membrane localization. Journal of Cell Communication and Signaling 2021; 15(2):223-36

Bodenstine TM, Chandler GS, Reed DW, Margaryan NV, Gilgur A, Atkinson J, Ahmed N, Hyser M, Seftor EA, Strizzi L, Hendrix MJ. Nodal expression in triple-negative breast cancer: cellular effects of its inhibition following doxorubicin treatment. Cell Cycle 2016; 15(9):1295-302

Strizzi L, Sandomenico A, Margaryan NV, Focà A, Sanguigno L, Bodenstine TM, Chandler GS, Reed DW, Gilgur A, Seftor EA, Seftor RE, Khalkhali-Ellis Z, Leonardi A, Ruvo M, Hendrix MJ. Effects of a novel Nodal-targeting monoclonal antibody in melanoma. Oncotarget 2015; 6(33):34071-86

Khalkhali-Ellis Z, Kirschmann DA, Seftor EA, Gilgur A, Bodenstine TM, Hinck AP, Hendrix MJ. Divergence(s) in nodal signaling between aggressive melanoma and embryonic stem cells. International Journal of Cancer 2015; 136:E242-E251

Bodenstine TM, Seftor RE, Seftor EA, Khalkhali-Ellis Z, Samii NA, Monarrez JC, Chandler GS, Pemberton PA, Hendrix MJ. Internalization by multiple endocytic pathways and lysosomal processing impact Maspin-based therapeutics. Molecular Cancer Research 2014; 12:1480-1891

Bodenstine TM, Vaidya KS, Ismail A, Beck BH, Diers AR, Edmonds MD, Kirsammer GT, Landar A, Welch DR. Subsets of ATP-sensitive potassium channel (KATP) inhibitors increase gap junctional intercellular communication in metastatic cancer cell lines independent of SUR expression. FEBS Letters 2012; 586(1): 27-31

Bodenstine TM, Beck BH, Cao X, Cook LM, Ismail A, Powers JK, Mastro AM, Welch DR. MC3T3-E1 promote breast cancer growth in bone in a murine xenograft model. Chinese Journal of Cancer 2011; 30(3): 189-96

Bodenstine TM, Vaidya KS, Ismail A, Beck BH, Cook LM, Diers AR, Landar A, Welch DR. Homotypic gap junctional communication associated with metastasis suppression increases with PKA activity and is unaffected by PI3K inhibition. Cancer Research 2010; 70(23): 10002-10011

Diers AR, Dranka BP, Ricart KC, Oh JY, Johnson MS, Zhou F, Pallero MA, Bodenstine TM, Murphy-Ullrich JE, Welch DR, Landar A. Modulation of mammary cancer cell migration by 15-deoxy-Δ12,14-prostaglandin J2: implications for anti-metastatic therapy. Biochemical Journal 2010; 430(1):69-78

Frolova N, Edmonds MD, Bodenstine TM, Seitz R, Johnson MR, Feng R, Accavitti-Loper MA, Welch DR, Frost AR. A shift from nuclear to cytoplasmic breast cancer metastasis suppressor 1 expression is associated with highly proliferative estrogen receptor-negative breast cancers. Tumor Biology 2009; 30:148-159

Kim M, Bodenstine TM, Sumerel LA, Rivera AA, Baker AH and Douglas JT. Tissue inhibitor of metalloproteinases-2 improves antitumor efficacy of a replicating adenovirus in vivo. Cancer Biology and Therapy 2006; 5:12, 1647-1653


Review Articles

Jones JC, Bodenstine TM. Connexins and Glucose Metabolism in Cancer. International Journal of Molecular Sciences 2022; 23(17):10172

Bodenstine TM, Chandler GS, Seftor RE, Seftor EA, Hendrix MJ. Plasticity underlies tumor progression: Role of Nodal in Cancer. Cancer and Metastasis Reviews 2016; 35(1):21-39

Bodenstine TM, Seftor RE, Khalkhali-Ellis Z, Seftor EA, Pemberton PA, Hendrix MJ. Maspin: molecular mechanisms and therapeutic implications. Cancer and Metastasis Reviews 2012; 31: 529-551

Bodenstine TM, Welch DR. Metastasis suppressors and the tumor microenvironment. Cancer Microenvironment 2008; 1:1-11


Book Chapters

Kristjansdottir K, Bodenstine TM, Noronha S. Chapter: Neoplasia. Advanced Physiology and Pathophysiology: Essentials for Clinical Practice. 2020; 215-240

Strizzi L, Hardy KM, Bodenstine TM, Hendrix JC. Targeting tumor cell plasticity. Stem Cells Handbook, Second Edition, Humana Press Inc. 2013; 441-448


Educational Manuscripts

Verdone M, Joshi MD, Bodenstine TM, Green JM, Lynch SM, Gettig JP, Fjortoft N. Impact of an online, self-directed pre-pharmacy bridging course on students’ academic performance. American Journal of Pharmaceutical Education 2020; ajpe7864


American Association for Cancer Research (AACR)

Metastasis Research Society (MRS)