Brock Humphries, PHD

The Humphries lab studies cell signaling in tumor recurrence and metastasis. We use our expertise in cell biology and molecular imaging to uncover the mechanisms that contribute to cancer cell heterogeneity, including mitochondrial morphology, cell metabolism, and interactions with the extracellular matrix. Ultimately, we aim to utilize the new information we find out about these processes and transition them into targeted therapies for cancer. Please explore our website for more information.

1. Mitochondria and Cellular Metabolism
Tumor-initiating cells (TICs, also known as cancer stem cells (CSCs)) are a major contributor to breast tumor heterogeneity, leading to breast cancer initiation, progression, metastasis, and recurrence. Our current understanding of mechanisms that establish and maintain TIC physiology is incompletely defined. However, we have previously shown that phosphatidylserine decarboxylase (PISD) is a novel regulator of TICs by regulating multiple facets of mitochondrial morphology, physiology, and cellular metabolism, underlining mitochondrial functions as critical drivers of TICs. Therefore, this project aims to understand mitochondria as central regulators of TIC and breast cancer physiology.

2. Interactions with the Extracellular Matrix
The behavior of cancer cells is directly influenced by the extracellular matrix (ECM), which provides both mechanical and biochemical cues to the cell. These cues activate intracellular signaling networks that drive metabolic reprogramming, survival, proliferation and motility. We have previously shown that biochemical cues, such as chemokines and chemotherapeutics, greatly influences key signaling molecules in breast cancer cells, contributing to overall cellular heterogeneity. Therefore, this project aims to understand ECM-dependent mechanisms linking signaling heterogeneity and metabolic reprogramming to differences in breast tumor initiation, progression, and treatment.