Teton™ CytoProfiling, Drug-induced liver injury (HepG2 cells)

Background

Drug-induced liver injury (DILI) is a major barrier in drug development and a leading cause of acute liver failure. To better understand hepatotoxic mechanisms, HepG2 cells were exposed to four well-characterized hepatotoxins for 24-hours: acetaminophen, diclofenac, tunicamycin, and amiodarone, along with positive and negative controls. Learn more about this study in our data spotlight.

Methods

Using the Teton Immuno Panel Kit and three 24-plex protein Teton Focus Panels (Cell Metabolism, Cell Stress & Apoptosis, and Innate Immunity​), we simultaneously measured 343 RNA, 122 protein and phospho-protein, and 6 cell paint markers across approximately 70,000 single cells with subcellular spatial resolution. Protocol details can be found in the Teton CytoProfiling User Guide.

Results

Multiomic integration revealed both shared and compound-specific signatures of hepatotoxicity, including mitochondrial stress, inflammatory signaling, and cell cycle dysregulation. Acetaminophen uniquely promoted a proliferative response, while diclofenac, tunicamycin, and amiodarone suppressed proliferation and induced stress pathways. This multidimensional approach demonstrates the power of high-content, single-cell profiling to dissect mechanisms of DILI and identify pathways for biomarker discovery.