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Related Experiment Video

Updated: May 20, 2025

A Biomimetic Model for Liver Cancer to Study Tumor-Stroma Interactions in a 3D Environment with Tunable Bio-Physical Properties

A Biomimetic Model for Liver Cancer to Study Tumor-Stroma Interactions in a 3D Environment with Tunable Bio-Physical Properties

Published on: August 7, 2020

Adaptation to Volumetric Compression Drives an Apoptosis-Resistant and Invasive Phenotype in Liver Cancer.

Xiangyu Gong^1,2, Noriyoshi Ogino^3,4, M Fátima Leite⁵

¹Department of Pharmacological Sciences, Renaissance School of Medicine, Stony Brook University, Stony Brook, New York.

Cancer Research

|May 19, 2025

Summary

Prolonged compression in liver cancer induces adaptive cell changes, promoting invasion and survival. Counteracting these effects via Rac1 inhibition or calcium modulation can trigger cancer cell death.

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Area of Science:

Biophysics
Cancer Biology
Cellular Mechanics

Background:

Physical forces like compression significantly impact cancer cell behavior.
Liver cancer involves dense tumor matrices, leading to substantial cell compression.
Understanding the mechanical microenvironment's role in liver cancer is crucial.

Purpose of the Study:

To investigate the adaptive responses of liver cells to prolonged compression.
To elucidate the molecular mechanisms underlying compression-induced cell state transitions.

Main Methods:

Transcriptomic analysis to identify gene expression changes.
Biochemical assays to measure Rac1 activity and YAP localization.
Intracellular calcium signaling analysis.
Inhibition of Rac1 and manipulation of calcium signaling to assess cell viability.

Main Results:

Compression caused liver cells to lose specific markers and gain epithelial-to-mesenchymal transition (EMT) gene signatures.
Elevated Rac1 activity under compression promoted cell protrusions, YAP nuclear translocation, and survival.
Compression disrupted calcium signaling, conferring resistance to apoptosis.
Inhibiting Rac1 or altering calcium levels induced death in adapted liver cancer cells.

Conclusions:

Compression acts as a critical biophysical signal in the liver microenvironment.
This signal drives adaptive cell state transitions and promotes aggressive phenotypes in liver cancer.
Targeting Rac1 or calcium signaling offers potential therapeutic strategies against compression-adapted liver cancer.