# Sulforaphane as a Multi-Scale Mechano-Modulator in Cancer: An Integrative Perspective

**Authors:** Xin Zhang, Lili Cheng, Yifan Han, Tailin Chen, Xinbin Zhao

PMC · DOI: 10.3390/biology15020167 · Biology · 2026-01-17

## TL;DR

This paper explores how sulforaphane, a compound from broccoli, may fight cancer by altering the physical environment of tumors.

## Contribution

The paper introduces sulforaphane as a 'mechano-modulator' that disrupts cancer progression through biomechanical effects.

## Key findings

- Sulforaphane targets force-sensitive pathways like YAP/TEAD and Rho/ROCK to disrupt cancer cell invasion.
- It destabilizes structures like the cytoskeleton and invadopodia that cancer cells use to spread.
- Sulforaphane promotes extracellular matrix remodeling, altering the tumor's physical environment.

## Abstract

Scientists are discovering that a tumor’s physical stiffness and pressure help it grow and spread. This review looks at a natural compound from broccoli, called sulforaphane, through this new “biomechanical” lens. We suggest sulforaphane works as a “mechano-modulator”—it fights cancer not just chemically, but by helping to normalize the tumor’s distorted physical environment. By disrupting the forces and structures cancer cells use to invade, its wide range of effects can be seen as part of a single, powerful strategy. This fresh perspective could guide the development of sulforaphane as a novel, mechanics-informed approach for cancer prevention and treatment.

Cancer progression is driven not only by biochemical signals but also by abnormal physical forces within a stiffened tumor microenvironment. This review re-examines the anticancer compound sulforaphane (SFN) through the integrative lens of tumor biomechanics. We propose SFN functions as a “mechano-modulator,” whose pleiotropic effects converge to disrupt pro-invasive mechanotransduction. SFN targets key force-sensitive pathways (e.g., YAP/TEAD, Rho/ROCK), destabilizes invasion machinery (cytoskeleton, invadopodia), and promotes tissue-level changes such as extracellular matrix remodeling. While preclinical evidence for this mechano-modulatory role is compelling, this perspective also highlights the critical need for clinical validation and discusses the key translational challenges. By systematically linking SFN’s molecular actions to the biophysics of tumor progression, this synthesis provides a novel framework for understanding its efficacy and outlines a rational path for its future development as a mechano-inspired therapeutic.

## Linked entities

- **Genes:** YAP1 (Yes1 associated transcriptional regulator) [NCBI Gene 10413], sd (scalloped) [NCBI Gene 32536], RHO (rhodopsin) [NCBI Gene 6010], ROCK (Rho kinase) [NCBI Gene 579202]
- **Chemicals:** sulforaphane (PubChem CID 5350)
- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** YAP1 (Yes1 associated transcriptional regulator) [NCBI Gene 10413] {aka COB1, YAP, YAP-1, YAP2, YAP65, YKI}, RHO (rhodopsin) [NCBI Gene 6010] {aka CSNBAD1, OPN2, RP4}
- **Diseases:** Cancer (MESH:D009369)
- **Chemicals:** SFN (MESH:C016766)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12838123/full.md

## References

97 references — full list in the complete paper: https://tomesphere.com/paper/PMC12838123/full.md

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Source: https://tomesphere.com/paper/PMC12838123