Extracellular Matrix Topography Drives Adrenergic to Mesenchymal Transition in Neuroblastoma

A Antonios Chronopoulos (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) C Chandra Kaladhar Vemula (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) V Vic Zamloot (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) I Ivan Chavez (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) R Rebekah Kennedy (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) W Woochan Kim (Department of Convergence Biosystems Engineering Chonnam National University Gwangju Republic of Korea) D Devon Bell (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) Y Yuanzhong Pan (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) B Babak Moghimi (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) J Jangho Kim (Department of Convergence Biosystems Engineering Chonnam National University Gwangju Republic of Korea) S Shahab Asgharzadeh (Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA) J Jinseok Park (Department of Immunology)

Abstract

Abstract Neuroblastoma (NB), the most common extracranial solid tumor in children, exhibits intra‐tumoral heterogeneity with two interconvertible identities: adrenergic (ADRN) and mesenchymal (MES). Compared to ADRN cells, MES cells exhibit phenotypes associated with metastasis and therapy resistance. Thus, the transition from ADRN to MES may contribute to poor clinical outcomes, necessitating further investigation into this ADRN‐to‐MES transition (AMT) to improve clinical responses. The extracellular matrix (ECM), a critical component of the tumor microenvironment (TME), provides structural support and delivers mechanical signals that influence oncogenic processes. This research demonstrates that high‐risk NB tumors contain more topographically aligned ECM fibers than low‐risk NB tumors. Using nano‐fabricated biomaterials designed to mimic the aligned ECM, ECM topography is revealed to drive AMT through transcriptional and epigenetic changes, accompanied by enhanced MES phenotypic features. Furthermore, ECM topography is shown to stimulate Rho‐associated kinase and YAP signaling pathways, which mediate ECM‐driven reprogramming. These findings introduce ECM‐driven AMT as a novel mechanism in NB progression and provide insights into TME‐targeted therapeutic strategies aimed at suppressing MES cells to improve clinical outcomes in NB.

Article Details

Volume / Issue Vol. 37, Issue 37
Published September 01, 2025
ISSN 0935-9648
Publisher Unknown Publisher

Journal Info

Advanced Materials

Unknown Publisher

ISSN: 0935-9648 Physical Sciences

Authors (12)

A

Antonios Chronopoulos

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

C

Chandra Kaladhar Vemula

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

V

Vic Zamloot

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

I

Ivan Chavez

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

R

Rebekah Kennedy

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

W

Woochan Kim

Department of Convergence Biosystems Engineering Chonnam National University Gwangju Republic of Korea

D

Devon Bell

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

Y

Yuanzhong Pan

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

B

Babak Moghimi

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

J

Jangho Kim

Department of Convergence Biosystems Engineering Chonnam National University Gwangju Republic of Korea

S

Shahab Asgharzadeh

Cancer and Blood Disease Institute Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles California 90027 USA

J

Jinseok Park

Department of Immunology