Search research articles

Search research articles

Home
An Integrin Alpha(v)beta(3)-c-src Oncogenic Unit Promotes Anchorage-independence And Tumor Progression.

Home
An Integrin Alpha(v)beta(3)-c-src Oncogenic Unit Promotes Anchorage-independence And Tumor Progression.

Related Concept Videos

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Experiment Videos

An integrin alpha(v)beta(3)-c-Src oncogenic unit promotes anchorage-independence and tumor progression.

Jay S Desgrosellier¹, Leo A Barnes, David J Shields

¹Department of Pathology, Moores University of California-San Diego Cancer Center, La Jolla, California, USA.

Nature Medicine

|September 8, 2009

View abstract on PubMed

Summary

This summary is machine-generated.

Integrin alpha(v)beta(3) promotes tumor growth and metastasis independently of cell adhesion. Blocking its associated c-Src signaling pathway inhibits these aggressive cancer behaviors.

Related Experiment Videos

Area of Science:

Oncology
Cell Biology
Molecular Biology

Background:

Integrins are key regulators of cell adhesion, influencing tumor cell growth, survival, and invasion.
Integrin alpha(v)beta(3) expression is linked to the progression of various human cancers.
A known role of integrins involves adhesion-dependent processes in cancer.

Purpose of the Study:

To investigate a potential adhesion-independent role of integrin alpha(v)beta(3) in pancreatic cancer and other carcinomas.
To elucidate the molecular mechanisms underlying this adhesion-independent function.
To explore therapeutic strategies targeting this pathway.

Main Methods:

Investigated the role of integrin alpha(v)beta(3) in anchorage-independent growth in vitro and metastasis in vivo.
Examined the involvement of c-Src kinase, Crk-associated substrate (CAS) phosphorylation, and focal adhesion kinase (FAK) activation.
Utilized pharmacological blockade of c-Src and gene silencing of alpha(v)beta(3) integrin and c-Src.

Main Results:

Integrin alpha(v)beta(3) expression enhanced anchorage-independent tumor growth and lymph node metastasis.
These effects were mediated by c-Src recruitment and activation, leading to CAS phosphorylation, independent of cell adhesion or FAK.
Inhibition of c-Src or alpha(v)beta(3) /c-Src expression suppressed tumor growth and metastasis without affecting migration or invasion.

Conclusions:

Integrin alpha(v)beta(3) plays a critical role in mediating anchorage independence in cancer cells.
An alpha(v)beta(3)-c-Src signaling module drives aggressive tumor behavior, including metastasis.
Targeting this integrin-c-Src pathway represents a potential therapeutic strategy for aggressive carcinomas.