Inhibition of Proliferation by PERK Regulates Mammary Acinar Morphogenesis and Tumor Formation
2007

How Cell Adhesion Affects Tumor Growth and Development

publication 10 minutes Evidence: moderate

Author Information

Author(s): Sequeira Sharon J., Ranganathan Aparna C., Adam Alejandro P., Iglesias Bibiana V., Farias Eduardo F., Aguirre-Ghiso Julio A.

Primary Institution: University at Albany, State University of New York

Hypothesis

Adhesion-dependent regulation of PERK signaling might determine cell fate.

Conclusion

The PERK pathway is essential for proper acinar morphogenesis and in preventing mammary tumor formation.

Supporting Evidence

  • Loss of adhesion to a suitable substratum induces PERK-dependent phosphorylation of eIF2α.
  • Inhibition of endogenous PERK signaling during acinar morphogenesis results in hyper-proliferative acini.
  • MCF10A cells expressing PERKΔC were tumorigenic in vivo upon implantation.

Takeaway

Cells need to stick to their surroundings to grow properly; if they don't, they can grow too much and form tumors.

Methodology

The study used 3D Matrigel cultures to analyze the role of PERK in mammary acinar morphogenesis and tumor formation.

Limitations

The study primarily focused on in vitro models and may not fully represent in vivo conditions.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0000615

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication