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  1. Home
  3. Functions Of P120-catenin In Physiology And Diseases.
  1. Home
  3. Functions Of P120-catenin In Physiology And Diseases.

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Functions of p120-catenin in physiology and diseases.

Xin Jin1, Ting Lin2, Yunjuan Wang1

  • 1The First Affiliated Hospital (The First School of Clinical Medicine), Guangdong Pharmaceutical University, Guangzhou, China.

Frontiers in Molecular Biosciences
|November 5, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

p120-catenin (p120) is crucial for cell adhesion and cadherin stability. This review highlights p120

Keywords:
P120cancercell-cell adhesioninflammationnon-coding RNAs

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • p120-catenin (p120) is a key regulator of cell-cell adhesion at adherens junctions.
  • p120 interacts with the E-cadherin juxtamembrane domain (JMD), influencing cadherin stability at the cell surface.
  • Known roles of p120 extend to tumor progression and inflammation.

Purpose of the Study:

  • To review recent advancements concerning p120-catenin in physiological processes and disease.
  • To focus on the specific functions of p120 in the regulation of cancer and inflammation.

Main Methods:

  • Literature review of recent scientific publications.
  • Synthesis of findings on p120-catenin's role in cancer and inflammation.
  • Analysis of p120's interactions with E-cadherin and its impact on cell adhesion.

Main Results:

  • p120-catenin significantly impacts cell-cell adhesion dynamics.
  • p120 plays a critical role in the stability of E-cadherin at the plasma membrane.
  • Emerging evidence links p120 function to the development and progression of cancer and inflammatory diseases.

Conclusions:

  • p120-catenin is a multifaceted protein with critical roles in fundamental cellular processes.
  • Understanding p120's functions in cancer and inflammation is vital for therapeutic strategies.
  • Further research into p120 regulation and its downstream effects is warranted.