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Impaired formation of homotypic cell-in-cell structures in human tumor cells lacking alpha-catenin expression

Manna Wang1, Xiangkai Ning1, Ang Chen2

  • 11] Institute of Molecular Immunology, School of Biotechnology, Southern Medical University, Guangzhou 510515, P. R. China [2] Laboratory of Cell Engineering, Institute of Biotechnology, 20 Dongda Street, Beijing 100071, P. R. China.

Scientific Reports
|July 21, 2015
PubMed

Insights

Alpha-catenin (α-catenin) loss impairs homotypic cell-in-cell (CIC) formation in tumors. Restoring α-catenin expression re-establishes cell adhesion and promotes CICs, identifying it as a key regulator alongside E- and P-cadherin.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Oncology

Background:

  • Cell-in-cell structures (CICs) are observed in human tumors, but homotypic CICs (formed between identical tumor cells) occur infrequently.
  • Previous research indicated that E- and P-cadherin expression is crucial for homotypic CIC formation via entosis.
  • Tumor cells lacking E- or P-cadherin cannot form homotypic CICs, while their re-expression restores this capability.

Purpose of the Study:

  • To investigate the role of alpha-catenin (α-catenin) in homotypic CIC formation in human tumor cells.
  • To identify molecular mechanisms that regulate homotypic CIC formation beyond cadherin expression.
  • To understand how α-catenin loss affects cell-cell adhesion and CIC development in cancer.

Main Methods:

  • Analysis of homotypic CIC formation in tumor cell lines with varying cadherin and α-catenin expression levels.
  • Functional assays to assess the impact of α-catenin re-expression on cell-cell adhesion.
  • Investigation of the involvement of ROCK kinase signaling in α-catenin-mediated CIC formation.

Main Results:

  • Homotypic CIC formation was impaired in tumor cells expressing high levels of E-cadherin but lacking α-catenin.
  • Re-expression of α-catenin in these cells restored cell-cell adhesion and promoted CIC formation.
  • α-catenin-dependent CIC formation was found to be regulated by ROCK kinase signaling.

Conclusions:

  • Alpha-catenin (α-catenin) is identified as a critical molecule, in addition to E- and P-cadherin, that regulates homotypic CIC formation in human tumors.
  • Loss of α-catenin can inactivate homotypic CIC formation in tumors, even in the presence of cadherins.
  • Targeting α-catenin and its downstream pathways, like ROCK kinase, may offer new strategies for cancer therapy.

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