Cell adhesion system and human cancer morphogenesis

  title={Cell adhesion system and human cancer morphogenesis},
  author={Setsuo Hirohashi and Yae Kanai},
  journal={Cancer Science},
Cell‐cell adhesion determines the polarity of cells and participates in the maintenance of the cell societies called tissues. Cell‐cell adhesiveness is generally reduced in human cancers. Reduced intercellular adhesiveness allows cancer cells to disobey the social order, resulting in destruction of histological structure, which is the morphological hallmark of malignant tumors. Reduced intercellular adhesiveness is also indispensable for cancer invasion and metastasis. A tumor‐suppressor gene… 


It is shown that overexpression of Pfn1 can restore adherence junctions and phenotypic reversion to an epithelioid-type through junctional stabilization of an endogenously expressed cadherin molecule, and also sensitizes MDA-MB-231 cells to apoptosis suggesting the survival of breast cancer cells can also be modulated Pfn 1.

Cell adhesion molecules, the extracellular matrix and oral squamous carcinoma.

  • A. J. LyonsJ. Jones
  • Biology, Medicine
    International journal of oral and maxillofacial surgery
  • 2007

Adhesion strength and anti-tumor agents regulate vinculin of breast cancer cells

The results showed that the post-treatment spreading rate was significantly decreased in both types of breast cancer, suggesting a lower metastatic potential and the probability of cell motility, migration, and metastasis was confined.

T-cadherin negatively regulates the proliferation of cutaneous squamous carcinoma cells.

The findings suggest that T-cadherin acts as an endogenous negative regulator of keratinocytes proliferation and its inactivation is the cause for keratinocyte hyperproliferation in SCC or in psoriasis vulgaris.

Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer

CADM1 could be a potential biomarker for early diagnosis and a target for cancer treatment in future clinical practices and some long non-coding RNAs or miRNAs directly or indirectly act on CADM1 to regulate tumor growth and motility.

The Integrin Tail: A Tale of Cell Motility and Division

A novel molecular mechanism by which Rab21, through association with the integrin subunits, drives integrin endosomal traffic during mitotic phases is revealed and firmly suggest that genetic alterations in integrin traffic may lead to progression of tumorigenesis as a result of failed cell division.

Actinin-4 increases cell motility and promotes lymph node metastasis of colorectal cancer.

Actinin-4 actively increases cell motility and promotes lymph node metastasis of colorectal cancer.

Downregulation of N-cadherin Expression Inhibits Invasiveness, Arrests Cell Cycle and Induces Cell Apoptosis in Esophageal Squamous Cell Carcinoma

The data showed that knock-down of N-cadherin in ESCC cell line could arrest cell cycle at G0/G1 phase, induce cell apoptosis, reduce the invasiveness in vitro, and inhibit the tumor formation in vivo.

Transcriptional regulation of cell polarity in EMT and cancer

Re-examined data related to the effect of EMT related transcription factors on epithelial cell plasticity and genetic interactions that highlight the existence of complex regulatory networks converging on the regulation of cell polarity by EMT inducers in human breast carcinomas are analyzed.



Dissecting tumor cell invasion: epithelial cells acquire invasive properties after the loss of uvomorulin-mediated cell-cell adhesion

It is shown that nontransformed Madin-Darby canine kidney epithelial cells acquire invasive properties when intercellular adhesion is specifically inhibited by the addition of antibodies against the cell adhesion molecule uvomorulin; the separated cells then invade collagen gels and embryonal heart tissue.

Disruption of E‐Cadherin‐mediated Cell Adhesion Systems in Gastric Cancers in Young Patients

The E‐cadherin‐mediated cell adhesion system in the cancer cells of all the patients examined appeared to be disrupted, indicating that somatically acquired dysfunction of this system plays an important role in early‐onset diffuse‐type gastric cancers.

E-cadherin gene mutations in human gastric carcinoma cell lines.

  • T. OdaY. Kanai S. Hirohashi
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1994
The E-cadherin gene had been inactivated by two hits (mutation and allele loss), similar to the mechanism for inactivation of tumor suppressor genes in "diffusely invasive" human carcinomas.

Frequent Loss of α Catenin Expression in Scirrhous Carcinomas with Scattered Cell Growth

It is suggested that down‐regulation of either α catenin or E‐cadherin plays a critical role in the disruption of cell adhesion in carcinomas with scattered cell growth.

The cadherins: cell-cell adhesion molecules controlling animal morphogenesis.

It appears that each cadherin subclass has binding specificity and this molecular family is involved in selective cell-cell adhesion, indicating a crucial role in construction of tissues and the whole animal body.

Dysadherin, a cancer-associated cell membrane glycoprotein, down-regulates E-cadherin and promotes metastasis

The cloning and characterization of a cancer-associated cell membrane glycoprotein, which down-regulates E-cadherin and promotes metastasis, dysadher in is reported, and named.

Cadherin cell-adhesion molecules in human epithelial tissues and carcinomas.

Two distinct calcium-sensitive cell-cell adhesion molecules were identified in human epithelial tissues and carcinomas using two monoclonal antibodies raised against vulvar epidermoid carcinoma A-431

Cadherin dysfunction in a human cancer cell line: possible involvement of loss of alpha-catenin expression in reduced cell-cell adhesiveness.

A human lung cancer cell line, PC 9, was analyzed to elucidate the molecular mechanisms of dysfunction of cadherin-mediated cell-cell adhesion in cancer, and it was revealed that PC 9 cells did not express alpha-catenin, a cadher in-associated protein, suggesting that this was the cause of the Cadherin dysfunction in the cell line.

A Truncated β-Catenin Disrupts the Interaction between E-Cadherin and α-Catenin: A Cause of Loss of Intercellular Adhesiveness in Human Cancer Cell Lines

The findings indicate that genetic abnormality of beta-catenin is one of the mechanisms responsible for loosening of cell-cell contact, and may be involved in enhancement of tumor invasion in human cancers.