Related Experiment Video

Updated: Jun 20, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

AsialoGM1 and integrin alpha2beta1 mediate prostate cancer progression

Severine Van Slambrouck1, John Hilkens, Marco Bisoffi

  • 1Department of Chemistry, Laboratory of Biochemical and Biomedical Research, New Mexico Tech, Socorro, NM 87801, USA. severine@nmt.edu

International Journal of Oncology
|September 3, 2009
PubMed

Insights

AsialoGM1 enhances prostate cancer metastasis by interacting with integrin alpha2beta1, promoting cell adhesion, migration, and invasion. This discovery offers new therapeutic targets for advanced cancer treatment.

Area of Science:

  • Oncology
  • Cell Biology
  • Glycobiology

Background:

  • Metastasis is the primary cause of cancer mortality.
  • Integrin alpha2beta1 and matrix metalloproteinases (MMPs) are implicated in prostate cancer invasion.
  • Previous research linked alpha2beta1 integrin reorganization to C4-2B cell invasiveness.

Purpose of the Study:

  • To investigate the role of asialoGM1 in prostate cancer progression and metastasis.
  • To elucidate the molecular mechanisms linking asialoGM1 to cancer cell behavior.
  • To identify potential therapeutic targets for metastatic prostate cancer.

Main Methods:

  • Analysis of asialoGM1 expression in C4-2B prostate cancer cells.
  • Assessment of cell adhesion, migration, and invasion assays.
  • Immunofluorescence microscopy to study colocalization of asialoGM1 and integrin alpha2beta1.
  • Investigation of downstream signaling pathways.

Main Results:

  • AsialoGM1 expression correlates with increased cancer progression in C4-2B cells.
  • AsialoGM1 influences cell adhesion, migration, and invasion.
  • AsialoGM1 reorganizes and colocalizes with integrin alpha2beta1.
  • A novel complex of asialoGM1 with integrin alpha2beta1 was identified, activating known signaling pathways.

Conclusions:

  • AsialoGM1 plays a significant role in promoting prostate cancer metastasis.
  • The interaction between asialoGM1 and integrin alpha2beta1 enhances cancer cell invasiveness via established signaling.
  • These findings reveal glycosphingolipids as modulators of malignant properties and suggest new therapeutic strategies.

More Related Videos

Growing Desmoplastic Three-Dimensional Pancreatic Cancer Spheroids from Co-Culture03:42

Growing Desmoplastic Three-Dimensional Pancreatic Cancer Spheroids from Co-Culture

Published on: September 27, 2024

In vitro Method to Observe E-selectin-mediated Interactions Between Prostate Circulating Tumor Cells Derived From Patients and Human Endothelial Cells11:56

In vitro Method to Observe E-selectin-mediated Interactions Between Prostate Circulating Tumor Cells Derived From Patients and Human Endothelial Cells

Published on: May 15, 2014

Related Concept Videos

Activation of Integrins01:15

Activation of Integrins

Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.
Integrins01:10

Integrins

Animal and protozoan cells do not have cell walls to help maintain shape and provide structural stability. Instead, these eukaryotic cells secrete a sticky mass of carbohydrates and proteins into the spaces between adjacent cells. This network of proteins and molecules is called an extracellular matrix or ECM.
Some ECM proteins assemble into a basement membrane to which the remaining components adhere. Proteoglycans typically form the bulk of the ECM while fibrous proteins, like collagen,...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...