Related Experiment Video
Updated: May 9, 2026
09:58
RhoC GTPase Activation Assay
Published on: August 22, 2010
CCL2 increases αvβ3 integrin expression and subsequently promotes prostate cancer migration
Tien-Huang Lin1, Hsin-Ho Liu, Tsung-Hsun Tsai
1School of Chinese Medicine, China Medical University, Taichung, Taiwan.
Biochimica Et Biophysica Acta
|July 13, 2013
Summary
Chemokine ligand 2 (CCL2) enhances prostate cancer cell migration and integrin expression via the CCR2 receptor. This interaction is a critical factor in prostate cancer metastasis.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Chemokine ligand 2 (CCL2), also known as monocyte chemoattractant protein-1 (MCP-1), is implicated in cancer progression.
- Prostate cancer, a prevalent malignancy in men, frequently metastasizes to bone.
- The specific role of CCL2 in prostate cancer cell behavior remained largely uncharacterized.
Purpose of the Study:
- To investigate the influence of CCL2 on integrin expression in prostate cancer cells.
- To determine the effect of CCL2 on the migratory activity of prostate cancer cells.
- To elucidate the signaling pathways involved in CCL2-mediated prostate cancer cell migration.
Main Methods:
- Utilized Transwell, wound healing, and invasion assays to assess prostate cancer cell migration.
- Employed western blotting to analyze PKCδ and c-Src phosphorylation.
- Conducted qPCR for integrin mRNA expression and transient transfection for AP-1 activity assessment.
Main Results:
- CCL2 stimulation increased migration and integrin αvβ3 expression in prostate cancer cell lines (PC3, DU145, LNCaP).
- CCR2 receptor, but not CCR4, mediated CCL2-induced migration and integrin expression.
- CCL2 activated a signaling cascade involving PKCδ, c-Src, and AP-1, crucial for cell migration and integrin upregulation.
Conclusions:
- CCL2 interaction with CCR2 receptor promotes prostate cancer cell migration by upregulating integrin αvβ3.
- CCL2 plays a significant role in the metastatic potential of prostate cancer.
Related Concept Videos
01:10Integrins
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,...
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,...
01:17Intracellular 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...
Some...
01:15Activation 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.
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.
01:35Cancer 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...
02:30Metastasis
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...
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...
01:25Selectins
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...