Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

The Tumor Microenvironment

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

Metastasis

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...

Tumor Immunotherapy

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Claudin-1 targeting suppresses tumor growth, invasion, and metastasis in patient-derived cholangiocarcinoma models.

Science translational medicine·2026

Same author

Pancreatic cancer induces B cell lineage plasticity via Pax5 inhibition to sustain immunosuppression.

Cell death discovery·2026

Same author

Cancer prevention through metabolic remission.

Nature reviews. Endocrinology·2026

Same author

EASL position paper on preclinical models of steatotic liver disease.

Journal of hepatology·2026

Same author

Electrophilic compound screening identifies GPX4-dependent ferroptosis as a senescence vulnerability.

Nature cell biology·2026

Same author

Spliceosome induction is a druggable dependency of RAS-driven senescence and cancer.

Nature communications·2026

Same journal

Peptidomics in the Spotlight: Advanced Sample Treatment Techniques and Analytical Insights.

Advances in experimental medicine and biology·2026

Same journal

Methods for the Investigation of Protein-Ligands Interactions.

Advances in experimental medicine and biology·2026

Same journal

Sample Preparation Strategies for Microbial Cell Surface Proteomics: Integrating Shaving and Shotgun Approaches.

Advances in experimental medicine and biology·2026

Same journal

Proteomic Sample Preparation for the Petroleum Industry: A Biocorrosion Case Study.

Advances in experimental medicine and biology·2026

Same journal

Proteomic and Functional Comparison of Extracellular Vesicles from Wild-Type and Lyn-Deficient Stromal Cells.

Advances in experimental medicine and biology·2026

Same journal

Proteomic Analysis of Histone Sequence Variants and Post-translationally Modified Forms.

Advances in experimental medicine and biology·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Oct 27, 2025

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

CCL2 in the Tumor Microenvironment.

Tracy O'Connor^1,2,3,4, Mathias Heikenwalder^5,6,7,8

¹Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany. tracy.oconnor@helmholtz-muenchen.de.

Advances in Experimental Medicine and Biology

|July 21, 2021

Summary

This summary is machine-generated.

The C-C motif chemokine ligand 2 (CCL2) drives cancer progression by recruiting immune cells and directly impacting tumor cells. Targeting the CCL2-CCR2 pathway offers a promising therapeutic strategy for various cancers.

Keywords:

Angiogenesis CCL2 CCR2 Cancer Extravasation Immunity Immunosuppression Invasion MCP-1 Macrophage Metastasis Microenvironment NFκB TAM Tumor

More Related Videos

Mass Cytometry Analysis of Systemic and Local Immune Responses in Hepatocellular Carcinoma

Mass Cytometry Analysis of Systemic and Local Immune Responses in Hepatocellular Carcinoma

Published on: April 25, 2025

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Published on: April 13, 2015

Related Experiment Videos

Last Updated: Oct 27, 2025

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

Mass Cytometry Analysis of Systemic and Local Immune Responses in Hepatocellular Carcinoma

Mass Cytometry Analysis of Systemic and Local Immune Responses in Hepatocellular Carcinoma

Published on: April 25, 2025

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Published on: April 13, 2015

Area of Science:

Immunology
Oncology
Molecular Biology

Background:

C-C motif chemokine ligand 2 (CCL2) is implicated in immune responses and cancer.
CCL2 overexpression correlates with aggressive cancers, metastasis, and poor patient outcomes.
CCL2 influences tumor microenvironment and cancer cell behavior.

Purpose of the Study:

To elucidate the multifaceted roles of CCL2 in cancer progression.
To highlight the significance of the CCL2-CCR2 signaling axis as a therapeutic target.

Main Methods:

Literature review and synthesis of existing research on CCL2 in cancer.
Analysis of CCL2's functions in immune cell recruitment, tumor cell interactions, and metastasis.
Examination of the CCL2-CCR2 signaling pathway's therapeutic potential.

Main Results:

CCL2 recruits tumor-associated macrophages (TAMs) with pro-tumorigenic functions.
CCL2 directly promotes tumor cell growth, motility, and angiogenesis.
CCL2 facilitates the metastatic cascade, including pre-metastatic niche formation and extravasation.
CCL2 contributes to an immunosuppressive tumor microenvironment.

Conclusions:

CCL2 is a key driver of tumorigenesis and metastasis through diverse mechanisms.
The CCL2-CCR2 axis represents a viable therapeutic target for combating cancer progression and metastasis.