C-C motif chemokine 7 Antibodies

C-C motif chemokine 7 (CCL7)

Chemotactic factor that attracts monocytes and eosinophils, but not neutrophils. Augments monocyte anti-tumor action.

Additionally induces the release of gelatinase B. This protein can bind heparin.

Gene Information

Human
Gene Name:	CCL7
Uniprot:	P80098
Entrez:	6354

Family

Belongs to:
intercrine beta (chemokine CC) family

Alternative Names

C-C motif chemokine 7; CCL7; chemokine (C-C motif) ligand 7; FIC; MARC; MCP-3; MCP3Monocyte chemotactic protein 3; MCP-3Small-inducible cytokine A7; MGC138465; Monocyte chemoattractant protein 3; NC28SCYA6; SCYA7MGC138463; small inducible cytokine A7 (monocyte chemotactic protein 3)

Molecular Weight

Mass (kDA):
11.2 kDA

Genomic Context

Human
Location:	17q12
Sequence:	17; NC_000017.11 (34270221..34272242)

Subcellular Localizations

Secreted.

Diseases

• Inflammation
• Cholangiocarcinoma
• Asthma
• Neoplasms
• Malignant Neoplasms
• Inflammatory Response
• Hiv Infections
• Tissue Adhesions
• Fibrosis
• Sclerosis
• Autoimmune Reaction
• Nervousness
• Multiple Sclerosis

• Immunologic Deficiency Syndromes
• Neoplasm Metastasis
• Allergy
• Atherosclerosis
• Pneumonia
• Granuloma
• Lung Diseases

Interacting Proteins

• TNFAIP6
• UBQLN1

Pathways

• Chemotaxis
• Pathogenesis
• Immune Response
• Secretion
• Cell Migration
• Inflammatory Response
• Chemokine Production
• Granuloma Formation
• Cytokine Production
• Angiogenesis
• Regeneration
• Cell Adhesion
• Cell Activation

• Innate Immune Response
• Neutrophil Chemotaxis
• Wound Healing
• Monocyte Chemotaxis
• Hypersensitivity
• Leukocyte Migration
• Viral Replication

PTMs

• Cleavage
• Phosphorylation
• Glycosylation
• Acetylation

• Demethylation
• Nitration
• Carboxylation
• Biotinylation

• Methylation

Research Areas

• Cancer

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CCL7

The Best Uses of the CCL7 Marker From Boster Bio

The CCL7 Marker is a powerful attractant of immunocompetent cells. This antitumor proteins can also mimic CCL2-mediated angiogenesis. In this article, we discuss some of the best uses of CCL7 and how you can make the most of this biomarker. To get started, read the article below. For more information on CCL7, you can return to this article later.

CCL7 is an attractive attractant for immunocompetent cell lines

A chemokine called CCL7 is a strong attractant of immune-competent cells. This chemokine can be used for many purposes. It has been shown to promote tumor invasion, growth, and metastasis. Lung adenomas from old mice express higher levels of CCL7 and show increased accumulation of immune cells. They are also more dangerous. Metastatic renal cell carcinoma also expresses high levels of CCL7 and triggers the recruitment tumor-associated macrophages. It also promotes vascular permeability, which allows tumor cells crossing the blood-brain border to reach the brain tissues.

CCL7 is well-known for its anti-inflammatory, tumor-fighting and anti-inflammatory properties. It also promotes the recruitment and activation of leukocytes. CCL7 can be overexpressed to increase monocyte recruitment to tumor sites, and facilitate their transformation into cancer-fighting cells. It also induces a response in type I T cells, triggering a cascade of anti-tumor immune responses.

Anti-inflammatory substances and pathogens activate monocytes in the immune system. The immune system polarizes towards Th2 cells and Th27 cells. Non-hematopoietic cells of the skin, such as cutaneous Fibroblasts, can express CCL7. CCL7 expression 2 weeks after Leishmania infection in the tissue stroma enhances the immune system.

It activates antitumor immune responses

A CCL7 marker could be useful in cancer patients to increase anti-tumor immunity. CCL7 has been proven to play an important role in the interaction between tumor cells stromal cells. CCL7 overexpressing tumors can increase leukocyte recruitment and activate antitumor immuno responses.

CCL7 has an anti-tumor effect by activating immune reactions by targeting tumor-associated macrophages. CCL7 binds at the CCR2 and promotes tumor-associated macrophage recruitment. CCL7-expressing MSCs in tumors stimulate macrophage growth and interaction with immune cell. In addition, tumor-associated microphages promote growth of metastatic tumor cells.

Boster Bio and STEMCELL researchers isolated neutrophils in mouse bone marrow using a mouse model. Cell migration chambers were coated in 5 mg/ml of recombinant mouse ICAM-1, and the indicated chemicals. The neutrophils were then kept at 37°C in L15 media. Video microscopy was performed to capture migration data from the neutrophils. Volocity software was used for migration analysis.

The discovery of a biomarker to CCL7 in cancer patients could help speed up anti-tumor immunotherapy. This protein plays an essential role in limiting cutaneous irritation following L. major. CCL7 may also be crucial for controlling visceral parasites. These researchers will therefore use Boster Bio's CCL7 to boost antitumor immune responses.

It mimics CCL2-mediated tumor angiogenesis

In this study, the CCL7 marker from Boster Bio mimicked the effect of tumor angiogenesis-promoting CCL2 on cancer growth. CCL7 is a marker for tumor growth and plays a crucial role in the interaction between tumor cells, stromal cells, and each other. Because of this, it may be a promising tool for tumor immunotherapy.

The chemokine CCL7 is produced by certain types of tumor cells, including breast cancer, colon, and prostate cancers. It has been shown to promote invasion and growth of these types of cancers. Additionally, it is more prevalent in metastatic tissue than in primary tissues. CCL7 expression is thought to increase the recruitment of macrophages in the tumor, which encourages vascular permeability. Tumor cells can also cross the blood brain barrier, which promotes tumor metastasis.

Researchers used lentiviral transduction (LCL7) to overexpress CCL7 within HCT116 and cells HT29. They observed mesenchymal effects in cells that were overexpressed for CCL7, including spindle cell shape and loss cell-to cell adhesion. CCL7 expression was confirmed using western blot and real-time PCR analyses.

The CCL7 marker also had an impact on colon carcinoma cell migration and invasion in HCT116 cell lines. CCL7-overexpressing CCT116 cells had lower levels of E-cadherin or N-cadherin expression than GFP-overexpressing CCT116 cells. CCL7 overexpression led to an increase in twist expression, which represses epithelial gene expression.

It prevents L. major.

A recent study on mice lacking CCL7 found that inflammation increased in response to L. major infected. The number of immune cells recruited into the skin infected with L. major infection increased and was characterized by an elevated IL-17 profile. This is associated to increased neutrophil infiltration. CCL7 inhibits neutrophil migration in vitro and adding it back to the immune response reduced neutrophil infiltration into the infected skin.

However, these studies have not proven the benefits of Boster Bio CCL7 inhibitors. Ccr2 nil mice were more likely to contract L. major infection than mice without Ccr2 ill. However, the mice's immune systems protected them. The inactivation Ccr2 resulted in a higher production and level of cytokine and Th2 in these mice. The nature and severity of the immunological challenge were not sufficient to cause the Th reaction.

It promotes tumor metastasis

The CCL7 gene plays an important role in the tumor environment. This cytokine promotes cancer cell growth and metastasis. In addition, it increases the number and activity of CD8+ T cells, which promote antitumor immunity. There are many possible explanations for these findings. We will be discussing three of these pathways.

The CC chemokine CC7 has a wide distribution and is widely recognized as an inflammatory cytokine. It mediates immune reactions and attracts different subgroups of leukocytes. It plays an important role in the immune system and overexpression in tumors could make it a promising target for antitumor treatments. Numerous mouse tumor models show that CCL7 overexpression can inhibit tumor growth.

In mouse lung cells, CCL7 expression was found in lungs and blood. It was most abundant in non-ciliated airway epithelial cells, although it was absent in ciliated airway epithelial cells. cDC1 levels were lower in tumor-burden lungs in mice lacking CCL7 expression. This suggests that tumors lacking CCL7 expression are less likely to spread to the bone.

It prevents neutrophil migration

A new study found that soluble Syndecan-3 (SCN-3), an indicator for the chemokine CCL7 inactivates neutrophil migration. These findings suggest that SCN-3 may be a therapeutic option for cancer. TAMs produce the molecule SCN-3. It regulates the migrations of neutrophils monocytes and macrophages.

CCL7 plays a role in tumorigenesis, although it is still not clear what its role is. However, it is well-known that it can promote leukocyte recruiting and type I T cell dependent reactions. CCL7 has been shown to promote tumor-promoting actions in many types of cells, and it also inhibits neutrophil movement. Researchers may need to identify tumor-associated genes.

In vitro experiments on a monocytic line of human cells were conducted. CCL7 inhibited leukocyte growth. Also, soluble synthecan-3 inhibited this process. CCL7 induced the greatest effect at 10 mg/ml. However, it was not significantly different than baseline migration levels. The inhibitory effect of any other syndecan member was not significant. No soluble syndecan-1, -2, or 4 affected the migration of THP-1 cells.