C-X-C motif chemokine 5 Antibodies

C-X-C motif chemokine 5 (CXCL5)

Involved in neutrophil activation. In vitro, ENA-78(8- 78) and ENA-78(9-78) show a threefold higher chemotactic activity for neutrophil granulocytes.

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Gene Information

Human
Gene Name:	CXCL5
Uniprot:	P42830
Entrez:	6374

Family

Belongs to:
intercrine alpha (chemokine CxC) family

Alternative Names

LIX

Molecular Weight

Mass (kDA):
11.972 kDA

Genomic Context

Human
Location:	4q13.3
Sequence:	4; NC_000004.12 (73995642..73998677, complement)

Subcellular Localizations

Secreted.

Diseases

• Inflammation
• Neoplasms
• Malignant Neoplasms
• Tumor Angiogenesis
• Inflammatory Response
• Tissue Adhesions
• Pathologic Neovascularization
• Carcinoma
• Neoplasm Metastasis
• Arthritis
• Pneumonia
• Rheumatoid Arthritis

• Cholangiocarcinoma
• Infective Disorder
• Fibrosis
• Cell Invasion
• Colitis
• Lung Neoplasms
• Cell Transformation, Neoplastic

Pathways

• Pathogenesis
• Angiogenesis
• Secretion
• Chemotaxis
• Inflammatory Response
• Chemokine Production
• Cell Migration
• Immune Response
• Cell Proliferation
• Cell Adhesion
• Cell Growth
• Neutrophil Chemotaxis
• Localization

• Tube Formation
• Chemokine Secretion
• Regeneration
• Neutrophil Activation
• Reverse Transcription
• Wound Healing
• Virulence

PTMs

• Phosphorylation
• Cleavage
• Methylation

• Citrullination
• Acetylation
• Demethylation

• Reduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CXCL5

Best Uses Of The CXCL5 Marker

This biomarker is crucial in detecting CXCL5 protein expression in human cells. This protein is released from neutrophils which are responsible for lymph node metastasis. This article examines the mechanisms that CXCL5 induces EMT as well as its clinical applications. Continue reading to find out more. This article also includes information about CXCL5 and its implications in treating cancer.

CXCL5 expression might be an adverse prognostic marker for cancer

In addition to its role in regulating tumor growth, CXCL5 also affects metastasis and promotes the development of a variety of cancers. It is a proangiogenic factor cytokine and regulates tumor development through a variety mechanism, including activation via the STAT pathway. Additionally, CXCL5/CXCR2 signaling in tumors promotes the growth of new blood vessels, which serve as channels for tumor metastasis. CXCL5/CXCR2 sends signals to tumors through the release of the enzyme matrix-metalloproteinase-9. This enzyme damages endothelial cells as well as the matrix barrier that protects against invasion. CXCL5/CXCR2 expression has also been reported.

CXCL5 also promotes the development of mitomycin resistance. It activates NF-kB. This finding makes CXCL5 an important novel chemoresistance-related biomarker in NSCLC. It also provides new therapeutic targets in lung cancer. CXCL5 high expression has been associated with poor overall survival, poor response to immunotherapy and poor prognosis.

High levels of CXCL5 expression in tumors could also impact the immune response. CXCL5 levels in cancer patients had shorter overall survival (DFS). However, there were no significant associations between CXCL5 protein and tumor-associatedfibroblasts. This study also shows CXCL16 to be a potent chemokine which plays a critical role in breast cancer development.

CXCL5 expression could also be associated to the progression and spread of gastric cancer. It is not yet clear what role it plays in gastric cancer. It has been proven to be important for tumor differentiation, angiogenesis, immunosuppression, and immune suppression. It may even be a prognostic factor in pancreatic tumors. Thus, CXCL5 expression might be an adverse prognostic marker for cancer.

In a recent study, researchers found that high levels of CXCL5 mRNA were associated with a poor prognosis in HCC patients. In addition, CXCL5 expression was found to correlate with tumor stage, T-classification, and ONCOMINE score. High CXCL5 levels were found to predict poor overall survival among HCC patients.

Mechanisms by CXCL5 that induce EMT

We are still not able to fully understand the mechanism by which CXCL5 induces EMET among gastric cancer cells. Molecular studies have shown that CXCL5 regulates EMT in gastric cancer cells via its ability to stimulate neutrophils, which in turn promotes GC cell metastasis. But what is EMT exactly? In this article, we discuss the mechanisms by which CXCL5 induces EMT in gastric cancer cells.

MET is a fundamental process that causes tumors. Invasive tumors cells spread faster and do better than non-metastatic. EMT is complex and context-dependent. Boster Bio cells express a wide variety of MET proteins, including adiponectin, thrombospondin, and osteocalcin. In fact, EMT is an important process in OS metastases.

Recent research revealed that the PDGFRb receptor, PDGFRb binds directly to the ligand activating the PI3K/AKT/mTOR signals pathway. This signaling pathway regulates genes important in the EMT process. EMT targets EpCAM, ZEB1 & ZEB2, a SMA, and the Snail/Twist Family.

CXCL5 plays a key role in the progression cancer. It is directly implicated in a series of cellular functions, including migration and invasion. CXCL5-primed neutrophils secrete IL-6 & IL-23 which promote tumor growth and metastasis, according to a study. Although the mechanism of EMT is still not known, it appears CXCL5 activates neutrophils, which is a crucial cellular factor to cancer progression. This may play an important role for the development of gastric Cancer.

Previous studies have shown CXCL5 has a positive effect on breast cancer cells' metastatic potential. This molecule activates the ERK/GSK-3b/Snail pathway, which promotes EMT. CXCL5 from cancer-associated fibroblasts enhances PD-L1 expression in melanoma cells, further suggesting its role in tumor development.

While CXCL5 induces EMT in various ways, its effect on lymphatic metastasis is more complicated. It is involved with many processes that influence tumor size, invasion depth, differentiation, and size. CXCL5 is also known for its chemotactic capabilities. The ERK/p38 signaling pathway activates neutrophils, which promotes tumor growth.

Contribution to lymph node metastasis by neutrophils

Neutrophils are thought to play a crucial role in the metastatic progression of cancer. They may also contribute to the spread and spread of tumours via lymph node metastasis. Their functions could include the release and activation of cytokines which affect cancer cells. They also play a role in anti-tumour immunity. However, it is not yet clear exactly how neutrophils contribute to the metastasis of cancer.

Although previously thought to being homogeneous, neutrophils have large phenotypic heterogeneity. They also exhibit functional versatility. This variability is reflected in the microenvironment that can prompt neutrophils to acquire specific specialised functions. For example, neutrophils found in the lung accumulate within the vascular lumen or interstitial space. This allows them to regain expression of the CXCR4 protein. The neutrophils in the spleen, however, migrate to the marginal lymph nodes where they produce cytokines. They also induce antibody production in marginal lymphocytes.

Neben ihrem anti-tumor effects, neutrophils also play a role in the proliferation of CD4+ cells in the dLNs. Neutrophils are essential for the proliferation of CD4+ T cells in the dLNs. Incubation of neutrophils with IC in vitro induces the production of specific antibodies. As a result, a specific anti-tumor immune response is induced.

A recent study has found that cancer patients have a reduced neutrophil count. This ratio was found to be elevated in lung cancer patients, which is indicative of poor survival. This ratio is strongly linked to cancer progress, but it is not known if neutrophils contribute to this process. Cancer patients have a higher ratio between neutrophils and lymphocytes. This suggests that cancer-related neutrophils may be involved in the metastasis.

Recent studies have shown that neutrophils could play a role during lymph node metastasis. Their recruitment in dLNs could limit the proliferation and activation of CD4+ T cell. The activity of other immune cells within the dLN may also be affected by neutrophils. Despite these findings, these neutrophils could still contribute to the metastasis cancer cells.

Clinical applications

The CXCL5 chemokine marker is part of the CXC family of chemokines, also known as chemoselectins. This molecule plays important roles in tumorigenesis and tumor progression. However, the prognostic significance of CXCL5 has been controversial. In an attempt to identify the prognostic value of CXCL5, we systematically searched PubMed, Embase, and Web of Science for studies assessing the expression of CXCL5 in cancer patients. We used the 95% confidence intervals (HR) to evaluate CXCL5's prognostic ability.

Our results show that CXCL5 stimulates the production of various chemokines within cancer cells. CXCL5 also promotes EMT among gastric cancer cells. CXCL5 also modulates neutrophils, allowing for it to play a pivotal part in the progression and treatment of GC. CXCL5 might be a promising marker for GC.

CXCL5 can be used clinically to detect cancer patients who have high levels of this protein in their tumors. The protein's high expression promotes granulocyte movement and invasion. CXCL5 expression is associated with a poorer outcome for lung cancer patients. The study by Roca et al. CXCL5 may promote tumor migration and metastasis. It may also aid in the development new drugs to combat cancer.

CXCL5 is not only a cancer cell marker, but it also affects other genes. CXCL5 inhibits CD44 expression, which is important for T24-L cell invasion and migration. Both CXCL5 (and CD44) inhibit the expression of these chemicals, suggesting that the marker could be useful in future studies. CXCL5 does not detect cancer cells in other situations.

The presence of CXCL5 in a tumor's tissue correlates with the TNM stage, tumor size, and T-cell count. Patients with high CXCL5 level have a shorter survival rate. These results indicate that CXCL5 is an important biomarker of NSCLC. But, before we can make these predictions, we need to understand its role in cancer progression.