| + |
CXCL5 | up-regulates 
|
Metastasis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277733 |
|
|
Homo sapiens |
Pancreatic Cancer Cell |
| pmid |
sentence |
| 34237033 |
We demonstrate that collagen-induced DDR1 activation in cancer cells is a major stimulus for CXCL5 production, resulting in the recruitment of tumor-associated neutrophils (TANs), the formation of neutrophil extracellular traps (NETs), and subsequent cancer cell invasion and metastasis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL5 | up-regulates activity 
binding
|
CXCR2 |
0.765 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277730 |
|
|
Homo sapiens |
Pancreatic Cancer Cell |
| pmid |
sentence |
| 38339310 |
CXCL5 is another ELR+ CXC chemokine and, thus, also potently attracts neutrophils. Just like CXCL1, CXCL5 also signals through CXCR2, explaining why, often, CXCL5 and CXCL1 are seen to function in parallel in PDAC. CXCL5 was increased in human pancreatic tissue compared to the normal pancreas, and the knockdown of CXCL5 in pancreatic cancer cell lines reduced the proliferation and migration ability of cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DDR1 | up-regulates quantity by expression
transcriptional regulation
|
CXCL5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277731 |
|
|
Homo sapiens |
MDA-Panc-28 Cell |
| pmid |
sentence |
| 34237033 |
We demonstrate that collagen-induced DDR1 activation in cancer cells is a major stimulus for CXCL5 production, resulting in the recruitment of tumor-associated neutrophils (TANs), the formation of neutrophil extracellular traps (NETs), and subsequent cancer cell invasion and metastasis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL5 | up-regulates
|
Neutrophil_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277732 |
|
|
Homo sapiens |
Neutrophil |
| pmid |
sentence |
| 34237033 |
We demonstrate that collagen-induced DDR1 activation in cancer cells is a major stimulus for CXCL5 production, resulting in the recruitment of tumor-associated neutrophils (TANs), the formation of neutrophil extracellular traps (NETs), and subsequent cancer cell invasion and metastasis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CXCL5 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-282637 |
|
|
Homo sapiens |
PANC-1 Cell |
| pmid |
sentence |
| 37541772 |
Our results showed that CRIP1 was frequently upregulated in PDAC tissues with low immune activation. Elevated CRIP1 expression induced high levels of myeloid-derived suppressor cell (MDSC) infiltration and fostered an immunosuppressive tumour microenvironment. Mechanistically, we primarily showed that CRIP1 bound to nuclear factor kappa-B (NF-κB)/p65 and facilitated its nuclear translocation in an importin-dependent manner, leading to the transcriptional activation of CXCL1/5. PDAC-derived CXCL1/5 facilitated the chemotactic migration of MDSCs to drive immunosuppression. SX-682, an inhibitor of CXCR1/2, blocked tumour MDSC recruitment and enhanced T-cell activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
CXCL5
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