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Editorial

The potential of CXCL5 as a target for liver cancer – what do we know so far?

, MD PhD, , , & , MD PhD

Figures & data

Figure 1. Regulators of CXCL5 and signal pathways activated by CXCL5. (1) Cytokines such as TNF-α, IL-17, IL-1β, KLF4 or Ron could activate the NF-κB signal pathways to induce CXCL5 production; (2) IL-27 could suppress the expression of CXCL5 though a STAT1-dominant pathway; (3) EGF could activate EGFR-downstream signal pathways e.g., PI3K or ERK or p38 MAPK to promote the production of CXCL5 in liver cancer; (4) CXCL5 activates Ras/MEK/ERK, PI3K/AKT, JAK/STAT, MSK1/Elk-1, Egr-1/cdk4 signal pathways and up-regulates transcript factors such as snail and NF-κB to promoteproliferation, migration, invasion, EMT, and neutrophils chemoattraction.

Figure 1. Regulators of CXCL5 and signal pathways activated by CXCL5. (1) Cytokines such as TNF-α, IL-17, IL-1β, KLF4 or Ron could activate the NF-κB signal pathways to induce CXCL5 production; (2) IL-27 could suppress the expression of CXCL5 though a STAT1-dominant pathway; (3) EGF could activate EGFR-downstream signal pathways e.g., PI3K or ERK or p38 MAPK to promote the production of CXCL5 in liver cancer; (4) CXCL5 activates Ras/MEK/ERK, PI3K/AKT, JAK/STAT, MSK1/Elk-1, Egr-1/cdk4 signal pathways and up-regulates transcript factors such as snail and NF-κB to promoteproliferation, migration, invasion, EMT, and neutrophils chemoattraction.
Supplemental material

IETT_A_993317_SM1869.doc

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