Tumors with KIR3DL2 mutations expressed low levels of
CXCL5 and its receptor CXCR1 and CXCR2, a potential mechanism of resistance to tipifarnib.
Chronic inflammation is the early pathological characteristic, including abnormal expression of inflammatory cytokines such as monocyte chemoattractant protein 1 (MCP-1) or chemokine C-X-C motif ligand 5 (
CXCL5) [1].
In vitro studies revealed that IL-6 transsignaling increases chemokine activation of
CXCL5, CXCL6, and CCL8 [16].
The expression of other Th1/Th17-related soluble factors (IL22, NFKB1, IL23A, STAT3, CCR5, IL17RA, CX3CL1, CXCL12, and
CXCL5) was also assessed by RT-PCR, and the amount of mRNA calculated as above described.
Sharma, "Increased serum CXCL1 and
CXCL5 are linked to obesity, hyperglycemia, and impaired islet function," The Journal of Endocrinology, vol.
Li, "Curcumin suppresses NTHi-induced
CXCL5 expression via inhibition of positive IKK[beta] pathway and up-regulation of negative MKP-1 pathway," Scientific Reports, vol.