Table 1.

Possible therapeutic approaches based on CXCL17/CXCR8 targeting

Strategy	Details of study	Outcomes	Ref
Deletion of CXCL17	¬ cSCC ¬ Animal model ¬ Metastatic and non-metastatic cSCC cells	¬ ↓ Tumor cell proliferation ¬ ↓ Migration and invasion ¬ Suppressing the AKT/mTOR/STAT3 pathways ¬ ↓ The expression of the CD31 biomarker and neovascularization	(Khandelwal et al. 2022)
Inhibiting CXCL17	¬ Lung adenocarcinoma	¬ ↓ Monocyte migration and TAMs to the lung ¬ ↓ The Src/FAK pathway signals ¬ ↓ Polarization of TAMs to the M2 phenotype ¬ ↓ Infiltration of immunosuppressive cells	(Liu et al. 2020)
CXCL17 silencing + CA	¬ HCC ¬ In vitro	¬ ↑ LKB1/AMPK pathway ¬ ↑ Autophagy in tumor cells ¬ Inhibiting VEGFR2/Src/FAK/cdc42 axis ¬ ↓ F-actin formation and reducing HCC cell locomotion ¬ ↓ Tumor growth	(Ku et al. 2015; Wang et al. 2019)
CXCL17 targeting by miR-325-3p	¬ HCC	¬ ↓ CXCL17 activity ¬ ↓ Tumor progression	(Li et al. 2021)
CXCL17 and miR-1252-3p targeting by THUMPD3-AS1	¬ GC	¬ ↓ CXCL17 activity ¬ ↓ Tumor progression	(Tan et al. 2022)
CXCL17 deletion	¬ cSCC ¬ In vitro/ animal model ¬ SCCB cells	¬ ↓ CXCL17 activity ¬ ↓ Infiltration of macrophages, Tregs, and MDSCs ¬ ↓ Tumor progression	(Khandelwal et al. 2020)
Knockdown of CXCR8	¬ NSCLC ¬ in vitro and in vivo	¬ ↓ Tumor cell chemoresistance in NSCLC	(Wang et al. 2018)
Genetic depletion of CXCR8	¬ Colon cancer ¬ Animal model	¬ ↓ ion transportation via the Na/K-ATPase channel ¬ ↓ Src signaling ¬ ↓ tumor growth via the epidermal growth factor receptor/Src/Ras/ERK pathway ¬ ↓ Intestinal tumorigenesis	(Kim et al. 2009; Schneditz et al. 2019)
Pepducin	¬ Colitis ¬ CRC	¬ ↓ CXCR8 activation ¬ ↓ Tumor burden	(Quon et al. 2020)
Pamoic acid	¬ Colitis ¬ DSS-induced colitis mouse model	¬ ↑ CXCR8 activation ¬ ↓ Chronic inflammation ¬ ↑ Lipid metabolism ¬ ↓ The severity of the disease	(Tsukahara et al. 2017)