Table 3.
Summary of studies evaluating the role of TANs in HCC therapy.
| Study (year) | Study Subjects | Outcome |
|---|---|---|
| Zhou et al. [56] (2016) | Human/Animal | The combination of sorafenib and TAN depletion inhibits tumor growth and neovascularization to a greater extent than sorafenib alone |
| Calvente et al. [61] (2019) | Animal | Neutrophils contribute to spontaneous resolution of liver inflammation and fibrosis via microRNA-223 mediated activation of restorative macrophages that release IL-10 |
| He et al. [67] (2017) | Animal | Deletion of the ICAM-1 gene ameliorates neutrophil infiltration and liver injury in miR-223 knockout mice |
| He et al. [69] (2019) | Human/Animal | Neutrophil-expressed miR-223 hinders the progression of HCC by targeting multiple inflammatory and oncogenic genes |
| Finisguerra et al. [70] (2015) | Human/Animal | Administration of MET kinase inhibitor counters the therapeutic benefit of MET targeting in cancer cells by the pro-tumoral effect arising from MET blockade in neutrophils |
| Marques et al. [84] (2012) | Human/Animal | Blockage of neutrophil infiltration by GR-1 depletion or combined CXCR2-FPR1 antagonism significantly prevents hepatotoxicity |
| Zhou et al. [85] (2018) | Animal | Blockade of CXCL1 or ICAM-1 expression reduces hepatic neutrophil infiltration and ameliorates liver injury and fibrosis |
| Imai et al. [93] (2005) | Human | The increased invasive activity of tumor cells co-cultured with neutrophils in patients with HCC is significantly suppressed by the addition of anti-HGF antibody |
| Yang et al. [76] (2020) | Human/Animal | Inhibition of TLR4/9-COX2 signaling abrogates the NET-aroused metastatic potential of HCC |
TAN: tumor-associated neutrophil; HCC: hepatocellular carcinoma; HGF: hepatocyte growth factor; GR-1: anti-granulocyte receptor-1; CXCR: C-X-C motif chemokine receptor; FPR: formyl peptide receptor; MET: hepatocyte growth factor receptor; ICAM: intercellular adhesion molecule; miR: microRNA; CXCL: chemokine C-X-C motif ligand; TLR: toll-like receptor; IL: interleukin; COX: cyclooxygenase; NET: neutrophil extracellular trap.