TY - JOUR
T1 - Blocking CXCR3B Expression Increases Tumor Aggressiveness in Hepatocellular Carcinoma
AU - Lee, Hwan Hee
AU - Oh, Seoyeon
AU - Kang, Hyojeung
AU - Cho, Hyosun
N1 - Publisher Copyright:
© 2024 International Institute of Anticancer Research. All rights reserved.
PY - 2024/12
Y1 - 2024/12
N2 - Background/Aim: CXCR3B has been positively involved in the inhibition of cancer and angiogenesis. The present study investigated the role of CXCR3B in a cell model of hepatocellular carcinoma, SK-Hep1. Materials and Methods: The blockade of CXCR3B expression in SK-Hep1 was investigated in terms of cell viability, cell cycle, and cell apoptosis using MTT assay and flow cytometry. In addition, the effect of blocking CXCR3B expression on cell migration and invasion was examined using scratch motility, transwell migration, and invasion assays. Furthermore, the cytotoxic effect of NK-92 cells against CXCR3B blocked SK-Hep1 was analyzed using the CytoTox96 assay, and the expression of NKp30+, NKG2D+, and NKG2C+ on NK-92 cells in a coculture with SK-Hep1 was measured using flow cytometry. Results: Blocking CXCR3B expression had no effect on the viability, cell cycle or apoptosis of SK-Hep1 cells. However, blockade of CXCR3B expression significantly increased the migratory and invasive ability of SK-Hep1 along with increased protein expression of slug, vimentin, and N-cadherin. CXCR3B blockade reduced the cytotoxicity of NK-92 against SK-Hep1 and inhibited the expression of activating receptors, NKp30+, NKG2D+, and NKG2C+ in NK-92 cells. Conclusion: CXCR3B may play a positive role in suppressing HCC by attenuating natural killer cell cytotoxicity against HCC.
AB - Background/Aim: CXCR3B has been positively involved in the inhibition of cancer and angiogenesis. The present study investigated the role of CXCR3B in a cell model of hepatocellular carcinoma, SK-Hep1. Materials and Methods: The blockade of CXCR3B expression in SK-Hep1 was investigated in terms of cell viability, cell cycle, and cell apoptosis using MTT assay and flow cytometry. In addition, the effect of blocking CXCR3B expression on cell migration and invasion was examined using scratch motility, transwell migration, and invasion assays. Furthermore, the cytotoxic effect of NK-92 cells against CXCR3B blocked SK-Hep1 was analyzed using the CytoTox96 assay, and the expression of NKp30+, NKG2D+, and NKG2C+ on NK-92 cells in a coculture with SK-Hep1 was measured using flow cytometry. Results: Blocking CXCR3B expression had no effect on the viability, cell cycle or apoptosis of SK-Hep1 cells. However, blockade of CXCR3B expression significantly increased the migratory and invasive ability of SK-Hep1 along with increased protein expression of slug, vimentin, and N-cadherin. CXCR3B blockade reduced the cytotoxicity of NK-92 against SK-Hep1 and inhibited the expression of activating receptors, NKp30+, NKG2D+, and NKG2C+ in NK-92 cells. Conclusion: CXCR3B may play a positive role in suppressing HCC by attenuating natural killer cell cytotoxicity against HCC.
KW - CXCR3B
KW - HCC
KW - NK cells
KW - SK-Hep1
UR - http://www.scopus.com/inward/record.url?scp=85211421308&partnerID=8YFLogxK
U2 - 10.21873/anticanres.17357
DO - 10.21873/anticanres.17357
M3 - Article
C2 - 39626933
AN - SCOPUS:85211421308
SN - 0250-7005
VL - 44
SP - 5293
EP - 5301
JO - Anticancer Research
JF - Anticancer Research
IS - 12
ER -