BACKGROUND:Interleukin-8 is an important inflammatory chemokine that plays an important role in the regulation of tumor cel proliferation and angiogenesis.
OBJECTIVE:To investigate the effect of interleukin-8 on the invasion and metastasis of CD133+hepatocel ular carcinoma stem cel s.
METHODS:After isolation and culture of MHCC97-H cel lines, CD133+/CD133-MHCC97-H cel s were sorted using immunomagnetic beads. CD133 expression was detected using flow cytometry, and interleukin-8 level in supernatant was measured using ELISA method. Cloning efficiency, tumorigenic capacity, cel migration and invasion ability were detected through colony formation assay, tumorigenesis experiment in nude mice, and Transwel detection. Additional y, other cel s were neutralized using interleukin-8 neutralizing antibody. Measurement results were compared between cel s undergoing different treatments.
RESULTS AND CONCLUSION:The CD133 level, interleukin-8 level, cloning efficiency and cel membrane permeability of CD133+MHCC97-H cel s were significantly higher than those of CD133-MHCC97-H cel s (P<0.05). Transplantation of CD133+MHCC97-H cel s at 1×106/L and 1×107/L resulted in subcutaneous tumors in some mice, whereas no subcutaneous tumors appeared in mice undergoing transplantation of CD133-MHCC97-H cel s at the same concentrations. After interleukin-8 neutralizing antibody treatment, the CD133 level, interleukin-8 level, and cloning efficiency of CD133+/CD133-MHCC97-H cel s were significantly decreased (P<0.05), especial y in the CD133+MHCC97-H cel s (P<0.01);the migration and invasion ability and cel membrane permeability of CD133+MHCC97-H cel s were significantly reduced (P<0.05), but these changes were not obvious in CD133-MHCC97-H cel s (P>0.05). These results show that interleukin-8 could be specifical y involved in the invasion and metastasis of CD133+MHCC97-H cel s.

BACKGROUND:As the existence of tumor stem cel s, it is difficult to completely eliminate tumors in clinic.
OBJECTIVE:To explore the tumor-kil ing effect of gastric cancer stem cel s as antigen to stimulate dendritic cel s combined with cytokine-induced kil er cel s.
METHODS:Side population cel s from human gastric cancer cel lines were isolated, and tumor antigen was prepared by freeze thawing method. After coculture with dendritic cel s, dendritic cel s combined with cytokine-induced kil er cel s, gastric cancer cel antigen, and gastric cancer stem cel antigen, kil ing rates of gastric cancer cel s were detected using MTT assay. Expression rate of CD83, a mature dendritic cel surface marker, was also detected.
RESULTS AND CONCLUSION:The CD83 expression level and kil ing rate of gastric cancer cel s were both significantly lower in the gastric cancer stem cel antigen group than the other groups (both P<0.05). These results indicate that gastric cancer stem cel s as antigen to stimulate dendritic cel s combined with cytokine-induced kil er cel s can promote the proliferation of gastric cancer cel s and elevate the ability to kil ing gastric cancer cel s.