Gastric cancer remains the second leading cause of
cancer-related deaths worldwide. Adjuvant
therapy has been shown to improve survival and is delivered either postoperatively (
chemoradiotherapy) or perioperatively (
chemotherapy) in Western countries. Debate continues regarding which of these approaches is an optimal strategy. Radioresistance in
gastric cancer cells remains a serious concern. B7 homologue 3 (B7-H3, CD276), a newly found member of B7 immunoregulatory family, was found to be expressed in aberrant
gastric cancer cells, and played a direct role in
gastric cancer progression systems in a previous study. With upregulation or downregulation of B7-H3, it was observed that B7-H3 could increase
radiotherapy resistance of
gastric cancer cells by modulating apoptosis, cell cycle progression, and
DNA double-strand breaks. Furthermore, it was found that B7-H3 could regulate baseline levels of cell autophagy. B7-H3 expression was negatively correlated with LC3-B expression in
gastric cancer tissues. It was found that increasing baseline levels of cell autophagy with
rapamycin in B7-H3-overexpressing cells could improve their sensitivity to radiation. This
protein also exerted its function by modulating apoptosis and
DNA double-strand breaks. Overall, it is demonstrated that B7-H3 increases the
radiotherapy resistance of
gastric cancer cells through regulating baseline levels of cell autophagy.