Neuroblastoma (NB) is a type of solid extracranial tumor that usually occurs in babies and children. Chemotherapy is a common method for NB treatment, however, the drug resistance exerts during the chemotherapy of NB. Galectin-1 is a member of galectin family and plays a potent role in the development of chemotherapy and radiotherapy resistance. However, the effect of galectin-1 on cisplatin resistance in NB remains unknown. The present study aimed to investigate the role of galectin-1 in cisplatin resisitance and the potential mechanism. Human neuroblastoma SH-SY5Y and SK-N-SH cells were treated with cisplatin and/or galectin-1/siRNA targeting galectin-1 (si-Gal-1). The cell viability was measured by MTT assay. The IC₅₀ values for cisplatin of neuroblastoma cells were calculated. The expression levels of autophagy markers including microtubule-associated protein light chain 3 (LC3B), Beclin-1, and p62 were detected by western blot. We found that cisplatin inhibited cell viability of SH-SY5Y and SK-N-SH in a dose-dependent manner. Cisplatin induced the ratio of LC3B-II/LC3B-I and Beclin-1 expression, and inhibited the p62 expression. Knockdown of galectin-1 decreased the IC₅₀ for cisplatin of SH-SY5Y and SK-N-SH cells and inhibited cisplatin-induced autophagy. Moreover, inhibition of autophagy suppressed galectin-1-induced increase in IC₅₀ for cisplatin. In conclusion, galectin-1 knockdown enhanced cisplatin sensitivity of neuroblastoma cells by inhibiting autophagy. The findings might provid a novel therapeutic target to overcome cisplatin resistance in chemotherapy of NB.

神经母细胞瘤（NB）是一类实体颅外肿瘤，通常发生在婴儿和儿童中。化学疗法是NB治疗的一种常见方法，但是，在NB的化学疗法中会产生耐药性。Galectin-1是Galectin家族的成员，在化学疗法和放疗耐药性的发展中起着重要作用。但是，galectin-1对NB中顺铂耐药性的影响仍然未知。本研究旨在探讨galectin-1在顺铂耐药性中的作用及其潜在机制。用顺铂和/或galectin-1 / siRNA靶向galectin-1（si-Gal-1）处理人神经母细胞瘤SH-SY5Y和SK-N-SH细胞。通过MTT测定法测量细胞活力。IC ₅₀计算成神经细胞瘤细胞的顺铂值。通过蛋白质印迹检测自噬标志物的表达水平，包括微管相关蛋白轻链3（LC3B），Beclin-1和p62。我们发现顺铂以剂量依赖性方式抑制SH-SY5Y和SK-N-SH的细胞活力。顺铂诱导LC3B-II / LC3B-1和Beclin-1的表达比例，并抑制p62的表达。galectin-1的组合降低SH-SY5Y和SK-N-SH细胞顺铂的IC ₅₀并抑制顺铂诱导的自噬。此外，自噬的抑制抑制了galectin-1诱导的IC ₅₀升高用于顺铂。总之，galectin-1敲低通过抑制自噬增强神经母细胞瘤细胞的顺铂敏感性。该发现可能为克服NB化疗中顺铂耐药性提供了新的治疗靶点。