Abstract：
Aim: This study aimed to investigate the role of brain-derived neurotrophic factor (BDNF) in colon adenocarcinoma, specifically its impact on sensitivity to carboplatin. Methods: mRNA and clinical information of colon adenocarcinoma samples were obtained from TCGA database. Differential expression analysis, transcription factor prediction, gene set enrichment analysis were performed in silico. qRT-PCR, western blot, CCK-8 and CHIP assay were employed. Results: BDNF demonstrated high expression in colon adenocarcinoma. Silencing of BDNF enhanced carboplatin sensitivity, while exerting opposite effects on epithelial-mesenchymal transition (EMT). BDNF was enriched in Hedgehog (HH) signaling pathway. SALL4 was identified as an upstream regulator of BDNF. Upregulation of BDNF by SALL4 promoted EMT and inhibited carboplatin sensitivity. Conclusion: SALL4 promoted BDNF expression to facilitate the aggressive phenotypes of colon adenocarcinoma.
[Box: see text].
[Box: see text].
摘要：
目的:探讨脑源性神经营养因子(BDNF)在结肠腺癌中的作用,特别是它对卡铂敏感性的影响。办法：从TCGA数据库获得结肠腺癌标本的mRNA和临床信息。差异表达分析,转录因子预测，在计算机上进行基因集富集分析。qRT-PCR,westernblot,采用CCK-8和CHIP测定。结果:BDNF在结肠腺癌中高表达。沉默BDNF可增强卡铂敏感性，同时对上皮-间质转化（EMT）产生相反的作用。BDNF富集在Hedgehog(HH)信号通路中。SALL4被鉴定为BDNF的上游调节剂。SALL4上调BDNF可促进EMT并抑制卡铂敏感性。结论:SALL4可促进BDNF的表达,促进结肠腺癌的侵袭性表型。
[方框：见正文]。
[方框：见正文]。
