结肠癌是全球癌症死亡的第三大原因。虽然自1970年以来，早期筛查和治疗技术的进步已经减少了死亡率，但需要找到治疗干预的新靶点以解决肿瘤的异质性和复发问题。先前的工作已经确定醛脱氢酶1B1(ALDH1B1)在结肠肿瘤发生中起到了关键作用。为了进一步研究这个问题，我们利用了一个人类结肠腺癌细胞系(SW480)，通过shRNA使ALDH1B1蛋白表达降低了80%。通过多组学（转录组学、蛋白质组学和非靶向代谢组学）分析，我们确定了ALDH1B1 RNA干扰对结肠癌细胞分子特征的影响。抑制ALDH1B1表达导致了357个差异表达基因(DEGs)、191个差异表达蛋白(DEPs)和891个差异代谢物(DAMs)。功能注释和富集分析表明：(1) DEGs在整合素连接激酶(ILK)信号通路和生长发育途径中富集；(2) DEPs主要涉及凋亡信号和细胞应激反应通路；(3) DAMs与生物合成、细胞间和第二信使信号传导相关。总之，本研究提供了与ALDH1B1的细胞功能相关的新的分子信息，有助于引导对结肠癌的未来研究。版权所有 © 2023 Elsevier B.V. 发表。

Colon cancer is the third leading cause of cancer death globally. Although early screenings and advances in treatments have reduced mortality since 1970, identification of novel targets for therapeutic intervention is needed to address tumor heterogeneity and recurrence. Previous work identified aldehyde dehydrogenase 1B1 (ALDH1B1) as a critical factor in colon tumorigenesis. To investigate further, we utilized a human colon adenocarcinoma cell line (SW480) in which the ALDH1B1 protein expression has been knocked down by 80% via shRNA. Through multi-omics (transcriptomics, proteomics, and untargeted metabolomics) analysis, we identified the impact of ALDH1B1 knocking down (KD) on molecular signatures in colon cancer cells. Suppression of ALDH1B1 expression resulted in 357 differentially expressed genes (DEGs), 191 differentially expressed proteins (DEPs) and 891 differentially altered metabolites (DAMs). Functional annotation and enrichment analyses revealed that: (1) DEGs were enriched in integrin-linked kinase (ILK) signaling and growth and development pathways; (2) DEPs were mainly involved in apoptosis signaling and cellular stress response pathways; and (3) DAMs were associated with biosynthesis, intercellular and second messenger signaling. Collectively, the present study provides new molecular information associated with the cellular functions of ALDH1B1, which helps to direct future investigation of colon cancer.Copyright © 2023. Published by Elsevier B.V.