Berberine (BBR) is one of isoquinoline alkaloids from and possesses extensive pharmacological activities, including anti-colorectal cancer (CRC) activity. However, the detailed mechanisms remain to be determined. The current study aims to investigate the ability and the potential mechanism of BBR against CRC. By mining recognized CRC datasets and RNA-seq results of cells and tumors treated with BBR for perform bioinformatics analysis to find key targets IGF2BP3. Overexpression and knockdown of IGF2BP3 assays were used to explore the biological role of IGF2BP3 in the process of BBR against CRC. Our results showed that BBR inhibits proliferation and induces G0/G1 phase arrest in CRC cells by downregulating IGF2BP3. Specifically, Knockdown of IGF2BP3 could suppress the PI3K/AKT pathway to inhibit cell proliferation and cycle transition. The negative effects of BBR in CRC cells could be rescued by overexpressing IGF2BP3. Our data might provide a theoretical basis for the future use of BBR in colorectal cancer prevention.

中文翻译：

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小檗碱通过下调 IGF2BP3 抑制结直肠癌细胞增殖并诱导 G0/G1 期阻滞


小檗碱 (BBR) 是一种异喹啉生物碱，具有广泛的药理活性，包括抗结直肠癌 (CRC) 活性。然而，详细机制仍有待确定。本研究旨在探讨 BBR 对抗 CRC 的能力和潜在机制。通过挖掘公认的CRC数据集以及BBR处理的细胞和肿瘤的RNA-seq结果进行生物信息学分析，以找到IGF2BP3的关键靶点。通过过表达和敲低 IGF2BP3 检测来探讨 IGF2BP3 在 BBR 对抗 CRC 过程中的生物学作用。我们的结果表明，BBR 通过下调 IGF2BP3 抑制 CRC 细胞增殖并诱导 G0/G1 期停滞。具体来说，敲除 IGF2BP3 可以抑制 PI3K/AKT 通路，从而抑制细胞增殖和周期转变。 BBR 对 CRC 细胞的负面影响可以通过过度表达 IGF2BP3 来缓解。我们的数据可能为未来 BBR 在结直肠癌预防中的应用提供理论基础。