Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Department of Pharmacy, Luzhou Naxi District People's Hospital, Luzhou 646000, China.
J Tradit Chin Med. 2023 Oct;43(5):876-886. doi: 10.19852/j.cnki.jtcm.20230802.004.
To detect the effects of active compounds of Caodoukou () (ACAK) on the proliferation, migration and invasion of pancreatic cancer, and explain the possible molecular mechanism of ACAK interacting with these processes.
Cell counting kit-8 method, cell scratch repair experiment, Transwell migration and invasion experiment, immunohistochemistry, western blot assay and real-time polymerase chain reaction experiment were used to evaluate the effect of ACAK on the proliferation, migration and invasion of pancreatic cancer cells. The levels of active molecules involved in the phosphoinosmde-3-kinase (PI3K)/Akt/the mammalian target of rapamycin (mTOR) signal transduction were detected by Western blot assay. In addition, the function of ACAK was evaluated by xenotransplantation tumor model in nude mice.
The inhibitory effect of ACAK on the proliferation of pancreatic cancer cells showed certain time-dose dependence. The results of scratch repair test, Transwell test, Western blotting and real time polymerase chain reaction assay showed that ACAK could inhibit the migration and invasion of pancreatic cancer cells . In addition, the regulatory effect of ACAK on epithelial-mesenchymal transition (EMT) is partly attributed to PI3K/Akt/mTOR signaling pathway. The experimental results showed that ACAK regulated the development of pancreatic cancer.
ACAK can partly inhibit the activity of EMT and matrix metallopeptidases by down-regulating the downstream proteins of PI3K/Akt/mTOR signal pathway, thus inhibiting the ability of migration and invasion of pancreatic cancer.
检测草豆蔻素（ACAK）活性成分对胰腺癌增殖、迁移和侵袭的影响，并阐明 ACAK 与这些过程相互作用的可能分子机制。
采用细胞计数试剂盒-8 法、细胞划痕修复实验、Transwell 迁移和侵袭实验、免疫组织化学法、Western blot 法和实时聚合酶链反应实验，评估 ACAK 对胰腺癌细胞增殖、迁移和侵袭的影响。Western blot 法检测磷酸肌醇 3-激酶（PI3K）/Akt/哺乳动物雷帕霉素靶蛋白（mTOR）信号转导中涉及的活性分子的水平。此外，通过裸鼠异种移植肿瘤模型评估 ACAK 的功能。
ACAK 对胰腺癌增殖的抑制作用呈一定的时间-剂量依赖性。划痕修复试验、Transwell 试验、Western blot 法和实时聚合酶链反应试验结果表明，ACAK 可抑制胰腺癌细胞的迁移和侵袭。此外，ACAK 对上皮-间充质转化（EMT）的调节作用部分归因于 PI3K/Akt/mTOR 信号通路。实验结果表明，ACAK 调控胰腺癌的发生发展。
ACAK 通过下调 PI3K/Akt/mTOR 信号通路的下游蛋白，部分抑制 EMT 和基质金属蛋白酶的活性，从而抑制胰腺癌的迁移和侵袭能力。
