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地榆苷通过上调 PTEN/KLF4/EMT 信号通路抑制非小细胞肺癌细胞转移。

Deguelin Attenuates Non-Small-Cell Lung Cancer Cell Metastasis by Upregulating PTEN/KLF4/EMT Signaling Pathway.

机构信息

Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.

Departments of Medical Oncology and Pathology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.

出版信息

Dis Markers. 2022 May 21;2022:4090346. doi: 10.1155/2022/4090346. eCollection 2022.

DOI:10.1155/2022/4090346
PMID:35637651
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9148257/
Abstract

Non-small-cell lung cancer (NSCLC) is the most common lung cancer and a major cause of cancer mortality worldwide. Deguelin plays a vital inhibitory role in NSCLC initiation and development. However, the downstream mechanism of deguelin-suppressed metastasis of NSCLC cells is still not completely understood. Interestingly, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and Krüppel-like factor 4 (KLF4) also contribute to inhibition of metastasis in NSCLC cells. Here, we demonstrated that deguelin significantly upregulated PTEN and KLF4 expressions and PTEN positively upregulated KLF4 expression in NSCLC cells including A549 and PC9 cells. Moreover, overexpressions of PTEN and KLF4 inhibited the migration and invasion of NSCLC cells, an effect similar to that of deguelin. Furthermore, overexpressions of PTEN and KLF4 could suppress the epithelial-mesenchymal transition (EMT), an effect also similar to that of deguelin. Additionally, deguelin displayed a significant antitumor ability by upregulating PTEN and KLF4 expressions in mice model with NSCLC cells. Together, these results indicated that deguelin could be a potential therapeutic agent through upregulating PTEN and KLF4 expressions for NSCLC therapy.

摘要

非小细胞肺癌（NSCLC）是最常见的肺癌类型，也是全球癌症死亡的主要原因。丹皮酚在非小细胞肺癌的发生和发展中起着至关重要的抑制作用。然而，丹皮酚抑制非小细胞肺癌细胞转移的下游机制仍不完全清楚。有趣的是，第 10 号染色体缺失的磷酸酶和张力蛋白同源物（PTEN）和 Kruppel 样因子 4（KLF4）也有助于抑制非小细胞肺癌细胞的转移。在这里，我们证明丹皮酚能显著上调 PTEN 和 KLF4 的表达，且在包括 A549 和 PC9 细胞在内的非小细胞肺癌细胞中，PTEN 能正向上调 KLF4 的表达。此外，PTEN 和 KLF4 的过表达抑制了非小细胞肺癌细胞的迁移和侵袭，其作用与丹皮酚相似。此外，PTEN 和 KLF4 的过表达还可以抑制上皮-间充质转化（EMT），其作用也与丹皮酚相似。此外，丹皮酚通过上调 NSCLC 细胞模型中的 PTEN 和 KLF4 表达，显示出显著的抗肿瘤能力。综上所述，这些结果表明，丹皮酚可能是一种通过上调 PTEN 和 KLF4 表达来治疗非小细胞肺癌的潜在治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/c5390e52ab00/DM2022-4090346.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/c88ee2c0bf52/DM2022-4090346.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/f20764a87a15/DM2022-4090346.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/5440fdc53468/DM2022-4090346.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/e6f2c2a9c044/DM2022-4090346.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/c5390e52ab00/DM2022-4090346.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/c88ee2c0bf52/DM2022-4090346.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/f20764a87a15/DM2022-4090346.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/328642aa3655/DM2022-4090346.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/5440fdc53468/DM2022-4090346.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/e6f2c2a9c044/DM2022-4090346.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdd8/9148257/c5390e52ab00/DM2022-4090346.006.jpg

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