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CUEDC1 通过 TβRI/Smad 信号通路抑制上皮-间充质转化，抑制非小细胞肺癌肿瘤进展。

CUEDC1 inhibits epithelial-mesenchymal transition via the TβRI/Smad signaling pathway and suppresses tumor progression in non-small cell lung cancer.

机构信息

The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.

Department of Orthopedic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

出版信息

Aging (Albany NY). 2020 Oct 25;12(20):20047-20068. doi: 10.18632/aging.103329.

DOI:10.18632/aging.103329
PMID:33099540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7655170/
Abstract

Lung cancer remains the most lethal cancer worldwide because of its high metastasis potential. Epithelial-mesenchymal transition (EMT) is known as the first step of the metastasis cascade, but the potential regulatory mechanisms of EMT have not been clearly established. In this study, we first found that low CUEDC1 expression correlated with lymph node metastasis in non-small cell lung cancer (NSCLC) patients using immunohistochemistry (IHC). CUEDC1 knockdown promoted the metastasis of NSCLC cells and EMT process and activated TβRI/Smad signaling pathway. Overexpression of CUEDC1 decreased the metastatic potential of lung cancer cells and inhibited the EMT process and inactivated TβRI/Smad signaling pathway. Immunoprecipitation (IP) assays showed that Smurf2 is a novel CUEDC1-interacting protein. Furthermore, CUEDC1 could regulate Smurf2 expression through the degradation of Smurf2. Overexpression of Smurf2 abolished CUEDC1 knockdown induced-EMT and the activation of TβRI/Smad signaling pathway, while siRNA Smurf2 reversed CUEDC1 overexpression-mediated regulation of EMT and TβRI/Smad signaling pathway. Additionally, CUEDC1 inhibited proliferation and promoted apoptosis of NSCLC cells. , CUEDC1-knockdown cells promoted metastasis and tumor growth compared with control cells. In conclusion, our findings indicate that the crucial role of CUEDC1 in NSCLC progression and provide support for its clinical investigation for therapeutic approaches.

摘要

肺癌仍然是全球最致命的癌症，因为它具有很高的转移潜力。上皮-间充质转化（EMT）被认为是转移级联的第一步，但 EMT 的潜在调节机制尚未明确确立。在这项研究中，我们首先通过免疫组织化学（IHC）发现低 CUEDC1 表达与非小细胞肺癌（NSCLC）患者的淋巴结转移相关。CUEDC1 敲低促进了 NSCLC 细胞的转移和 EMT 过程，并激活了 TβRI/Smad 信号通路。CUEDC1 的过表达降低了肺癌细胞的转移潜力，并抑制了 EMT 过程和失活了 TβRI/Smad 信号通路。免疫沉淀（IP）实验表明，Smurf2 是 CUEDC1 的一种新型相互作用蛋白。此外，CUEDC1 可以通过降解 Smurf2 来调节 Smurf2 的表达。Smurf2 的过表达消除了 CUEDC1 敲低诱导的 EMT 和 TβRI/Smad 信号通路的激活，而 siRNA Smurf2 逆转了 CUEDC1 过表达介导的 EMT 和 TβRI/Smad 信号通路的调节。此外，CUEDC1 抑制了 NSCLC 细胞的增殖并促进了其凋亡。在体内实验中，与对照细胞相比，CUEDC1 敲低细胞促进了转移和肿瘤生长。总之，我们的研究结果表明 CUEDC1 在 NSCLC 进展中起着关键作用，并为其临床研究提供了治疗方法的支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/5ef3d6b7b454/aging-12-103329-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/f6d9ad287c6b/aging-12-103329-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/1646d618da9b/aging-12-103329-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/5ef3d6b7b454/aging-12-103329-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/f6d9ad287c6b/aging-12-103329-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/848c490cf9ce/aging-12-103329-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/ef8f63961615/aging-12-103329-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/a8764f88aa06/aging-12-103329-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc6e/7655170/5ef3d6b7b454/aging-12-103329-g008.jpg

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