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TRIM66 通过靶向 MMP9 促进非小细胞肺癌细胞的恶性进展。

TRIM66 Promotes Malignant Progression of Non-Small-Cell Lung Cancer Cells via Targeting MMP9.

机构信息

Department of Oncology, Affiliated Hospital of Jiaxing University, No. 1882, Zhonghuan South Road, Nanhu District, Jiaxing, Zhejiang Province 314001, China.

Department of Respiratory Medicine, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang Province 314001, China.

出版信息

Comput Math Methods Med. 2022 Jul 21;2022:6058720. doi: 10.1155/2022/6058720. eCollection 2022.

DOI:10.1155/2022/6058720
PMID:35912155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9334090/
Abstract

Lung cancer has a higher incidence and mortality rate than other cancers, and over 80% of lung cancer cases were classified as non-small-cell lung cancer (NSCLC). TRIM66 is one of the crucial members of TRIM, which has a deep connection with the behavior of various malignant tumors. But it remains uncertain regarding its exact function and underlying mechanism in NSCLC. In our study, qRT-PCR and Western blot were employed to validate that TRIM66 was overexpressed in NSCLC. The migration, invasion, and epithelial-mesenchymal transformation (EMT) progression of NSCLC cells were determined by Western blotting and Transwell experiments after knocking down TRIM66, and it was found that knockdown TRIM66 inhibited the migration, invasion, and EMT processes of NSCLC cells. Next, the binding relationship between TRIM66 and MMP9 was verified by Co-IP assay. After determining the interaction between them, rescue assays showed that overexpression of MMP9 was capable to promote the migration, invasion, and EMT of NSCLC cells. However, the transfection of si-TRIM66 could reverse this facilitating effectiveness. To sum up, we concluded that by targeting MMP9, TRIM66 could exert a cancer-promoting role in the progression of NSCLC cells.

摘要

肺癌的发病率和死亡率均高于其他癌症,超过 80%的肺癌病例被归类为非小细胞肺癌(NSCLC)。TRIM66 是 TRIM 家族的关键成员之一,与各种恶性肿瘤的行为有很深的联系。但它在 NSCLC 中的确切功能和潜在机制仍不确定。在我们的研究中,qRT-PCR 和 Western blot 被用来验证 TRIM66 在 NSCLC 中过表达。敲低 TRIM66 后,通过 Western blot 和 Transwell 实验确定了 NSCLC 细胞的迁移、侵袭和上皮-间充质转化(EMT)进程,结果发现敲低 TRIM66 抑制了 NSCLC 细胞的迁移、侵袭和 EMT 过程。接下来,通过 Co-IP 测定验证了 TRIM66 和 MMP9 之间的结合关系。确定它们之间的相互作用后,挽救实验表明过表达 MMP9 能够促进 NSCLC 细胞的迁移、侵袭和 EMT。然而,si-TRIM66 的转染可以逆转这种促进作用。总之,我们得出结论,通过靶向 MMP9,TRIM66 可以在 NSCLC 细胞的进展中发挥促进癌症的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/b412a089ef15/CMMM2022-6058720.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/97e050daa0ef/CMMM2022-6058720.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/8b494a36e3fd/CMMM2022-6058720.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/62dd42a9f93f/CMMM2022-6058720.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/b412a089ef15/CMMM2022-6058720.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/97e050daa0ef/CMMM2022-6058720.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/8b494a36e3fd/CMMM2022-6058720.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/62dd42a9f93f/CMMM2022-6058720.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc16/9334090/b412a089ef15/CMMM2022-6058720.004.jpg

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1
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2
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Life Sci. 2019 Oct 15;235:116799. doi: 10.1016/j.lfs.2019.116799. Epub 2019 Aug 28.
3
Overexpression of matrix metalloproteinase-9 in breast cancer cell lines remarkably increases the cell malignancy largely via activation of transforming growth factor beta/SMAD signalling.
[小细胞肺癌骨转移机制及诊断标志物的研究进展]
Zhongguo Fei Ai Za Zhi. 2024 Sep 20;27(9):697-703. doi: 10.3779/j.issn.1009-3419.2024.106.24.
4
Enhancing the revelation of key genes and interaction networks in non-small cell lung cancer with major depressive disorder: A bioinformatics analysis.增强对伴有重度抑郁症的非小细胞肺癌中关键基因及相互作用网络的揭示:一项生物信息学分析
Health Sci Rep. 2024 Jun 25;7(6):e2167. doi: 10.1002/hsr2.2167. eCollection 2024 Jun.
5
Diagnostic value of matrix metalloproteinases 2, 7 and 9 in urine for early detection of colorectal cancer.尿液中基质金属蛋白酶2、7和9对早期结直肠癌的诊断价值
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Cell Prolif. 2019 Sep;52(5):e12633. doi: 10.1111/cpr.12633. Epub 2019 Jul 2.
4
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9
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10
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