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POLR1D 沉默通过抑制 PI3K-Akt 通路抑制肺癌细胞的增殖和迁移。

POLR1D silencing suppresses lung cancer cells proliferation and migration via inhibition of PI3K-Akt pathway.

机构信息

Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University, No. 507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.

Institute of Thoracic Oncology, Fudan University, Shanghai, China.

出版信息

J Cardiothorac Surg. 2024 Jun 6;19(1):322. doi: 10.1186/s13019-024-02791-y.

DOI:10.1186/s13019-024-02791-y
PMID:38844975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11155163/
Abstract

AIM

The most common type of cancer that leads to death worldwide is lung cancer. Despite significant surgery and chemotherapy improvements, lung cancer patient's survival rate is still poor. The RNA polymerase I subunit D (POLR1D) gene can induce various cancers. A current study reported that POLR1D plays a vital role in cancer prognosis. However, its biological function in the development of lung cancer remains unclear.

METHODS

Reverse transcription PCR (RT-PCR) measured the relative POLR1D protein expression level in lung cancer cell lines. Lung cancer cell proliferation, migration, and invasion were analyzed by performing cell counting kit-8 (CCK-8), and transwell. The phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) signaling pathway-related protein expressions were examined by Western blotting assay.

RESULTS

POLR1D protein expression was elevated in lung cancer. Lung cancer cell loss-of-function tests showed that POLR1D silencing could attenuate cell viability both in SK-MES-1 and in H2170 cells. Furthermore, silencing POLR1D inhibited SK-MES-1 and H2170 cells proliferation, migration, and invasion. Moreover, SK-MES-1 and H2170 cells' migration and invasion capacity were potentially suppressed by the knockdown of POLR1D. The progression of multiple cancers has been implicated in the PI3K/AKT pathway. Here, we observed that POLR1D silencing suppressed lung cancer progression by inhibition of the PI3K-Akt pathway.

CONCLUSIONS

The study speculated that POLR1D might provide a new potential therapeutic possibility for treating lung cancer patients via targeting PI3K/AKT.

摘要

目的

全球导致死亡的最常见癌症类型是肺癌。尽管手术和化疗有了显著的改进,但肺癌患者的生存率仍然很差。RNA 聚合酶 I 亚基 D(POLR1D)基因可诱发多种癌症。目前的一项研究报告称,POLR1D 在癌症预后中起着至关重要的作用。然而,其在肺癌发展中的生物学功能尚不清楚。

方法

逆转录 PCR(RT-PCR)测量肺癌细胞系中相对 POLR1D 蛋白表达水平。通过细胞计数试剂盒-8(CCK-8)和 Transwell 分析肺癌细胞增殖、迁移和侵袭。通过 Western blot 检测法检测磷酸肌醇 3-激酶/丝氨酸-苏氨酸激酶(PI3K/AKT)信号通路相关蛋白的表达。

结果

POLR1D 蛋白在肺癌中表达上调。肺癌细胞功能丧失试验表明,POLR1D 沉默可减弱 SK-MES-1 和 H2170 细胞的细胞活力。此外,沉默 POLR1D 抑制 SK-MES-1 和 H2170 细胞的增殖、迁移和侵袭。此外,沉默 POLR1D 可能抑制 SK-MES-1 和 H2170 细胞的迁移和侵袭能力。PI3K/AKT 通路与多种癌症的进展有关。在这里,我们观察到 POLR1D 沉默通过抑制 PI3K-Akt 通路抑制肺癌的进展。

结论

该研究推测,通过靶向 PI3K/AKT,POLR1D 可能为治疗肺癌患者提供新的潜在治疗可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/27379077a814/13019_2024_2791_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/cb4b45c6c80b/13019_2024_2791_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/58b4be015cc9/13019_2024_2791_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/6293a6ebd8ef/13019_2024_2791_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/6e5211b30b11/13019_2024_2791_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/27379077a814/13019_2024_2791_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/cb4b45c6c80b/13019_2024_2791_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/58b4be015cc9/13019_2024_2791_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/6293a6ebd8ef/13019_2024_2791_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/6e5211b30b11/13019_2024_2791_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9102/11155163/27379077a814/13019_2024_2791_Fig5_HTML.jpg

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