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CDC45 通过影响细胞周期促进肺腺癌的干性和转移。

CDC45 promotes the stemness and metastasis in lung adenocarcinoma by affecting the cell cycle.

机构信息

School of Medicine, Anhui University of Science and Technology, Chongren Building, No 168, Taifeng St, Huainan, 232001, People's Republic of China.

Anhui Province Engineering Laboratory of Occupational Health and Safety, Anhui University of Science and Technology, Huainan, People's Republic of China.

出版信息

J Transl Med. 2024 Apr 8;22(1):335. doi: 10.1186/s12967-024-05038-5.

DOI:10.1186/s12967-024-05038-5
PMID:38589907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11000299/
Abstract

OBJECTIVE

This study aimed to assess the functions of cell division cycle protein 45 (CDC45) in Non-small cell lung cancer (NSCLC) cancer and its effects on stemness and metastasis.

METHODS

Firstly, differentially expressed genes related to lung cancer metastasis and stemness were screened by differential analysis and lasso regression. Then, in vitro, experiments such as colony formation assay, scratch assay, and transwell assay were conducted to evaluate the impact of CDC45 knockdown on the proliferation and migration abilities of lung cancer cells. Western blotting was used to measure the expression levels of related proteins and investigate the regulation of CDC45 on the cell cycle. Finally, in vivo model with subcutaneous injection of lung cancer cells was performed to verify the effect of CDC45 on tumor growth.

RESULTS

This study identified CDC45 as a key gene potentially influencing tumor stemness and lymph node metastasis. Knockdown of CDC45 not only suppressed the proliferation and migration abilities of lung cancer cells but also caused cell cycle arrest at the G2/M phase. Further analysis revealed a negative correlation between CDC45 and cell cycle-related proteins, stemness-related markers, and tumor mutations. Mouse experiments confirmed that CDC45 knockdown inhibited tumor growth.

CONCLUSION

As a novel regulator of stemness, CDC45 plays a role in regulating lung cancer cell proliferation, migration, and cell cycle. Therefore, CDC45 may serve as a potential target for lung cancer treatment and provide a reference for further mechanistic research and therapeutic development.

摘要

目的

本研究旨在评估细胞分裂周期蛋白 45（CDC45）在非小细胞肺癌（NSCLC）中的作用及其对干性和转移的影响。

方法

首先，通过差异分析和套索回归筛选与肺癌转移和干性相关的差异表达基因。然后，在体外通过集落形成实验、划痕实验和 Transwell 实验评估 CDC45 敲低对肺癌细胞增殖和迁移能力的影响。Western blot 用于测量相关蛋白的表达水平，并研究 CDC45 对细胞周期的调节作用。最后，通过肺癌细胞皮下注射的体内模型验证 CDC45 对肿瘤生长的影响。

结果

本研究确定 CDC45 是一个潜在影响肿瘤干性和淋巴结转移的关键基因。CDC45 敲低不仅抑制了肺癌细胞的增殖和迁移能力，而且导致细胞周期在 G2/M 期停滞。进一步分析显示，CDC45 与细胞周期相关蛋白、干性相关标志物和肿瘤突变呈负相关。小鼠实验证实，CDC45 敲低抑制了肿瘤生长。

结论

作为一种新的干性调节因子，CDC45 在调节肺癌细胞增殖、迁移和细胞周期方面发挥作用。因此，CDC45 可能成为肺癌治疗的潜在靶点，并为进一步的机制研究和治疗开发提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/a5c75c3129e6/12967_2024_5038_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/f43351df2c2d/12967_2024_5038_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/5113b8e19dab/12967_2024_5038_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/57344dc00c6e/12967_2024_5038_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/a5c75c3129e6/12967_2024_5038_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/f43351df2c2d/12967_2024_5038_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/68f9fb8cdf10/12967_2024_5038_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/fe035d59264a/12967_2024_5038_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/d4a78d2ae776/12967_2024_5038_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/231641246e5d/12967_2024_5038_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/892ce0fec249/12967_2024_5038_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/5113b8e19dab/12967_2024_5038_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/57344dc00c6e/12967_2024_5038_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1592/11000299/a5c75c3129e6/12967_2024_5038_Fig9_HTML.jpg

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