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EIF3A 通过 PI3K/AKT 信号通路介导结直肠癌细胞的恶性生物学行为。

eIf3a mediates malignant biological behaviors in colorectal cancer through the PI3K/AKT signaling pathway.

机构信息

Department of Anus and Intestines, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.

Hongshan Community Hospital, People's Hospital of Longhua District, Shenzhen, Guangdong, China.

出版信息

Cancer Biol Ther. 2024 Dec 31;25(1):2355703. doi: 10.1080/15384047.2024.2355703. Epub 2024 May 23.

DOI:10.1080/15384047.2024.2355703
PMID:38782896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11123456/
Abstract

Colorectal cancer (CRC) is among the most common gastrointestinal malignancies worldwide. eIF3a is highly expressed in a variety of cancer types, yet its role in CRC remains unclear. We introduced ectopic eIF3a expression in CRC cells to investigate its relevance to various malignant behaviors. Further, we silenced eIF3a to explore its effect on tumor growth in a nude mouse tumor xenograft model. Finally, the molecular mechanisms through which eIF3a regulates malignancy in CRC cells were explored through bioinformatics analysis combined with the use of a specific PI3K inhibitor (LY294002). eIF3a was highly expressed in the peripheral blood and cancer tissue of CRC patients. Malignancy and tumor growth were significantly inhibited by silencing eIF3a, while overexpression promoted malignant behaviors, with a positive correlation between PI3K/AKT activation and eIF3a expression. Taken together, eIF3a plays an oncogenic role in CRC by regulating PI3K/AKT signaling and is a potential biomarker for CRC diagnosis and prognostic monitoring.

摘要

结直肠癌（CRC）是全球最常见的胃肠道恶性肿瘤之一。eIF3a 在多种癌症类型中高度表达，但它在 CRC 中的作用尚不清楚。我们在 CRC 细胞中引入异位 eIF3a 表达，以研究其与各种恶性行为的相关性。此外，我们通过沉默 eIF3a 来探索其在裸鼠肿瘤异种移植模型中对肿瘤生长的影响。最后，通过生物信息学分析结合使用特定的 PI3K 抑制剂（LY294002），探索了 eIF3a 调节 CRC 细胞恶性的分子机制。eIF3a 在 CRC 患者的外周血和癌组织中高表达。沉默 eIF3a 显著抑制了恶性和肿瘤生长，而过表达则促进了恶性行为，PI3K/AKT 激活与 eIF3a 表达呈正相关。综上所述，eIF3a 通过调节 PI3K/AKT 信号通路在 CRC 中发挥致癌作用，是 CRC 诊断和预后监测的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6fd16bd0b0b4/KCBT_A_2355703_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/bb52b8e315f0/KCBT_A_2355703_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/390bfe7d3a76/KCBT_A_2355703_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6a93e5e472d8/KCBT_A_2355703_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/3599cde0894d/KCBT_A_2355703_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/20cfee0c642c/KCBT_A_2355703_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6bbe2a37a9b6/KCBT_A_2355703_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/223cc11bef95/KCBT_A_2355703_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6fd16bd0b0b4/KCBT_A_2355703_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/bb52b8e315f0/KCBT_A_2355703_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/390bfe7d3a76/KCBT_A_2355703_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6a93e5e472d8/KCBT_A_2355703_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/3599cde0894d/KCBT_A_2355703_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/20cfee0c642c/KCBT_A_2355703_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6bbe2a37a9b6/KCBT_A_2355703_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/223cc11bef95/KCBT_A_2355703_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56a0/11123456/6fd16bd0b0b4/KCBT_A_2355703_F0008_OC.jpg

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