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

IF 4.4 4区 医学 Q2 ONCOLOGY Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-23 DOI:10.1080/15384047.2024.2355703
Chao Huo, Disheng Wu, Xiaodan Li, Yan Zhang, Baoguang Hu, Taoming Zhang, Jianwei Ren, Tianbao Wang, Yi Liu
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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.

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eIf3a 通过 PI3K/AKT 信号通路介导结直肠癌的恶性生物学行为。
大肠癌(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中的作用仍不清楚。我们在 CRC 细胞中引入了 eIF3a 的异位表达,以研究它与各种恶性行为的相关性。此外,我们还在裸鼠肿瘤异种移植模型中沉默了 eIF3a,以探讨其对肿瘤生长的影响。最后,我们通过生物信息学分析,结合使用特异性 PI3K 抑制剂(LY294002),探讨了 eIF3a 调节 CRC 细胞恶性程度的分子机制。沉默eIF3a能显著抑制恶性肿瘤的发生和生长,而过表达则会促进恶性行为,PI3K/AKT的激活与eIF3a的表达呈正相关。综上所述,eIF3a通过调控PI3K/AKT信号在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。
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来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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