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促进结直肠癌进展并作用于BCL2相关X蛋白(BAX)

Promotes Colorectal Cancer Progression and Targets BCL2-Associated X (BAX) Protein.

作者信息

Zeng Xiangyue, Yang Xinhui, Parhatsayim Shayim, Abudoukelimu Abulajiang, Shu Yin, Zhao Zeliang

机构信息

Department of Gastrointestinal Surgery (Inpatient Area 2), Cancer Hospital of Xinjiang Medical University, Urumqi, Xinjiang, 830011, China.

出版信息

Iran J Public Health. 2023 Feb;52(2):306-314. doi: 10.18502/ijph.v52i2.11883.

DOI:10.18502/ijph.v52i2.11883
PMID:37089159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10113591/
Abstract

BACKGROUND

Colorectal cancer is the third most common malignant tumor in the world and substantial death cases are reported each year. We aimed to explore the molecular mechanism underlying colorectal cancer tumor-igenesis and progression.

METHODS

The expression levels of () in colorectal cancer tissues were first analyzed using Gene Expression Profiling Interactive Analysis (GEPIA). More multiple in vitro experiments established the role of in colorectal cancer progression. The potential downstream target of was identified by Western blot analysis.

RESULTS

FOXA2 expression level was significantly up-modulated in colorectal cancer specimens and cells (<0.05). Silencing remarkably inhibited colorectal cancer cells growth, invasion and migration. BCL2-associated X (BAX) protein was identified as a potential downstream protein of .

CONCLUSION

Our findings demonstrated the essential role of in colorectal cancer progression and identified BAX protein as its potential target.

摘要

背景

结直肠癌是全球第三大常见恶性肿瘤,每年有大量死亡病例报告。我们旨在探讨结直肠癌发生和进展的分子机制。

方法

首先使用基因表达谱交互式分析(GEPIA)分析结直肠癌组织中()的表达水平。更多的体外实验确定了()在结直肠癌进展中的作用。通过蛋白质印迹分析确定了()的潜在下游靶点。

结果

FOXA2在结直肠癌标本和细胞中的表达水平显著上调(<0.05)。沉默()可显著抑制结直肠癌细胞的生长、侵袭和迁移。BCL2相关X蛋白(BAX)被确定为()的潜在下游蛋白。

结论

我们的研究结果证明了()在结直肠癌进展中的重要作用,并确定BAX蛋白为其潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/24f4fad06b10/IJPH-52-306-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/a9a80f339f74/IJPH-52-306-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/b5c8017c4153/IJPH-52-306-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/f9c13bf73611/IJPH-52-306-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/36cb501cd3d2/IJPH-52-306-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/24f4fad06b10/IJPH-52-306-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/a9a80f339f74/IJPH-52-306-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/b5c8017c4153/IJPH-52-306-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/f9c13bf73611/IJPH-52-306-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/36cb501cd3d2/IJPH-52-306-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/10113591/24f4fad06b10/IJPH-52-306-g005.jpg

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