文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

EIF3D 通过上调 RUVBL1 促进结直肠癌对 5-氟尿嘧啶的耐药性。

EIF3D promotes resistance to 5-fluorouracil in colorectal cancer through upregulating RUVBL1.

机构信息

Gastroenterology Department, Liaocheng People's Hospital, Liaocheng, China.

Gastrointestinal Surgery Department, Liaocheng People's Hospital, Liaocheng, China.

出版信息

J Clin Lab Anal. 2023 Jan;37(2):e24825. doi: 10.1002/jcla.24825. Epub 2023 Jan 2.

DOI:10.1002/jcla.24825
PMID:36592991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9937894/
Abstract

BACKGROUND: As EIF3D is oncogenic in colorectal cancer (CRC) and is associated with multidrug resistance, this study aims to investigate whether and how EIF3D regulates resistance to 5-fluorouracil (5-Fu) in CRC. METHODS: EIF3D-associated genes in CRC were predicted using bioinformatics tools. CRC cells and nude mice received 5-Fu treatment. Then, the impacts of EIF3D and the interaction between EIF3D and RUVBL1 on cell viability, colony formation, apoptosis, and DNA damage were detected through MTT, colony formation, flow cytometry, and immunofluorescence assays, and those on in vivo tumorigenesis through murine xenograft assay. IC50 value of 5-Fu for CRC cells was determined by probit regression analysis. Expressions of EIF3D, eIF4E, EIF3D-associated genes, γH2AX, Bcl-2, Bax, and Cleaved Caspase-3/Caspase-3 in CRC tissues, cells, and/or xenograft tumors were analyzed by qRT-PCR and/or Western blot. RESULTS: EIF3D and RUVBL1 were highly expressed and positively correlated with CRC tissues/cells. In CRC cells, except for eIF4E, both EIF3D and RUVBL1 levels were upregulated by 5-Fu treatment; in addition to that, RUVBL1 level was downregulated by EIF3D silencing rather than eIF4E. Meanwhile, EIF3D silencing diminished IC50 value of 5-Fu and potentiated 5-Fu-induced viability decrease, colony formation inhibition, apoptosis promotion, Bcl-2 downregulation, and γH2AX, Bax, and Cleaved Caspase-3/Caspase-3 upregulation but reversed 5-Fu-triggered RUVBL1 upregulation. RUVBL1 overexpression offsets EIF3D silencing-induced viability decrease and apoptosis promotion of 5-Fu-treated CRC cells, and tumorigenesis suppression and apoptosis promotion in 5-Fu-treated mice. CONCLUSION: EIF3D promotes resistance to 5-Fu in CRC through upregulating RUVBL1 level.

摘要

背景：EIF3D 在结直肠癌（CRC）中具有致癌性，并与多药耐药性相关，因此本研究旨在探讨 EIF3D 是否以及如何调节 CRC 对 5-氟尿嘧啶（5-Fu）的耐药性。

方法：使用生物信息学工具预测 CRC 中与 EIF3D 相关的基因。给予 CRC 细胞和裸鼠 5-Fu 处理。然后，通过 MTT、集落形成、流式细胞术和免疫荧光检测 EIF3D 及其与 RUVBL1 的相互作用对细胞活力、集落形成、细胞凋亡和 DNA 损伤的影响，并通过小鼠异种移植实验检测对体内肿瘤发生的影响。通过概率单位回归分析确定 CRC 细胞对 5-Fu 的 IC50 值。通过 qRT-PCR 和/或 Western blot 分析 CRC 组织、细胞和/或异种移植肿瘤中 EIF3D、eIF4E、EIF3D 相关基因、γH2AX、Bcl-2、Bax 和 Cleaved Caspase-3/Caspase-3 的表达。

结果：EIF3D 和 RUVBL1 在 CRC 组织/细胞中高表达且呈正相关。在 CRC 细胞中，除了 eIF4E，5-Fu 处理均上调 EIF3D 和 RUVBL1 水平；此外，EIF3D 沉默而非 eIF4E 下调 RUVBL1 水平。同时，EIF3D 沉默降低了 5-Fu 的 IC50 值，并增强了 5-Fu 诱导的活力下降、集落形成抑制、凋亡促进、Bcl-2 下调以及 γH2AX、Bax 和 Cleaved Caspase-3/Caspase-3 的上调，但逆转了 5-Fu 触发的 RUVBL1 上调。RUVBL1 过表达抵消了 EIF3D 沉默诱导的 5-Fu 处理的 CRC 细胞活力下降和凋亡促进作用，以及 5-Fu 处理的小鼠的肿瘤发生抑制和凋亡促进作用。

结论：EIF3D 通过上调 RUVBL1 水平促进 CRC 对 5-Fu 的耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/5688b1986732/JCLA-37-e24825-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/1ccb42baf5a9/JCLA-37-e24825-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/94e64857bcee/JCLA-37-e24825-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/0ee9200a5df4/JCLA-37-e24825-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/1c020b0d6389/JCLA-37-e24825-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/5c782c4df2ad/JCLA-37-e24825-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/6600856b1818/JCLA-37-e24825-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/c7e24eb36963/JCLA-37-e24825-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/d2c701af9d54/JCLA-37-e24825-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/edec1cc4f506/JCLA-37-e24825-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/5688b1986732/JCLA-37-e24825-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/1ccb42baf5a9/JCLA-37-e24825-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/94e64857bcee/JCLA-37-e24825-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/0ee9200a5df4/JCLA-37-e24825-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/1c020b0d6389/JCLA-37-e24825-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/5c782c4df2ad/JCLA-37-e24825-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/6600856b1818/JCLA-37-e24825-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/c7e24eb36963/JCLA-37-e24825-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/d2c701af9d54/JCLA-37-e24825-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/edec1cc4f506/JCLA-37-e24825-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec63/9937894/5688b1986732/JCLA-37-e24825-g003.jpg

相似文献

[1]
EIF3D promotes resistance to 5-fluorouracil in colorectal cancer through upregulating RUVBL1.

J Clin Lab Anal. 2023-1

[2]
LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer.

Cell Signal. 2020-2

[3]
FOXM1 evokes 5-fluorouracil resistance in colorectal cancer depending on ABCC10.

Oncotarget. 2017-1-31

[4]
The long non-coding RNA HOTAIRM1 suppresses cell progression via sponging endogenous miR-17-5p/ B-cell translocation gene 3 (BTG3) axis in 5-fluorouracil resistant colorectal cancer cells.

Biomed Pharmacother. 2019-6-29

[5]
CircDDX17 reduces 5-fluorouracil resistance and hinders tumorigenesis in colorectal cancer by regulating miR-31-5p/KANK1 axis.

Eur Rev Med Pharmacol Sci. 2020-2

[6]
Knockdown of circ_0004585 enhances the chemosensitivity of colorectal cancer cells to 5-fluorouracil via the miR-874-3p/CCND1 axis.

Histol Histopathol. 2023-1

[7]
Exosome-Mediated Transfer of circ_0000338 Enhances 5-Fluorouracil Resistance in Colorectal Cancer through Regulating MicroRNA 217 (miR-217) and miR-485-3p.

Mol Cell Biol. 2021-4-22

[8]
RUVBL1/2 Blockade Targets YTHDF1 Activity to Suppress m6A-Dependent Oncogenic Translation and Colorectal Tumorigenesis.

Cancer Res. 2024-9-4

[9]
Inhibition of semaphorin 4D enhances chemosensitivity by increasing 5-fluorouracile-induced apoptosis in colorectal cancer cells.

Mol Biol Rep. 2020-9

[10]
Patrinia scabiosaefolia Inhibits Growth of 5-FU-Resistant Colorectal Carcinoma Cells via Induction of Apoptosis and Suppression of AKT Pathway.

Chin J Integr Med. 2019-2

引用本文的文献

[1]
Surface Engineering of MXene and Functional Fullerenols for Cancer Biomarker 'eIFd'.

Langmuir. 2025-4-1

[2]
Identification of a 5-gene signature panel for the prediction of prostate cancer progression.

Br J Cancer. 2024-12

[3]
Development of a diagnostic model based on glycolysis-related genes and immune infiltration in intervertebral disc degeneration.

Heliyon. 2024-8-13

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索