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在MCF-7/ADR癌细胞系中鉴定与阿霉素耐药相关的共调控基因。

Identification of co-regulated genes associated with doxorubicin resistance in the MCF-7/ADR cancer cell line.

作者信息

Miri Ali, Gharechahi Javad, Samiei Mosleh Iman, Sharifi Kazem, Jajarmi Vahid

机构信息

Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Human Genetic Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.

出版信息

Front Oncol. 2023 Jun 15;13:1135836. doi: 10.3389/fonc.2023.1135836. eCollection 2023.

DOI:10.3389/fonc.2023.1135836
PMID:37397367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10311417/
Abstract

INTRODUCTION

The molecular mechanism of chemotherapy resistance in breast cancer is not well understood. The identification of genes associated with chemoresistance is critical for a better understanding of the molecular processes driving resistance.

METHODS

This study used a co-expression network analysis of Adriamycin (or doxorubicin)-resistant MCF-7 (MCF-7/ADR) and its parent MCF-7 cell lines to explore the mechanisms of drug resistance in breast cancer. Genes associated with doxorubicin resistance were extracted from two microarray datasets (GSE24460 and GSE76540) obtained from the Gene Expression Omnibus (GEO) database using the GEO2R web tool. The candidate differentially expressed genes (DEGs) with the highest degree and/or betweenness in the co-expression network were selected for further analysis. The expression of major DEGs was validated experimentally using qRT-PCR.

RESULTS

We identified twelve DEGs in MCF-7/ADR compared with its parent MCF-7 cell line, including 10 upregulated and 2 downregulated DEGs. Functional enrichment suggests a key role for RNA binding by IGF2BPs and epithelial-to-mesenchymal transition pathways in drug resistance in breast cancer.

DISCUSSION

Our findings suggested that , , , , , , , , and genes play an important role in doxorubicin resistance and could be targeted for developing novel therapies by chemical synthesis approaches.

摘要

引言

乳腺癌化疗耐药的分子机制尚未完全明确。鉴定与化疗耐药相关的基因对于更好地理解驱动耐药的分子过程至关重要。

方法

本研究利用耐阿霉素（或多柔比星）的MCF-7（MCF-7/ADR）及其亲本MCF-7细胞系进行共表达网络分析，以探究乳腺癌耐药机制。使用GEO2R网络工具从基因表达综合数据库（GEO）获得的两个微阵列数据集（GSE24460和GSE76540）中提取与多柔比星耐药相关的基因。选择共表达网络中度数和/或介数最高的候选差异表达基因（DEG）进行进一步分析。使用qRT-PCR实验验证主要DEG的表达。

结果

与亲本MCF-7细胞系相比，我们在MCF-7/ADR中鉴定出12个DEG，包括10个上调的和2个下调的DEG。功能富集表明IGF2BP的RNA结合和上皮-间质转化途径在乳腺癌耐药中起关键作用。

讨论

我们的研究结果表明， 、 、 、 、 、 、 、 和 基因在多柔比星耐药中起重要作用，可作为通过化学合成方法开发新疗法的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/acea26b1d86a/fonc-13-1135836-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/85e6f678ea09/fonc-13-1135836-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/a2aa65958df9/fonc-13-1135836-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/6a6babfd7c19/fonc-13-1135836-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/817fe8289b89/fonc-13-1135836-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/6f2ccac4190d/fonc-13-1135836-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/7d22e746b725/fonc-13-1135836-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/acea26b1d86a/fonc-13-1135836-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/85e6f678ea09/fonc-13-1135836-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/a2aa65958df9/fonc-13-1135836-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/6a6babfd7c19/fonc-13-1135836-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/817fe8289b89/fonc-13-1135836-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/6f2ccac4190d/fonc-13-1135836-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/7d22e746b725/fonc-13-1135836-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b9/10311417/acea26b1d86a/fonc-13-1135836-g007.jpg

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