B细胞特异性Moloney小鼠白血病病毒整合位点1的敲低削弱了癌症细胞对阿霉素的耐药性。

IF 1.1 4区 医学 Q4 GASTROENTEROLOGY & HEPATOLOGY Arab Journal of Gastroenterology Pub Date : 2023-08-01 DOI:10.1016/j.ajg.2023.02.004
Ning Ma, Sihui Zhao, Wei Yang, Yongfang Wang
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引用次数: 1

摘要

背景与研究目的:B细胞特异性Moloney小鼠白血病病毒整合位点1(BMI-1)与癌症(GC)的进展有关。然而,其在癌症干细胞(GCSC)耐药性中的作用尚不清楚。本研究旨在探讨BMI-1在GC细胞中的生物学功能及其在GC耐药性中的作用。患者和方法:我们在GEPIA数据库和收集的GC患者样本中评估了BMI-1的表达。我们使用siRNA沉默BMI-1来研究GC细胞的细胞增殖和迁移。我们还使用Hoechst 33342染色来验证阿霉素(ADR)对副群(SP)细胞的影响,并测量BMI-1对N-钙粘蛋白、E-钙粘蛋白和耐药性相关蛋白(多药耐药性突变1和肺耐药相关蛋白)表达的影响。最后,我们在STRING和GEPIA数据库中分析了BMI-1相关蛋白。结果:BMI-1 mRNA在GC组织和细胞系中上调,尤其是在MKN-45和HGC-27细胞中。沉默BMI-1降低GC细胞的增殖和迁移。敲除BMI-1显著降低ADR处理的GC细胞中上皮-间质转化进程、耐药蛋白的表达水平和SP细胞的数量。生物信息学分析表明,EZH2、CBX8、CBX4和SUZ12与GC组织中的BMI-1呈正相关。结论:我们的研究表明,BMI-1影响GC细胞的细胞活性、增殖、迁移和侵袭。在ADR处理的GC细胞中,沉默BMI-1基因显著减少SP细胞的数量和耐药蛋白的表达。我们推测,BMI-1的抑制通过影响GCSC增加GC细胞的耐药性,并且EZH2、CBX8、CBX4和SUZ12可能参与BMI-1诱导的GCSC样表型和生存能力的增强。
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B-cell-specific Moloney murine leukemia virus integration site 1 knockdown impairs adriamycin resistance of gastric cancer cells

Background and study aims

The B-cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) is associated with the progression of gastric cancer (GC). However, its role in drug resistance of gastric cancer stem cell (GCSC) remains unclear. This study aimed to explore the biological function of BMI-1 in GC cells and its role in drug resistance of GCSCs.

Patients and methods

We assessed BMI-1 expression in the GEPIA database and in our collected samples from patients with GC. We silenced BMI-1 using siRNA to study the cell proliferation and migration of GC cells. We also used Hoechst 33342 staining to verify the effect of adriamycin (ADR) on side population (SP) cells, and measured the effects of BMI-1 on the expression of N-cadherin, E-cadherin, and drug-resistance-related proteins (multidrug resistance mutation 1 and lung resistance-related protein). Finally, we analyzed BMI-1-related proteins uing the STRING and GEPIA databases.

Results

BMI-1 mRNA was upregulated in GC tissues and cell lines, especially in MKN-45 and HGC-27 cells. Silencing BMI-1 reduced the proliferation and migration of GC cells. Knocking down BMI-1 significantly decreased epithelial-mesenchymal transition progression, expression levels of drug-resistant proteins, and the number of SP cells in ADR-treated GC cells. Bioinformatics analysis showed that EZH2, CBX8, CBX4, and SUZ12 were positively correlated with BMI-1 in GC tissues.

Conclusion

Our study demonstrates that BMI-1 affects the cellular activity, proliferation, migration, and invasion of GC cells. Silencing the BMI-1 gene significantly reduces the number of SP cells and the expression of drug-resistant proteins in ADR-treated GC cells. We speculate that inhibition of BMI-1 increases the drug resistance of GC cells by affecting GCSCs, and that EZH2, CBX8, CBX4, and SUZ12 may participate in BMI-1-induced enhancement of GCSC-like phenotype and viability.

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来源期刊
Arab Journal of Gastroenterology
Arab Journal of Gastroenterology Medicine-Gastroenterology
CiteScore
2.70
自引率
0.00%
发文量
52
期刊介绍: Arab Journal of Gastroenterology (AJG) publishes different studies related to the digestive system. It aims to be the foremost scientific peer reviewed journal encompassing diverse studies related to the digestive system and its disorders, and serving the Pan-Arab and wider community working on gastrointestinal disorders.
期刊最新文献
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