实用肿瘤学杂志 ›› 2024, Vol. 38 ›› Issue (2): 88-95.doi: 10.11904/j.issn.1002-3070.2024.02.003

• 基础研究 • 上一篇    下一篇

DLX2对乳腺癌细胞增殖、迁移、侵袭、凋亡及乳腺癌干细胞特性的影响

孟凡岗, 陈飞, 甄立军   

  1. 大庆龙南医院普外科(大庆 163453)
  • 收稿日期:2023-12-26 修回日期:2024-02-08 出版日期:2024-04-28 发布日期:2024-07-12
  • 通讯作者: 孟凡岗,E-mail:oicqyinlang1999@163.com
  • 作者简介:孟凡岗,男,(1984-),本科,主治医师,从事乳腺癌相关的研究。

Effects of DLX2 on proliferation,migration,invasion,apoptosis of breast cancer cells and characteristics of breast cancer stem cells

MENG Fangang, CHEN Fei, ZHEN Lijun   

  1. Department of General Surgery,Longnan Hospital,Daqing 163453,China
  • Received:2023-12-26 Revised:2024-02-08 Online:2024-04-28 Published:2024-07-12

摘要: 目的 探索调控乳腺癌转移的关键基因,研究DLX2对乳腺癌细胞增殖、迁移、侵袭和凋亡的影响,探讨DLX2调控乳腺癌干细胞特性的作用及机制。方法 构建DLX2基因敲除的乳腺癌细胞系MCF7,使用CCK-8法检测细胞增殖活力,流式细胞术检测细胞凋亡情况,Transwell实验检测细胞迁移和侵袭能力,免疫荧光检测细胞和组织中SOX4表达水平,Western blot实验检测细胞及组织中CD44和ALDH1的蛋白表达情况,TUNEL试剂盒检测组织的凋亡情况,HE染色评估肿瘤组织恶性程度。结果 敲低DLX2后,细胞增殖活力减弱(P<0.001),细胞凋亡水平增加(P<0.001),细胞迁移、侵袭能力下降(P<0.05)。SOX4免疫荧光检测结果显示SOX4表达被抑制。Western blot结果显示细胞干性标志物CD44和ALDH1蛋白表达水平降低(P<0.05)。在Balb/c裸鼠乳腺癌移植瘤模型中,sh-DLX2组的肿瘤体积明显小于模型组(P<0.001),且肿瘤生长缓慢,肿瘤体积和重量也都较模型组低(P<0.05)。sh-DLX2组的凋亡水平较模型组高,SOX4、CD44以及ALDH1的表达与细胞水平一致,均被抑制(P<0.05)。结论 DLX2抑制乳腺癌细胞增殖、迁移和侵袭,促进乳腺癌细胞凋亡,并通过SOX4调控乳腺癌细胞干细胞特性。

关键词: 乳腺癌, DLX2, SOX4, 肿瘤干性

Abstract: Objective The Objective of this study was to explore the key genes regulating the metastasis of breast cancer,determine the effects of DLX2 on proliferation,migration,invasion,and apoptosis of breast cancer cells,and explore the role and mechanism of DLX2 in regulating the characteristics of breast cancer stem cells. Methods A DLX2 gene knockdown breast cancer MCF7 cell line was constructed.The cell viability was detected in breast cancer cells by CCK-8 assay,apoptosis was detected in breast cancer cells by flow cytometry,cell migration and invasive abilities were detected by Transwell assay,the expression of SOX4 protein was detected by immunofluorescence(IF)in breast cancer cells and xenografts,the expression of CD44 and ALDH1 protein was detected in breast cancer cells and xenografts by Western blot,apoptosis was detected in xenografts by TUNEL assay,and the malignancy degree of tumor tissues was assessed by HE staining. Results After knocking down DLX2,the cell viability decreased(P<0.001),apoptosis increased(P<0.001),and cell migration and invasion abilities decreased in breast cancer cells(P<0.05).The results of IF showed that the expression of SOX4 was inhibited.The results of Western blot showed a decrease in the expression of CD44 and ALDH1 proteins in breast cancer cells,which are cellular stemness markers(P<0.05).In the Balb/c nude mouse breast cancer transplantation tumor model,the volume of xenografts in the sh-DLX2 group was significantly smaller than that in the model group(P<0.001),the xenografts grew slowly,and the volume and weight of xenografts were also lower than those of the model group(P<0.05).Apoptosis in the sh-DLX2 group was higher than that in the model group,and the expression of SOX4,CD44 and ALDH1 was consistent with the cellular level,all of which were inhibited(P<0.05). Conclusion DLX2 inhibits proliferation,migration and invasion of breast cancer cells,promotes apoptosis of breast cancer cells,and regulates the characteristics of breast cancer stem cells through SOX4.

Key words: Breast cancer, DLX2, SOX4, Tumor stemness

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