Jiao Zhuo-Ya, Zhu Yong-Fu, Chen Shu-Tong, Pan Yun-Xia, Song Hang, Chen Feng-Yuan
School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine Hefei 230012, China.
the First Affiliated Hospital of Anhui University of Chinese Medicine Hefei 230012, China.
Zhongguo Zhong Yao Za Zhi. 2024 Jul;49(14):3868-3877. doi: 10.19540/j.cnki.cjcmm.20240412.705.
The study investigated the effect of Compound Shougong Powder(CSGP) on the biological functions of triple-negative breast cancer(TNBC) cells and whether its mechanism of action was related to the epithelial-mesenchymal transition(EMT) signaling pathway. TNBC cells(MDA-MB-231 and BT-549) were treated with different concentrations of CSGP-containing serum. MTS assay was used to detect the effect of CSGP on the proliferation of TNBC cells. The EdU staining was used to detect the effect of CSGP on the proliferation of TNBC cells. Flow cytometry was used to examine the impact of CSGP on apoptosis of TNBC cells. Wound-healing and Transwell assays were used to evaluate the effects of different concentrations of CSGP on the migration and invasion capabilities of TNBC cells. RNA sequencing technology was utilized to elucidate its mechanism. Subsequently, qRT-PCR was performed to measure the mRNA expression levels of E-cadherin, N-cadherin, Slug, Snail, Vimentin, Twist, Zinc finger E-box-Binding homeobox 1(Zeb1), and Zinc finger E-box-Binding homeobox 2(Zeb2). Western blot was used to assess the protein expression levels of Slug, Vimentin, and E-cadherin. After intervention with CSGP, the proliferation of MDA-MB-231 and BT-549 cells significantly decreased, while the apoptosis rate markedly increased. The expression levels of the epithelial marker protein E-cadherin significantly increased, while the expression levels of the EMT-related transcription factors Slug and Vimentin showed a decrease. In conclusion, CSGP inhibits the EMT, thereby suppressing the malignant progression of TNBC.
本研究探讨了复方守宫散(CSGP)对三阴性乳腺癌(TNBC)细胞生物学功能的影响,以及其作用机制是否与上皮-间质转化(EMT)信号通路相关。用不同浓度含CSGP血清处理TNBC细胞(MDA-MB-231和BT-549)。采用MTS法检测CSGP对TNBC细胞增殖的影响。采用EdU染色法检测CSGP对TNBC细胞增殖的影响。采用流式细胞术检测CSGP对TNBC细胞凋亡的影响。采用伤口愈合实验和Transwell实验评估不同浓度CSGP对TNBC细胞迁移和侵袭能力的影响。利用RNA测序技术阐明其作用机制。随后,进行qRT-PCR检测E-钙黏蛋白、N-钙黏蛋白、Slug、Snail、波形蛋白、Twist、锌指E盒结合同源框1(Zeb1)和锌指E盒结合同源框2(Zeb2)的mRNA表达水平。采用蛋白质免疫印迹法评估Slug、波形蛋白和E-钙黏蛋白的蛋白表达水平。经CSGP干预后,MDA-MB-231和BT-549细胞的增殖显著降低,而凋亡率明显升高。上皮标记蛋白E-钙黏蛋白的表达水平显著升高,而EMT相关转录因子Slug和波形蛋白的表达水平则降低。综上所述,CSGP抑制EMT,从而抑制TNBC的恶性进展。