在乳腺癌原代培养中,表皮生长因子诱导上皮-间充质转变

IF 0.1 Q4 ONCOLOGY
Brizio Moreno-Jaime , José Esparza-López , Andrea Castro-Sánchez , Elizabeth Escobar-Arriaga , Heriberto Medina-Franco , Eucario León-Rodríguez , María de Jesús Ibarra-Sánchez
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引用次数: 1

摘要

脱上皮-间充质转化(EMT)是一个生物过程,在这个过程中,固定的和极化的上皮细胞通过高迁移获得间充质特征。这一过程产生肿瘤细胞骨架的变化,其中E-cadherin的丢失和N-cadherin的获得是EMT的主要生化变化。本研究探讨了表皮生长因子(EGF)在乳腺癌细胞系和原代培养物中诱导EMT的作用。方法采用smcf -7细胞系和原代培养物MBCDF、MBCD25进行实验。EGF连续处理诱导EMT。通过Western blot检测以下标记物:pSTAT3、STAT3、E-cadherin的抑制和Snail的表达,评估间充质egf诱导的表型。结果EGF处理可诱导STAT3磷酸化,而MBCDF、MBCD25和MCF-7中STAT3的表达不发生变化。此外,EGF处理诱导EMT,如5天后E-cadherin和Snail表达的减少所示。结论egf在原发性乳腺癌细胞培养物、MBCDF、MBCD25和MCF-7细胞系中均能诱导EMT。这些结果表明,EGF产生一种假定的侵袭性表型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
El factor de crecimiento epidérmico induce transición epitelio-mesénquima en cultivos primarios de cáncer de mama

Background

Epithelial-mesenchymal transition (EMT) is a biological process where immobile and polarised epithelial cells acquire mesenchymal characteristics with high migration. This process produces changes in the cytoskeleton of the tumour cells, with the loss of E-cadherin and the acquisition of N-cadherin being the main biochemical changes of the EMT. This study investigates the role of epidermal growth factor (EGF) on the EMT induction in breast cancer cell lines and primary cultures.

Methods

MCF-7 cell line and the primary cultures MBCDF and MBCD25 were used in this study. EMT was induced by continuous EGF treatment. Mesenchymal EGF-induced phenotype was evaluated by Western blot of the following markers: pSTAT3, STAT3, repression of E-cadherin, and expression of Snail.

Results

Our results demonstrate that EGF treatment induced STAT3 phosphorylation without changes in STAT3 in MBCDF, MBCD25 and MCF-7. Additionally, EGF treatment induced EMT, as shown by the loss of E-cadherin and Snail expression after 5 days.

Conclusion

EGF was able to induce EMT in primary breast cancer cell cultures, MBCDF, MBCD25, as well as MCF-7 cell line. These results suggest that EGF produces a putative aggressive phenotype.

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