The activity of the Nrf2/Keap1 pathway regulates A549 Non-small-cell Lung Cancer (NSCLC) cells motility through RhoAROCK1 pathway

Jiahao Wu
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Abstract

Purpose: It is observed that Nrf2 transcription factors initiate the production of proteins that play a role in regulating tumor growth, the study aims to discover whether Nrf2 will regulate cell motility in A549 NSCLC cells. The ROCK-RhoA pathway is a significant contributor to cell growth and migration, which can relate to cell motility. There might be a connection between Nrf2 and ROCK-RhoA pathway, the study aims to see whether Nrf2 regulates A549 NSCLC cell motility through ROCK-RhoA pathway. Method: The study will use wound healing assay to visualize cell motility, comparison is made between positive control group(A549 cells treated with brusatol) and negative control group(A549 cells not treated with brusatol), respectively representing the expression level of Nrf2 where it is inhibited or normal. The pathway by which Nrf2 regulates cell motility is studied by western blotting and chemiluminescence. Possible result: There are four main possible results: (1), Nrf2 regulates cell motility in A549 NSCLC cells, the pathway involved in this regulation is ROCK-RhoA pathway. (2), Nrf2 regulates cell motility in A549 cells, however, the pathway involved in this regulation requires further studies to decide. (3), There is no obvious correlation between Nrf2 expression level and cell motility, the inhibition of Nrf2 results in change of expression level of the ROCK-RhoA pathway, however. (4), There is no obvious correlation between Nrf2 expression level and cell motility, ROCK-RhoA pathway is not significantly affected by inhibition of Nrf2 expression, further studies are needed to decide pathways involved. Conclusion: The result of this study provides valuable insights for studying the role of Nrf2 in regulating cell motility and the pathway in the process. It would improve understanding of Nrf2 transcription factor, and how it interacts with pathways to carry out regulation of cell motility. The study also provides future possibilities in terms of cancer treatment and development of gene-based medicine.
Nrf2/Keap1通路的活性通过RhoAROCK1通路调控A549非小细胞肺癌(NSCLC)细胞的活力
目的:据观察,Nrf2转录因子可启动调节肿瘤生长的蛋白质的产生,本研究旨在发现Nrf2是否会调节A549 NSCLC细胞的细胞运动性。ROCK-RhoA通路是细胞生长和迁移的重要因素,而细胞生长和迁移可能与细胞的运动性有关。Nrf2与ROCK-RhoA通路之间可能存在联系,本研究旨在探讨Nrf2是否通过ROCK-RhoA通路调控A549 NSCLC细胞的运动性。研究方法本研究将使用伤口愈合试验来观察细胞的运动性,并将阳性对照组(使用布芦沙托处理的 A549 细胞)与阴性对照组(未使用布芦沙托处理的 A549 细胞)进行比较,分别代表 Nrf2 被抑制或正常的表达水平。通过 Western 印迹和化学发光法研究 Nrf2 调节细胞运动的途径。可能的结果可能的结果主要有四种:(1),Nrf2 调节 A549 NSCLC 细胞的细胞活力,参与调节的途径是 ROCK-RhoA 途径。(2)、Nrf2 对 A549 细胞的细胞活力有调控作用,但参与调控的途径需要进一步研究才能确定。(3)、Nrf2 的表达水平与细胞运动性之间没有明显的相关性,但抑制 Nrf2 会导致 ROCK-RhoA 通路表达水平的变化。(4)、Nrf2 的表达水平与细胞运动无明显相关性,ROCK-RhoA 通路受 Nrf2 表达抑制的影响不明显,需要进一步研究以确定相关通路。结论本研究的结果为研究 Nrf2 在调控细胞运动中的作用及其过程中的通路提供了有价值的见解。它将加深人们对 Nrf2 转录因子及其如何与细胞运动调控途径相互作用的理解。这项研究还为未来的癌症治疗和基因药物开发提供了可能性。
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