Combination of AAV‑mediated NUPR1 knockdown and trifluoperazine induces premature senescence in human lung adenocarcinoma A549 cells in nude mice

AAV 介导的 NUPR1 敲低与三氟拉嗪联合使用可诱导裸鼠人肺腺癌 A549 细胞过早衰老

阅读:6
作者:Yanzhe Li, Yueyuan Yin, Jinyi Ma, Yanan Sun, Ruimin Zhou, Bo Cui, Yuxuan Zhang, Jie Yang, Xiaojie Yan, Zhe Liu, Zhenyi Ma

Abstract

Nuclear protein 1 (NUPR1)/p8, a transcriptional regulator, has the ability to facilitate lung cancer cell survival. Adeno‑associated virus (AAV)‑based vectors are efficient vehicles for gene transfer and expression. In this study, an AAV‑mediated NUPR1 shRNA vector was constructed that effectively inhibited the expression of NUPR1 in a tumor xenograft model derived from lung adenocarcinoma A549 cells. Trifluoperazine (TFP), which is an antipsychotic drug, has the ability to bind to NUPR1 and mimic NUPR1 deficiency in cancer cells. It was also found that the combination of TFP and AAV‑mediated NUPR1 shRNA delivery led to significant tumor growth inhibition in nude mice bearing human lung cancer xenografts. Moreover, AAV‑mediated NUPR1 shRNA therapy induced premature senescence in vitro and in vivo. Collectively, the findings of this study suggest a putative role for the combination of AAV‑NUPR1 shRNA and TFP in lung cancer therapy.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。