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鞣酸诱导未折叠蛋白反应引发 MDA-MB-231 乳腺癌细胞凋亡。

Induction of Unfolded Protein Response by Tannic Acid Triggers Apoptosis in MDA-MB-231 Breast Cancer Cells.

机构信息

Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran.

Department of Molecular Medicine and Biotechnology, Arak University of Medical Sciences, Arak, Iran.

出版信息

Asian Pac J Cancer Prev. 2023 Jun 1;24(6):2029-2035. doi: 10.31557/APJCP.2023.24.6.2029.

Abstract

INTRODUCTION

Endoplasmic reticulum (ER) stress can reduce cell survival and enhances the apoptosis of cancer cells. Plant polyphenols like tannic acid trigger ER stress and apoptosis and therefore can be a novel agent for the treatment of cancer. In this study, we investigated the effect of tannic acid on survival, migration, colony formation, ER stress pathway, and apoptosis of the MDA-MB-231 breast cancer cells.

METHODS

The MTT assay was performed to investigate the effect of tannic acid on the cell survival of breast cancer cells. We used the qPCR method to reveal the effect of tannic acid on the Bak, CHOP, ATF4, P21, MMP-2, and Bcl-2 expression. Also, colony formation, cell migration, and Hoechst staining assays were employed.

RESULTS

The results of the MTT test showed that tannic acid reduced the cell survival rate. In the qPCR assay, we found that tannic acid decreased the expression levels of MMP-2, Bcl-2, ATF4, and CHOP genes, paradoxically, enhanced the expression of Bak and P21 genes. The colony formation and cell migration assays indicated that tannic acid significantly diminished breast cancer cell proliferation and migration, respectively. In the apoptosis assay, tannic acid increased the number of apoptotic cells.

CONCLUSION

Tannic acid increases the rate of cell death but decreases viability and cell migration. Moreover, tannic acid induces apoptosis in breast cancer cells. Overall, our study demonstrates that tannic acid induces ER stress by increasing the genes which are playing role in ER stress pathway. These results show that tannic acid can be used as an effective agent for breast cancer treatment.

摘要

简介

内质网(ER)应激会降低细胞存活率并增强癌细胞的凋亡。植物多酚如鞣酸会引发 ER 应激和凋亡,因此可以成为治疗癌症的新药物。在这项研究中,我们研究了鞣酸对 MDA-MB-231 乳腺癌细胞的存活、迁移、集落形成、内质网应激途径和凋亡的影响。

方法

通过 MTT 法研究鞣酸对乳腺癌细胞存活的影响。我们使用 qPCR 方法揭示鞣酸对 Bak、CHOP、ATF4、P21、MMP-2 和 Bcl-2 表达的影响。此外,还进行了集落形成、细胞迁移和 Hoechst 染色实验。

结果

MTT 试验结果表明鞣酸降低了细胞存活率。在 qPCR 试验中,我们发现鞣酸降低了 MMP-2、Bcl-2、ATF4 和 CHOP 基因的表达水平,相反,增强了 Bak 和 P21 基因的表达。集落形成和细胞迁移实验表明,鞣酸显著减少了乳腺癌细胞的增殖和迁移。在凋亡实验中,鞣酸增加了凋亡细胞的数量。

结论

鞣酸增加了细胞死亡的速度,但降低了细胞活力和迁移能力。此外,鞣酸诱导乳腺癌细胞凋亡。总的来说,我们的研究表明,鞣酸通过增加参与内质网应激途径的基因来诱导内质网应激。这些结果表明,鞣酸可作为治疗乳腺癌的有效药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db1/10505879/41ab1357f8fb/APJCP-24-2029-g001.jpg

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