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来自人脐带干细胞的辐照和条件培养基可抑制乳腺癌细胞中的上皮-间质转化生物标志物。

Irradiation and conditioned media from human umbilical cord stem cells suppress epithelial-mesenchymal transition biomarkers in breast cancer cells.

作者信息

Ghanbarnasab Behbahani Rahil, Danyaei Amir, Shogi Hamed, Tahmasbi Mohammad Javad, Saki Ghasem, Neisi Niloofar

机构信息

Department of Medical Physics, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Department of Anatomical Sciences, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

出版信息

Iran J Basic Med Sci. 2023 Apr;26(4):486-491. doi: 10.22038/IJBMS.2023.68374.14919.

DOI:10.22038/IJBMS.2023.68374.14919
PMID:37009003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10008391/
Abstract

OBJECTIVES

Breast cancer cells developing radioresistance during radiation may result in cancer recurrence and poor survival. One of the main reasons for this problem is the changes in the regulation of genes that have a key role in the epithelial-mesenchymal transition (EMT). Utilizing mesenchymal stem cells can be an effective approach to overcome therapeutic resistance. In this study, we investigated the possibility of combining mesenchymal medium with cancer cell medium in sensitizing breast carcinoma cells to radiation.

MATERIALS AND METHODS

In this experimental study, the cells were irradiated at a dose of 4 Gy alone and in combination with stem cells and cancer cells media. Apoptosis, cell cycle, Western blotting, and real-time PCR assays evaluated the therapeutic effects.

RESULTS

We found that the CSCM could decrease the expression of several EMT markers (CD133, CD44, Vimentin, Nanog, Snail, and Twist), resulting in increased cell distribution in the G1 and G2/M phases, apoptosis rate, and protein levels of p-Chk2 and cyclin D1; furthermore, it exhibits synergetic effects with radiation treatment .

CONCLUSION

These findings show that CSCM inhibits the expansion of breast cancer cells and makes them more susceptible to radiotherapy, offering a unique approach to treating breast cancer by overcoming radioresistance.

摘要

目的

乳腺癌细胞在放疗过程中产生放射抗性可能导致癌症复发和生存率低下。该问题的主要原因之一是上皮-间质转化(EMT)中起关键作用的基因调控发生变化。利用间充质干细胞可能是克服治疗抗性的有效方法。在本研究中,我们研究了将间充质培养基与癌细胞培养基联合使用使乳腺癌细胞对放疗敏感的可能性。

材料与方法

在本实验研究中,细胞分别单独接受4 Gy剂量的照射,以及与干细胞和癌细胞培养基联合照射。通过凋亡、细胞周期、蛋白质印迹和实时PCR分析评估治疗效果。

结果

我们发现癌干细胞条件培养基(CSCM)可降低几种EMT标志物(CD133、CD44、波形蛋白、Nanog、Snail和Twist)的表达,导致G1期和G2/M期细胞分布增加、凋亡率升高以及p-Chk2和细胞周期蛋白D1的蛋白质水平升高;此外,它与放射治疗表现出协同作用。

结论

这些发现表明,CSCM可抑制乳腺癌细胞的增殖,并使其对放疗更敏感,为克服放射抗性治疗乳腺癌提供了一种独特的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/4478c20b454e/IJBMS-26-486-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/b6e35558facc/IJBMS-26-486-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/72b78a260910/IJBMS-26-486-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/a01ee3ffbbe3/IJBMS-26-486-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/4a77b9e87f08/IJBMS-26-486-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/4478c20b454e/IJBMS-26-486-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/b6e35558facc/IJBMS-26-486-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/72b78a260910/IJBMS-26-486-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/a01ee3ffbbe3/IJBMS-26-486-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/4a77b9e87f08/IJBMS-26-486-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca4/10008391/4478c20b454e/IJBMS-26-486-g005.jpg

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Nanog, as a key cancer stem cell marker in tumor progression.Nanog 作为肿瘤进展中的关键癌症干细胞标志物。
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