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二烯丙基三硫诱导乳腺导管原位癌和微浸润乳腺癌细胞凋亡。

Diallyl Trisulfide Induces Apoptosis in Breast Ductal Carcinoma In Situ Derived and Minimally Invasive Breast Cancer Cells.

机构信息

Department of Nutrition, College of Agriculture, Biotechnology and Natural Resources, University of Nevada, Reno, NV 89557, USA.

出版信息

Nutrients. 2022 Mar 31;14(7):1455. doi: 10.3390/nu14071455.

DOI:10.3390/nu14071455
PMID:35406068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9002892/
Abstract

Breast ductal carcinoma in situ (DCIS) is a localized form of breast cancer that can progress to invasive breast cancer. Diallyl trisulfide (DATS) is a bioactive compound from vegetables reported to induce anticancer effects in several cancer models. The objective of this study was to characterize DATS-induced apoptosis in breast DCIS and minimally invasive breast cancer cells. Breast DCIS cells SUM 102PT (ductal carcinoma in situ with areas of micro-invasion) and SUM 225CWN (chest wall recurrence of ductal carcinoma in situ) were used in this study. DATS induced a dose-dependent reduction in the colony formation ability of breast DCIS cells. DATS inhibited DCIS cell growth by inducing apoptosis as shown by a dose-dependent increase in cytoplasmic histone-associated DNA fragmentation. Induction of apoptosis was more pronounced in SUM 102PT cells than in SUM 225CWN cells at similar concentrations of DATS. DATS-induced apoptosis was characterized by a dose-dependent increase in cleaved poly-ADP ribose polymerase (PARP). DATS treatment resulted in an increase in the cytochrome levels and cleavage of caspases 3, 7, and 9. This study shows that DATS inhibits cell proliferation and induces apoptosis in breast DCIS derived and minimally invasive breast cancer cells, and supports further investigation of DATS as a potential chemopreventive agent for DCIS.

摘要

乳腺导管原位癌(DCIS)是一种局限性乳腺癌,可能进展为浸润性乳腺癌。二烯丙基三硫化物(DATS)是一种来自蔬菜的生物活性化合物,据报道,它在几种癌症模型中诱导抗癌作用。本研究的目的是描述 DATS 在乳腺 DCIS 和微侵袭性乳腺癌细胞中的诱导细胞凋亡作用。本研究使用了乳腺 DCIS 细胞 SUM 102PT(具有微浸润区域的导管原位癌)和 SUM 225CWN(导管原位癌的胸壁复发)。DATS 诱导乳腺 DCIS 细胞的集落形成能力呈剂量依赖性降低。DATS 通过诱导细胞凋亡抑制 DCIS 细胞生长,如细胞质组蛋白相关 DNA 片段化的剂量依赖性增加所示。在相似浓度的 DATS 下,SUM 102PT 细胞中诱导的细胞凋亡比 SUM 225CWN 细胞更明显。DATS 诱导的细胞凋亡的特征是切割的多聚 ADP 核糖聚合酶(PARP)呈剂量依赖性增加。DATS 处理导致细胞色素水平增加和半胱天冬酶 3、7 和 9 的切割。本研究表明,DATS 抑制乳腺 DCIS 衍生和微侵袭性乳腺癌细胞的增殖并诱导细胞凋亡,支持进一步研究 DATS 作为 DCIS 的潜在化学预防剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/539c/9002892/9cb65c0788bf/nutrients-14-01455-g006.jpg
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