Department of Biochemistry, Faculty of Science, Alexandria University, Alexandria, Egypt.
Department of Biotechnology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt.
Breast. 2018 Oct;41:34-41. doi: 10.1016/j.breast.2018.06.009. Epub 2018 Jun 22.
Studies have emphasized an antineoplastic effect of the non-psychoactive, phyto-cannabinoid, Cannabidiol (CBD). However, the molecular mechanism underlying its antitumor activity is not fully elucidated. Herein, we have examined the effect of CBD on two different human breast cancer cell lines: the ER-positive, well differentiated, T-47D and the triple negative, poor differentiated, MDA-MB-231 cells. In both cell lines, CBD inhibited cell survival and induced apoptosis in a dose dependent manner as observed by MTT assay, morphological changes, DNA fragmentation and ELISA apoptosis assay. CBD-induced apoptosis was accompanied by down-regulation of mTOR, cyclin D1 and up-regulation and localization of PPARγ protein expression in the nuclei and cytoplasmic of the tested cells. The results suggest that CBD treatment induces an interplay among PPARγ, mTOR and cyclin D1 in favor of apoptosis induction in both ER-positive and triple negative breast cancer cells, proposing CBD as a useful treatment for different breast cancer subtypes.
研究强调了非精神活性植物大麻素大麻二酚（CBD）的抗肿瘤作用。然而，其抗肿瘤活性的分子机制尚未完全阐明。在此，我们研究了 CBD 对两种不同的人乳腺癌细胞系的影响：ER 阳性、分化良好的 T-47D 和三阴性、分化不良的 MDA-MB-231 细胞。在这两种细胞系中，如 MTT 测定、形态变化、DNA 片段化和 ELISA 凋亡测定所观察到的，CBD 以剂量依赖的方式抑制细胞存活并诱导细胞凋亡。CBD 诱导的细胞凋亡伴随着 mTOR、细胞周期蛋白 D1 的下调以及 PPARγ 蛋白表达在核和细胞质中的定位。结果表明，CBD 处理诱导了 PPARγ、mTOR 和细胞周期蛋白 D1 之间的相互作用，有利于 ER 阳性和三阴性乳腺癌细胞的凋亡诱导，提示 CBD 可作为不同乳腺癌亚型的有效治疗方法。
