Abstract
Rhus verniciflua Stokes has long been used as a food supplement and traditional herbal medicine for various ailments in East Asia. We evaluated the anticancer effects of Rhus verniciflua Stokes extract (RVSE) on MCF-7 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, annexin V/7-AAD staining, and western blotting. In addition, the gallic acid content of RVSE was assayed using high-performance liquid chromatography. RVSE inhibited the growth of MCF-7 cells in a dose-dependent manner by inducing apoptosis in the sub-G1 phase. RVSE also significantly increased the number of apoptotic cells and increased the expression of p53 and p21 in a dose-dependent manner. Furthermore, RVSE treatment increased the Bax:Bcl-2 ratio and the levels of apoptosis-related factors, such as cleaved caspase-3 and -9 and PARP, in MCF-7 cells. Our findings suggest that the proapoptotic effect of RVSE on MCF-7 cells is mediated by p53, p21, and the intrinsic mitochondrial cascade. Thus, RVSE shows promise for the prevention and treatment of breast cancer.
Highlights
Cancer is characterized by the uncontrolled growth and spread of abnormal cells and is caused by hormones, immune conditions, and deregulation of oncogenes [1]
We investigated the effect of Rhus verniciflua Stokes extract (RVSE) on cell cycle arrest
Our findings showed that RVSE significantly inhibited the proliferation of MCF-7 cells in a dose-dependent manner
Summary
Cancer is characterized by the uncontrolled growth and spread of abnormal cells and is caused by hormones, immune conditions, and deregulation of oncogenes [1]. Deregulation of oncogenes results in explosive cell proliferation and induction of invasiveness, which promotes the acquisition of a malignant phenotype [2]. Breast cancer is one of the most common malignancies in women worldwide. 200,000 women are diagnosed with invasive breast cancer and around 40,000 die annually; breast cancer is the second leading cause of cancer-related deaths in women globally [1]. The estrogen receptor-positive MCF-7 breast cancer cell line was derived from the pleural effusion of a patient with metastatic breast cancer [3]. Several decades of use have facilitated the evolution of distinct MCF-7 lineages resistant to chemotherapy [3, 4]
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