Anti-breast cancer activity of the essential oil from grapefruit mint (Mentha suaveolens × piperita).

Grapefruit mint (Mentha suaveolens × piperita) is a hybrid, perennial, and aromatic plant widely cultivated all over the world and used in the food, cosmetics, and pharmaceutical industries mostly for its valuable essential oil. Herein, we evaluated the anticancer activity of the grapefruit mint essential oil, cultivated in Iran. For the chemical composition analysis of essential oil, GC-MS was used. MTT assay was utilized for assessing the cytotoxic activity of the essential oil. The type of cell death was determined by annexin V/PI staining. Essential oil effect on the expression of maternally expressed gene 3 (MEG3), a regulatory lncRNA involved in cell growth, proliferation, and metastasis, was studied using qRT-PCR. Linalool (43.9%) and linalool acetate (40.1%) were identified as the dominant compounds of essential oil. Compared with MCF-7, the MDA-MB-231 cells were more sensitive to essential oil (IC50 = 7.6 µg/ml in MCF-7 and 5.9 µg/ml in MDA-MB-231 after 48 h). Essential oil induced cell death by apoptosis. Wound healing scratch assay confirmed the anti-invasive effect of essential oil. In addition, essential oil upregulated the tumor suppressor MEG3 in breast cancer cells. These results provide new insights into grapefruit mint essential oil potential application as an anticancer adjuvant in combination treatments for breast cancer patients.

Silibinin to improve cancer therapeutic, as an apoptotic inducer, autophagy modulator, cell cycle inhibitor, and microRNAs regulator.

Silibinin is a natural plant polyphenol with high antioxidant and anticancer properties, which causes broad-spectrum efficacy against cancer, including cell cycle arrest and apoptosis in most cancer cell types. Silibinin, by modulating the apoptosis, cell cycle progression and autophagic pathways in various cellular and molecular routs might be used to design more effective anticancer strategies. Silibinin also regulates aberrant miRNAs expression linked to many aspects of cell biology in cancer. Maybe the most interesting aspect of silibinin is its ability to trigger multiple cellular signaling pathways to induce a particular biologic effect in various cell types. This review discusses investigations supporting the ability of silibinin to be as a natural modulator of involved cellular biological events in cancer progression. In this review, we introduce the salient features of silibinin therapy to optimize clinical outcomes for oncology patients. The goal of the treatments is to make it possible to eliminate the tumor with the minimum side effects and cure the patient in the early stage cancer. Therefore, plant extracts such as silibinin can be included in the treatments.

Influence of silibinin and ß-ß-dimethylacrylshikonin on chordoma cells.

BACKGROUND: Chordoma, slow growing bone tumours originating from remnants of the notochord, leave affected patients with a median survival of six years. The high recurrence rate of chordoma, together with limited treatment options and bad overall prognosis, make the development of new treatment options urgently necessary. PURPOSE: In this study, the potential of two natural products, silibinin and ß-ß-dimethylacrylshikonin (DMAS), was tested on clival (MUG-CC1 and UM-Chor1) as well as sacral (MUG-Chor1 and U-CH2) chordoma cell lines. The treatment was administered both as single- and combined therapy. METHODS: For investigation of cell viability, the Cell Titer 96 Aqueous Non-Radioactive Cell Proliferation Assay Kit was used. Apoptosis induction was studied by flow cytometry, (Annexin V/SYTOX Green, caspase-3) and RT-qPCR. Pathway analyses were performed by western blot. RESULTS: Both drugs were found to reduce cell viability alone as well as in combination in a dose dependent manner, with DMAS being more efficient than silibinin. The mode of cell death was mainly apoptosis in DMAS treated samples, while the combination therapy led to apoptosis as well as late-apoptosis/necrosis. Silibinin therapy alone, although reducing cell viability, did not lead to significant apoptotic effects in the performed assays. Focussing on the molecular mechanism of DMAS induced apoptosis, it was found that major genes of the mitochondrial apoptosis pathway, like NOXA and PUMA were overexpressed. Additionally, western blot experiments showed a decrease of ERK/pERK, STAT3/pSTAT3 (Tyr705) and AKT/pAKT expression/activation levels under DMAS treatment. CONCLUSION: DMAS is a promising new candidate for chordoma therapy, while silibinin or a combination of both is less favourable.