Combinatorial Cytotoxic Effects of Damnacanthal and Doxorubicin against Human Breast Cancer MCF-7 Cells in Vitro

Abstract

Despite progressive research being done on drug therapy to treat breast cancer, the number of patients succumbing to the disease is still a major issue. Combinatorial treatment using different drugs and herbs to treat cancer patients is of major interest in scientists nowadays. Doxorubicin is one of the most used drugs to treat breast cancer patients. The combination of doxorubicin to other drugs such as tamoxifen has been reported. Nevertheless, the combination of doxorubicin with a natural product-derived agent has not been studied yet. Morinda citrifolia has always been sought out for its remarkable remedies. Damnacanthal, an anthraquinone that can be extracted from the roots of Morinda citrifolia is a promising compound that possesses a variety of biological properties. This study aimed to study the therapeutic effects of damnacanthal in combination with doxorubicin in breast cancer cells. Collectively, the combination of both these molecules enhanced the efficacy of induced cell death in MCF-7 as evidenced by the MTT assay, cell cycle, annexin V and expression of apoptosis-related genes and proteins. The effectiveness of doxorubicin as an anti-cancer drug was increased upon addition of damnacanthal. These results could provide a promising approach to treat breast cancer patients.

In Vitro Studies on the Synergistic Effect of Morinda Citrifolia L. (Noni) and Methotrexate on Cytotoxicity of Hela Cell Lines

“…Sharma et al (2016) reported that cell cycle distribution in MCF -7 and MDA-MB-231 cell when exposed to Noni ethyl acetate extract at IC 50 for 24, 48, and 72 h showed a noticeable increase in the G1/S phase in a time-dependent manner [20]. They have reported 81% apoptotic cells which are comparable to our results for the same time duration [22]. Our results are also in accordance with Gupta et al (2013) and Alitheen et al (2016) [2,23].…”

Curcumin Analog DK1 Induces Apoptosis in Human Osteosarcoma Cells In Vitro through Mitochondria-Dependent Signaling Pathway

“…Acridine orange/propidium iodide (AO/PI) double staining assay was conducted to examine the cell death of osteosarcoma cells microscopically. By using this staining assay, the morphology and cellular profiles for viable, apoptotic and necrotic cells can be distinguished [ 13 ]. Viable cells with intact membranes will stain green, whilst early apoptotic cells will stain with a green color but are distinguished by occurrences of distinct features such as membrane disruption, while late apoptosis/necrosis will stain red [ 13 ].…”

“…By using this staining assay, the morphology and cellular profiles for viable, apoptotic and necrotic cells can be distinguished [ 13 ]. Viable cells with intact membranes will stain green, whilst early apoptotic cells will stain with a green color but are distinguished by occurrences of distinct features such as membrane disruption, while late apoptosis/necrosis will stain red [ 13 ]. Around 200 populations of cells were quantified for statistical analysis [ 13 ].…”

“…Viable cells with intact membranes will stain green, whilst early apoptotic cells will stain with a green color but are distinguished by occurrences of distinct features such as membrane disruption, while late apoptosis/necrosis will stain red [ 13 ]. Around 200 populations of cells were quantified for statistical analysis [ 13 ]. Based on MTT assay, three different inhibition concentrations (IC 25 , IC 50 , and IC 75 ) for DK1 were obtained and subsequently used to treat both MG-63 and U-2OS cell lines for 48 h. Figure 2 represents the fluorescence photomicrographs of MG-63 and U-2OS osteosarcoma cell lines 48 h post treatment with three different concentrations of DK1.…”

DK1 Induces Apoptosis via Mitochondria-Dependent Signaling Pathway in Human Colon Carcinoma Cell Lines In Vitro

“…During a cell cycle there are checkpoints that play significant roles. They help to regulate the cell cycle by temporarily arresting the cell, thereby allowing time for cellular repair mechanisms to take place and reversing any incurred DNA mutation, or activating programmed cell death in the case of irreversible cellular damage and causing DNA fragmentation that is usually accompanied by increased sub-G0/G1 population in these apoptotic cells [ 17 , 23 ]. Irregular cell cycle activity then leads to enhanced cancer proliferation as the cell is unable to activate cell death mechanisms, thus allowing cancerous cells to further proliferate.…”