Damnacanthal, an anthraquinone compound, is isolated from the roots of Morinda citrifolia L. (noni), which has been used for traditional therapy in several chronic diseases, including cancer. Although noni has long been consumed in Asian and Polynesian countries, the molecular mechanisms by which it exerts several benefits are starting to emerge. In the present study, the effect of damnacanthal on MCF-7 cell growth regulation was investigated. Treatment of MCF-7 cells with damnacanthal for 72 h indicated an antiproliferative activity. The MTT method confirmed that damnacanthal inhibited the growth of MCF-7 cells at the concentration of 8.2 μg/ml for 72 h. In addition, the drug was found to induce cell cycle arrest at the G1 checkpoint in MCF-7 cells by cell cycle analysis. Damnacanthal induced apoptosis, determined by Annexin V-fluorescein isothiocyanate/propidium iodide (PI) dual-labeling, acridine-orange/PI dyeing and caspase-7 expression. Furthermore, damnacanthal-mediated apoptosis involves the sustained activation of p21, leading to the transcription of p53 and the Bax gene. Overall, the present study provided significant evidence demonstrating that p53-mediated damnacanthal induced apoptosis through the activation of p21 and caspase-7.

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.

The Noni fruit, or scientifically known as Morinda citrifolia can be found in various parts of the world, especially in the pacific region. It is a small evergreen bushy-like tree originated from the Rubiaceae family. The plant has been used by polynesians as a medicinal herb for more than 2000 years. A substantial amount of phytochemicals can be found in the roots of this plant. Among all, damnacanthal has been found to be the most interesting, versatile and potent compound. Damnacanthal or chemically known as,3- hydroxy-1-methoxyanthraquinone-2-caboxaldehyde (C16H10O5), appears as pale yellow crystals with a melting point of 210-211 °C. This compound is of particular interest due to its striking pharmacological properties. Damnacanthal was shown to inhibit the oncogene Ras, p56lck tyrosine kinase, NF-KB pathway and induce apoptosis in vitro. This review aims to discuss the biological properties of damnacanthal, specifically on its anti-cancer activity that has been reported.

Gallic acid (GA) comes from benzoic acid or, more specifically, 3,4,5-tryhydroxybenzoic, which derives from the phenolic acid of the non-flavonoid part of the polyphenol compound. It is found ubiquitously in various plants and fruits, such as grapes, gallnuts, pomegranates, and tea leaves [1]. Many scientific journals and articles reported on the pharmacological properties of the photochemical like GA, which has antioxidant properties, antimicrobial, anti-inflammatory, anticancer, cardioprotective, gastroprotective, and neuroprotective activity [2]. Moreover, the anticancer properties of GA have been recognised in several cancers, such as lung cancers, oesophageal cancer cells and leukaemia [3].   The objective of this study is to examine the anti-proliferative and apoptosis inducing effects of GA on HL-60 cell lines. Six concentrations of GA were made using the stock solution of GA compound dissolved in dimethyl sulfide (DMSO). HL-60 cells were treated with concentrations of 100, 50, 25, 12.5, 6.25, and 3.125 µg/mL and was incubated at three incubation period which were 24, 48, and 72 hours. The quantitative measure was determined with cytotoxicity assay of 3- (4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and was read by microplate reader at 570 nm. For qualitative measure was through staining with acridine orang (AO) and propidium iodide (PI) and observed the morphological changes of the treated cells.   Results from the MTT assays show that GA has cytotoxicity effect on HL-60 cells especially for 72 hours incubation period. The maximal half inhibitory concentrations (IC50) value of GA decreases as incubation period increases. The IC50 of GA were 9.03, 6.76, and 3.65 µg/ml for 24-, 48-, and 72-hours incubation, respectively. The IC50 value of GA (p<0.05) was significantly different for different incubation periods. The morphological changes were seen through the AO/PI staining with the appearance of the cell blebbing, early apoptosis, and late apoptosis.   Figure 1 shows early apoptosis (EA), late apoptosis (LA), cell blebbing (CB), membrane loose (MB), nuclear fragmentation (NF), and apoptotic bodies (AB).   These findings show that GA has potential as anti-proliferative and apoptosis inducing effects on HL-60 cells line. More research is needed to determine the pathways of apoptosis in HL-60 treated with GA.

Curcuma Longa or also known as turmeric is a prominent natural remedy in Asia that has been utilized to heal diseases for decades. It has been demonstrated to have substantial biological activities, including anticarcinogenic, antimutagenic, antioxidant, anti-inflammatory, anti-infectious, hypocholesterolemic, and chemopreventive properties. Curcumin is a therapeutic substance extracted from Curcuma Longa that is thought to have anti-cancer properties against a variety of cancer types. However, its anti-cancer potential on acute myeloid leukemia (AML) remains uncertain [1,2].    The objective of this intervention study was to examine the anti-proliferative and apoptotic effects of curcumin on the HL-60 cell line of acute myeloid leukemia. A stock solution of pure curcumin compound was obtained by dissolving it in dimethyl sulfide (DMSO). HL-60 cells were treated with six different concentrations which were 100, 50, 25, 12.5, 6.25, 3.125 µg/ml and incubated at three distinct incubation period (24, 48 and 72 hours). The in vitro cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and quantified using a microplate reader at 570 nm. Acridine orange (AO) and propidium iodide (PI) staining were employed to evaluate morphological changes.    MTT assays results show that curcumin has a high cytotoxicity effect on HL-60 cells. The maximal half inhibitory concentration (IC50) value of curcumin was consistently decreased when the incubation time increased. The IC50 of curcumin on HL-60 cells were reported to be 13, 8, and 3.5 µg/ml at 24, 48 and 72 hours of incubation, respectively. There was a significantly different IC50 value (p<0.05) of curcumin between the incubation periods (Figure 1). The morphological alteration was shown in AO/PI staining by the appearance of early apoptosis, late apoptosis, and necrotic cells. These findings illustrated that curcumin revealed an effective anti-cancer action on human acute myeloid leukemia HL-60 cell line. Further research is required to determine the mechanism of cell death in HL-60 cells treated with pure curcumin compound.   In conclusion, the study revealed the role of putative targeted genes in the biological mechanism in gout pathogenesis has provides insight of the potential biomarkers in developing the personalized medicine better treatment for gout patient in ensuring better patient healthcare.