Moringa oleifera, a fast-growing deciduous tree that is widely cultivated in tropical and subtropical regions of the world, is well known for its abundant uses. The tree is a source of food, shelter, and traditional medicine for many people, especially in developing countries. Many studies have been conducted to evaluate the various claims of traditional medicine practitioners that the moringa tree can improve health and treat various diseases. The tree has a high nutritional profile, especially the nutrient rich leaves. Some reports also support the use of parts of the tree to reduce blood sugar and cholesterol levels. These attractive properties have led researchers to look for other novel uses for the moringa tree, especially as a source of anticancer drugs. Researchers have tested extracts from various parts of the moringa tree both in vitro and in vivo on several types of cancers with varying success. This review explores the state of current research on the anticancer properties of M. oleifera.

Background: Moringa oleifera, commonly known as "moringa", is widely cultivated in tropical and subtropical regions across the globe. Extensive studies have shown that various parts of the moringa tree exhibit anti-cancer properties. This study determined the effects of sequential moringa leaf extracts and silver nanoparticles synthesized from moringa leaf extract on Kasumi-1 leukemia cells. Methods and Results: Dried moringa leaf powder was sequentially extracted with the assistance of ultrasound starting with absolute ethanol, followed by 50% ethanol, and finally, deionized water. The aqueous extract was utilized to synthesize silver nanoparticles. The optimum conditions to generate moringa silver nanoparticles (MO-AgNPs) were eight hours of incubation at 60°C with 1 mM silver nitrate and 1% moringa aqueous extract from sequential extraction. The three extracts and MO-AgNPs were used to treat Kasumi-1 cells for 24, 48, 72 hours with concentrations ranging from 400 to 12.5 µg/mL, while cell viability was determined with 3(4, 5-dimethythiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. After 72 hours of treatment, the moringa leaf absolute ethanol extract displayed the strongest inhibitory effects on Kasumi-1 cells with IC 50 of 10 µg/mL, in comparison to moringa leaf 50% ethanol extract (25 µg/mL) and aqueous extract (>400 µg/mL). Interestingly, MO-AgNPs exhibited the strongest cytotoxic effects on Kasumi-1 cells with an IC 50 of 7.5 µg/mL. Cytotoxic study on normal CD34+ cells treated with up to 50ug/mL of either MO-AgNPs or ethanol extract still had more than 80% cell viability indicating that the treatments have selective cytotoxicity against the cancer cells. Morphological studies of Kasumi-1 cells treated with IC 50 of moringa leaf ethanolic extract and MO-AgNPs show a lot of shrinking, dying cells and cell debris. Cell cycle studies displayed an increase in cells at the G1 phase for ethanol leaf extract, while MO-AgNPs caused cell cycle arrest at the S phase after treatment with IC 50 dose for 24 hours. Moringa leaf ethanol extract and the nanoparticles induced apoptosis in Kasumi-1 cells as shown by annexin V -FITC assays. Gene expression analysis by qPCR verified these outcomes, as the moringa leaf ethanol extract led to significant upregulation of proapoptotic gene caspase 8, whereas the MO-AgNPs caused a significant increase of proapoptotic protein BID. Conclusion: This study reveals that moringa ethanolic leaf extract and MO-AgNPs induced potent antiproliferative effects in Kasumi-1 cells by apoptosis.

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The t(8;21) translocation is one of the most frequent chromosome abnormalities associated with acute myeloid leukaemia (AML). This abberation deregulates numerous molecular pathways including the ERK signalling pathway among others. Therefore, the aim of the present study was to investigate the gene expression patterns following siRNA-mediated suppression of RUNX1-RUNX1T1 and MAPK1 in Kasumi-1 and SKNO-1 cells and to determine the differentially expressed genes in enriched biological pathways. BeadChip microarray and gene ontology analysis revealed that RUNX1-RUNX1T1 and MAPK1 suppression reduced the proliferation rate of the t(8;21) cells with deregulated expression of several classical positive regulator genes that are otherwise known to enhance cell proliferation. RUNX1-RUNX1T1 suppression exerted an anti-apoptotic effect through the overexpression of BCL2, BIRC3 and CFLAR genes, while MAPK1 suppression induced apopotosis in t(8;21) cells by the apoptotic mitochondrial changes stimulated by the activity of upregulated TP53 and TNFSF10, and downregulated JUN gene. RUNX1-RUNX1T1 suppression supported myeloid differentiation by the differential expression of CEBPA, CEBPE, ID2, JMJD6, IKZF1, CBFB, KIT and CDK6, while MAPK1 depletion inhibited the differentiation of t(8;21) cells by elevated expression of ADA and downregulation of JUN. RUNX1-RUNX1T1 and MAPK1 depletion induced cell cycle arrest at the G 0 /G 1 phase. Accumulation of cells in the G 1 phase was largely the result of downregulated expression of TBRG4, CCNE2, FOXO4, CDK6, ING4, IL8, MAD2L1 and CCNG2 in the case of RUNX1-RUNX1T1 depletion and increased expression of RASSF1, FBXO6, DADD45A and P53 in the case of MAPK1 depletion. Taken together, the current results demonstrate that MAPK1 promotes myeloid cell proliferation and differentiation simultaneously by cell cycle progression while suppresing apoptosis.

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MicroRNAs (miRNAs) are short non-coding RNAs involved in post-transcriptional gene regulation. Over the past years, various studies have demonstrated the role of aberrant miRNA expression in the onset of cancer. The mechanisms by which miRNA exerts its cancer-promoting or inhibitory effects are apparent through the various cancer hallmarks, which include selective proliferative advantage, altered stress response, vascularization, invasion and metastasis, metabolic rewiring, the tumor microenvironment and immune modulation; therefore, this review aims to highlight the association between miRNAs and the various cancer hallmarks by dissecting the mechanisms of miRNA regulation in each hallmark separately. It is hoped that the information presented herein will provide further insights regarding the role of cancer and serve as a guideline to evaluate the potential of microRNAs to be utilized as biomarkers and therapeutic targets on a larger scale in cancer research.

Purpose: Vernonia amygdalina (VA) is a traditional African herbal medicine that has been reported to possess anticancer properties. However, the anticancer properties of VA silver nanoparticles have not been studied. The aim of the study was to examine and evaluate the anticancer activities of VA leaf extracts and VA silver nanoparticles on the human breast cancer cell line, MCF-7. Methods: VA leaves were extracted using sequential extraction assisted with ultrasound using three different solvents: ethanol, 50% ethanol, and deionized water. The silver nanoparticles were synthesised with VA aqueous extract. Results: The ethanol extract and VA silver nanoparticles inhibit MCF-7 cell proliferation with an average half-maximal inhibitory concentration (IC 50 ) value of 67µg/mL and 6.11µg/ mL, respectively, after 72 hours of treatment. The ethanol extract and VA silver nanoparticles also caused G1 phase cell cycle arrest, induced apoptosis and nuclear fragmentation in MCF-7 cells. Conclusion:VA ethanol extracts and VA silver nanoparticles decreased the cell viability in MCF-7 cells in a time and dose-dependent manner by inducing apoptosis and causing DNA damage. Further research is needed to elucidate the mechanism of action of VA leaf extracts and VA silver nanoparticles. This study is the first to report on the anticancer activity of VA silver nanoparticles in MCF-7 cells.