Preferential target is mitochondria in α-mangostin-induced apoptosis in human leukemia HL60 cells

Objective: The research aimed to study the effects of mitomycin on human leukemic K562 cells, and to explore the mechanism of mitomycin induced apoptosis．In order to provide previous experiment basis for mitomycin applying clinical treatments Methods: The multiplication and apoptosis status of K562 cells treated different time by different concentration mitomycin were observed by light microscope, fluorescence microscope, TEM, agrose gel electrophoresis of DNA and flow cytometry. Results: The results showed that mitomycin could induce K562 cells apoptosis, and the best concentration was 12.5μg/ml for 48 h. The optimal concentration of apoptosis induced by apoptosis rate is （28.8±1.04）% （P<0.01）. Mitomycin could affect the S phase among cellular multiplication, cell could be blocked by mitomycin and then apoptosis in this phase. Conclusions: Mitomycin can induce the apoptosis of human leukemic K562 cells. It is of great significance to guide clinical medication.

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Camel Milk Exosomes Potentiate The Anticancer Effect of Doxorubicin on Multidrug-Resistant Human Leukemia Hl60 Cells in Vitro and in Vivo

10.53350/pjmhs2115113313 ◽

2021 ◽

Vol 15 (11) ◽

pp. 3313-3320

Author(s):

Rashad Qasem Ali Othman ◽

Abdelnaser A. Badawy ◽

Mohammed M. Alruwaili ◽

Mohammed A. El-magd

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Multidrug Resistant ◽

Chemotherapeutic Agents ◽

Camel Milk ◽

Human Leukemia ◽

Anticancer Effect ◽

Hl60 Cells ◽

Cycle Arrest ◽

Mdr Genes

Background: Multidrug resistance (MDR) is one of the strategies developed by cancer cells to inhibit the anticancer potential of the majority of chemotherapeutic agents and almost results in treatment failure. Objective: This study aimed to evaluate the therapeutic potential of camel milk exosomes (CME) on multidrug-resistant human acute promyelocytic leukemia HL60 cells (HL60/RS) and to investigate whether this CME could potentiate the anticancer effect of Doxorubicin (DOX) and decrease its side effects. Results: CME alone or combined with DOX significantly induced HL60/RS cell viability loss, apoptosis, and cell cycle arrest at the G0/G1 phase, and downregulated MDR genes (Abcb1, Abcc1, Abcg2) as compared to cells treated with DOX alone. Additionally, CME and DOX co-treated nude mice had the lowest tumor volume, Abcb1, Abcc1, Abcg2, and Bcl2 expression, and the highest Bax and caspase3 expression in HL60/RS xenografts. This combined therapy also decreased DOX adverse effects as revealed by decreased liver damage enzymes and lipid peroxide (MDA) and increased hepatic antioxidant enzymes (SOD, CAT, GPx). Conclusion: CME increased sensitivity of HL60/RS to DOX through, at least in part, reduction of MDR genes, induction of apoptosis, and cell cycle arrest. Thus, CME may be used as safe adjuvants to DOX during cancer treatment. Keywords: Camel milk exosomes; Myeloid leukemia; HL60; Apoptosis; MDR

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A New Hybrid δ-Lactone Induces Apoptosis and Potentiates Anticancer Activity of Taxol in HL-60 Human Leukemia Cells

Molecules ◽

10.3390/molecules25071479 ◽

2020 ◽

Vol 25 (7) ◽

pp. 1479 ◽

Cited By ~ 1

Author(s):

Katarzyna Gach-Janczak ◽

Joanna Drogosz-Stachowicz ◽

Angelika Długosz-Pokorska ◽

Rafał Jakubowski ◽

Tomasz Janecki ◽

...

Keyword(s):

Cell Proliferation ◽

Anticancer Agents ◽

Biologically Active ◽

Human Leukemia ◽

Apoptosis Induction ◽

Hybrid Compound ◽

Drug Candidates ◽

Natural Substances ◽

High Cytotoxic Activity ◽

Induced Apoptosis

In the search for new drug candidates, researchers turn to natural substances isolated from plants which may be either used directly or may serve as a source for chemical modifications. An interesting strategy in the design of novel anticancer agents is based on the conjugation of two or more biologically active structural motifs into one hybrid compound. In this study, we investigated the anticancer potential of 4-benzyl-5,7-dimethoxy-4-methyl-3-methylidene-3,4-dihydro-2H-chroman-2-one (DL-247), a new hybrid molecule combining a chroman-2-one skeleton with an exo-methylidene bond conjugated with a carbonyl group, in human myeloid leukemia HL-60 cell line. The cytotoxicity of the new compound was tested using MTT assay. The effect of DL-247 on cell proliferation and apoptosis induction were studied by flow cytometry, fluorometric assay and ELISA analysis. DL-247 displayed high cytotoxic activity (IC50 = 1.15 µM, after 24 h incubation), significantly inhibited cell proliferation and induced apoptosis by both, the intrinsic and extrinsic pathways. A combination of DL-247 with taxol exhibited a strong synergistic effect on DNA damage generation, apoptosis induction and inhibition of cell growth.

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