Lipopolysaccharide-Binding Motif Derived Peptides Induce Cell Membrane Damages in Human Lung Cancer and Hepatoma Cell Lines

Sung, Hung-Hung; Jane, Wann‐Neng; Kao, Wen-Yi; Fu, Po-Ying; Ho, Shih-Ching; Yang, Chu‐Wen

doi:10.1007/s10989-015-9459-7

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“…Recently, several peptides have been found to suppress leukemia cancer like THP-1 leukemic cells by inducing plasma membrane damage, including LPSBD0 and LPSBD2 peptides [29]. Epinecidin-1 peptide also has been found to regulate the toll-like receptor (TLR)-2/MyD88 pathway in RAW264.7 macrophage [16] and exert anticancer activity for leukemia U937 cells [17].…”

Section: Discussionmentioning

confidence: 99%

Pardaxin Promoted Differentiation and Maturation of Leukemic Cells via Regulating TLR2/MyD88 Signal against Cell Proliferation

Uen

Choong

Tai

2019

Evidence-Based Complementary and Alternative Medicine

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Objective. Leukemia is a cancer of the blood cells. Leukemic THP-1 and U937 cells were used in this study as monocytic effectors cells for proliferation responses and macrophage-like cells induction in leukemia. Pardaxin is an antimicrobial peptide isolated from the marine fish species.Methods. After treatment for 5 days, pardaxin significantly suppressed cell viability and arrested cell cycle at G0/G1 phase in leukemic cells which were evaluated.Results. Pardaxin also induced cell differentiation and maturation of THP-1 and U937 cells into macrophage-like cells with phagocytotic ability. Moreover, pardaxin elevated the expression of MyD88 but not toll-like receptor (TLR)-2 in both leukemic cells. TLR-2 blocking peptide was used to confirm that pardaxin attenuated phagocytotic ability and superoxide anion production in leukemic cells via activating MyD88 protein.Conclusions. These findings suggested that pardaxin has a therapeutic potential for leukemia.

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Section: Discussionmentioning

confidence: 99%