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

Wu Ching Uen, Chen Yen Choong, Chen Jei Tai, Cheng Jeng Tai

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Article number7035087
JournalEvidence-based Complementary and Alternative Medicine
Volume2019
DOIs
Publication statusPublished - Jan 1 2019

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Cell Proliferation
Toll-Like Receptor 2
U937 Cells
Leukemia
Myeloid Differentiation Factor 88
Macrophages
Cell Cycle Resting Phase
Peptides
G1 Phase
Superoxides
pardaxin
Cell Differentiation
Blood Cells
Cell Survival
Cell Cycle
Fishes
Neoplasms
Therapeutics

ASJC Scopus subject areas

  • Complementary and alternative medicine

Cite this

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abstract = "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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AU - Choong, Chen Yen

AU - Tai, Chen Jei

AU - Tai, Cheng Jeng

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N2 - 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.

AB - 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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