Next Article in Journal
Regulation of the Rhythmic Emission of Plant Volatiles by the Circadian Clock
Previous Article in Journal
In Situ Synthesis of Silver Nanoparticles in a Hydrogel of Carboxymethyl Cellulose with Phthalated-Cashew Gum as a Promising Antibacterial and Healing Agent
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2017, 18(11), 2407; https://doi.org/10.3390/ijms18112407

Lp16-PSP, a Member of YjgF/YER057c/UK114 Protein Family Induces Apoptosis and p21WAF1/CIP1 Mediated G1 Cell Cycle Arrest in Human Acute Promyelocytic Leukemia (APL) HL-60 Cells

1
Department of Microbiology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, Liaoning, China
2
Institute of Cancer Stem Cell, Dalian Medical University, Dalian 116044, Liaoning, China
3
Department of Biotechnology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, Liaoning, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 23 September 2017 / Revised: 3 November 2017 / Accepted: 7 November 2017 / Published: 13 November 2017
(This article belongs to the Section Biochemistry)
Full-Text   |   PDF [6640 KB, uploaded 14 November 2017]   |  

Abstract

Lp16-PSP (Latcripin 16-Perchloric acid Soluble Protein) from Lentinula edodes strain C91-3 has been reported previously in our laboratory to have selective cytotoxic activity against a panel of human cell lines. Herein, we have used several parameters in order to characterize the Lp16-PSP-induced cell death using human acute promyeloid leukemia (HL-60) as a model cancer. The results of phase contrast microscopy, nuclear examination, DNA fragmentation detection and flow cytometry revealed that high doses of Lp16-PSP resulted in the induction of apoptosis in HL-60 cells. The colorimetric assay showed the activation of caspase-8, -9, and -3 cascade highlighting the involvement of Fas/FasL-related pathway. Whereas, Western blot revealed the cleavage of caspase-3, increased expression of Bax, the release of cytochrome c and decreased expression of Bcl-2 in a dose-dependent manner, suggesting the intrinsic pathway might be involved in Lp16-PSP-induced apoptosis as well. Low doses of Lp16-PSP resulted in the anchorage-independent growth inhibition, induction of G1 phase arrest, accompanied by the increased expression of p21WAF1/CIP1, along with the decreased expression of cyclin D, E, and cdk6. In addition, Lp16-PSP resulted in constitutive translocation inhibition of transcription factor nuclear factor kappa B (NF-κB) into the nucleus by decreasing the phosphorylation of IκBα. All these findings suggested Lp16-PSP as a potential agent against acute promyeloid leukemia; however, further investigations are ultimately needed. View Full-Text
Keywords: Lentinula edodes; Lp16-PSP; acute promyeloid leukemia; extrinsic and intrinsic apoptotic pathway; G1 phase cell cycle arrest; NF-κB signaling pathway Lentinula edodes; Lp16-PSP; acute promyeloid leukemia; extrinsic and intrinsic apoptotic pathway; G1 phase cell cycle arrest; NF-κB signaling pathway
Figures

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Joseph, T.P.; Chanda, W.; Mohammad, A.F.; Kanwal, S.; Batool, S.; Zhang, M.; Zhong, M.; Huang, M. Lp16-PSP, a Member of YjgF/YER057c/UK114 Protein Family Induces Apoptosis and p21WAF1/CIP1 Mediated G1 Cell Cycle Arrest in Human Acute Promyelocytic Leukemia (APL) HL-60 Cells. Int. J. Mol. Sci. 2017, 18, 2407.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top