Piperlongumine inhibits LMP1/MYC-dependent mouse B-lymphoma cells. Han, S., Tompkins, V. S., Son, D., Kamberos, N. L., Stunz, L. L., Halwani, A., Bishop, G. A., & Janz, S. Biochemical and biophysical research communications, 436(4):660–665, July, 2013. Place: United Statesdoi abstract bibtex Piperlongumine (PL), isolated from the fruit of Long pepper, Piper longum, is a cancer-inhibiting compound that selectively kills tumor cells while sparing their normal counterparts. Here we evaluated the efficacy with which PL suppresses malignant B cells derived from a newly developed, double-transgenic mouse model of human endemic Burkitt lymphoma (BL), designated mCD40-LMP1/iMyc(Eμ). PL inhibited tumor cell proliferation in a concentration-dependent manner and induced apoptosis of neoplastic but not normal B cells. Treatment with PL resulted in downregulation of EBV-encoded LMP1, cellular Myc, constitutive NF-κB activity, and a host of LMP1-Myc-NF-κB-regulated target genes including Aurka, Bcat1, Bub1b, Ccnb1, Chek1, Fancd2, Tfrc and Xrcc6. Of note, p21(Cip1)-encoding Cdkn1a was suppressed independent of changes in Trp53 mRNA levels and p53 DNA-binding activity. Considering the central role of the LMP1-NF-κB-Myc axis in B-lineage neoplasia, these findings further our understanding of the mechanisms by which PL inhibits B-lymphoma and provide a preclinical rationale for the inclusion of PL in new interventions in blood cancers.
@article{han_piperlongumine_2013,
title = {Piperlongumine inhibits {LMP1}/{MYC}-dependent mouse {B}-lymphoma cells.},
volume = {436},
copyright = {Copyright © 2013 The Authors. Published by Elsevier Inc. All rights reserved.},
issn = {1090-2104 0006-291X},
doi = {10.1016/j.bbrc.2013.06.012},
abstract = {Piperlongumine (PL), isolated from the fruit of Long pepper, Piper longum, is a cancer-inhibiting compound that selectively kills tumor cells while sparing their normal counterparts. Here we evaluated the efficacy with which PL suppresses malignant B cells derived from a newly developed, double-transgenic mouse model of human endemic Burkitt lymphoma (BL), designated mCD40-LMP1/iMyc(Eμ). PL inhibited tumor cell proliferation in a concentration-dependent manner and induced apoptosis of neoplastic but not normal B cells. Treatment with PL resulted in downregulation of EBV-encoded LMP1, cellular Myc, constitutive NF-κB activity, and a host of LMP1-Myc-NF-κB-regulated target genes including Aurka, Bcat1, Bub1b, Ccnb1, Chek1, Fancd2, Tfrc and Xrcc6. Of note, p21(Cip1)-encoding Cdkn1a was suppressed independent of changes in Trp53 mRNA levels and p53 DNA-binding activity. Considering the central role of the LMP1-NF-κB-Myc axis in B-lineage neoplasia, these findings further our understanding of the mechanisms by which PL inhibits B-lymphoma and provide a preclinical rationale for the inclusion of PL in new interventions in blood cancers.},
language = {eng},
number = {4},
journal = {Biochemical and biophysical research communications},
author = {Han, Seong-Su and Tompkins, Van S. and Son, Dong-Ju and Kamberos, Natalie L. and Stunz, Laura L. and Halwani, Ahmad and Bishop, Gail A. and Janz, Siegfried},
month = jul,
year = {2013},
pmid = {23764397},
pmcid = {PMC3749779},
note = {Place: United States},
keywords = {Animals, Cell Line, Tumor, Mice, *Genes, myc, BL, Burkitt lymphoma, Cancer therapy and prevention, Dioxolanes/*pharmacology, Epstein Barr virus, Lymphoma, B-Cell/genetics/*pathology, Mice, Inbred C57BL, NF-kappa B/metabolism, NF-κB, p21-Encoding Cdkn1a, Piperlongumine, PL, Transgenic mouse model of human endemic Burkitt lymphoma, Viral Matrix Proteins/*physiology},
pages = {660--665},
}
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PL inhibited tumor cell proliferation in a concentration-dependent manner and induced apoptosis of neoplastic but not normal B cells. Treatment with PL resulted in downregulation of EBV-encoded LMP1, cellular Myc, constitutive NF-κB activity, and a host of LMP1-Myc-NF-κB-regulated target genes including Aurka, Bcat1, Bub1b, Ccnb1, Chek1, Fancd2, Tfrc and Xrcc6. Of note, p21(Cip1)-encoding Cdkn1a was suppressed independent of changes in Trp53 mRNA levels and p53 DNA-binding activity. 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