Sanguinarine induces bimodal cell death in K562 but not in high Bcl-2-expressing JM1 cells

P. Weerasinghe, S. Hallock, S. C. Tang, A. Liepins

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Our previous studies with low Bcl-2-expressing K562 cells have shown that, when treated with the putative anti-cancer drug sanguinarine, concentrations of 1.5 μg/ml induced the morphology of apoptosis or programmed cell death (PCD), while concentrations of 12.5 μg/ml induced a morphology of blister formation or blister cell death (BCD). To elucidate the possible role of Bcl-2 in this dual cell death modality induced by sanguinarine, K562 and the high Bcl-2-expressing JM1 cells were treated with sanguinarine concentrations of 1.5 μg/ml and 12.5 μg/ml respectively, and multiple parameters of their effects were studied using light and electron microscopy, terminal deoxynucleotidyl transferase (TdT) end-labeling, 51Cr release, trypan blue exclusion, propidium iodide exclusion, and annexin-V binding. In general, we found that, while K562 cells underwent PCD and BCD when treated with sanguinarine, JM1 cells failed to undergo either PCD or BCD under the same experimental conditions. Thus, the over-expression of anti-apoptotic Bcl-2 may have prevented sanguinarine from inducing PCD and BCD in JM1 cells. These results indicate that the resistance of JM1 cells to the alkaloid sanguinarine may have been due to an anti-BCD role played by Bcl-2, in addition to its widely reported anti-apoptotic role.

Original languageEnglish (US)
Pages (from-to)717-726
Number of pages10
JournalPathology Research and Practice
Volume197
Issue number11
DOIs
StatePublished - Jan 1 2001

Fingerprint

Cell Death
Blister
K562 Cells
sanguinarine
Trypan Blue
DNA Nucleotidylexotransferase
Propidium
Annexin A5
Alkaloids
Electron Microscopy
Apoptosis
Light
Pharmaceutical Preparations
Neoplasms

Keywords

  • Apoptosis
  • Blebbing
  • Blister cell death
  • Chemoresistance
  • Sanguinarine

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Cell Biology

Cite this

Sanguinarine induces bimodal cell death in K562 but not in high Bcl-2-expressing JM1 cells. / Weerasinghe, P.; Hallock, S.; Tang, S. C.; Liepins, A.

In: Pathology Research and Practice, Vol. 197, No. 11, 01.01.2001, p. 717-726.

Research output: Contribution to journalArticle

Weerasinghe, P. ; Hallock, S. ; Tang, S. C. ; Liepins, A. / Sanguinarine induces bimodal cell death in K562 but not in high Bcl-2-expressing JM1 cells. In: Pathology Research and Practice. 2001 ; Vol. 197, No. 11. pp. 717-726.
@article{4b4971c646734f7ba234f52d7b68ce34,
title = "Sanguinarine induces bimodal cell death in K562 but not in high Bcl-2-expressing JM1 cells",
abstract = "Our previous studies with low Bcl-2-expressing K562 cells have shown that, when treated with the putative anti-cancer drug sanguinarine, concentrations of 1.5 μg/ml induced the morphology of apoptosis or programmed cell death (PCD), while concentrations of 12.5 μg/ml induced a morphology of blister formation or blister cell death (BCD). To elucidate the possible role of Bcl-2 in this dual cell death modality induced by sanguinarine, K562 and the high Bcl-2-expressing JM1 cells were treated with sanguinarine concentrations of 1.5 μg/ml and 12.5 μg/ml respectively, and multiple parameters of their effects were studied using light and electron microscopy, terminal deoxynucleotidyl transferase (TdT) end-labeling, 51Cr release, trypan blue exclusion, propidium iodide exclusion, and annexin-V binding. In general, we found that, while K562 cells underwent PCD and BCD when treated with sanguinarine, JM1 cells failed to undergo either PCD or BCD under the same experimental conditions. Thus, the over-expression of anti-apoptotic Bcl-2 may have prevented sanguinarine from inducing PCD and BCD in JM1 cells. These results indicate that the resistance of JM1 cells to the alkaloid sanguinarine may have been due to an anti-BCD role played by Bcl-2, in addition to its widely reported anti-apoptotic role.",
keywords = "Apoptosis, Blebbing, Blister cell death, Chemoresistance, Sanguinarine",
author = "P. Weerasinghe and S. Hallock and Tang, {S. C.} and A. Liepins",
year = "2001",
month = "1",
day = "1",
doi = "10.1078/0344-0338-00150",
language = "English (US)",
volume = "197",
pages = "717--726",
journal = "Pathology Research and Practice",
issn = "0344-0338",
publisher = "Urban und Fischer Verlag GmbH und Co. KG",
number = "11",

}

TY - JOUR

T1 - Sanguinarine induces bimodal cell death in K562 but not in high Bcl-2-expressing JM1 cells

AU - Weerasinghe, P.

AU - Hallock, S.

AU - Tang, S. C.

AU - Liepins, A.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - Our previous studies with low Bcl-2-expressing K562 cells have shown that, when treated with the putative anti-cancer drug sanguinarine, concentrations of 1.5 μg/ml induced the morphology of apoptosis or programmed cell death (PCD), while concentrations of 12.5 μg/ml induced a morphology of blister formation or blister cell death (BCD). To elucidate the possible role of Bcl-2 in this dual cell death modality induced by sanguinarine, K562 and the high Bcl-2-expressing JM1 cells were treated with sanguinarine concentrations of 1.5 μg/ml and 12.5 μg/ml respectively, and multiple parameters of their effects were studied using light and electron microscopy, terminal deoxynucleotidyl transferase (TdT) end-labeling, 51Cr release, trypan blue exclusion, propidium iodide exclusion, and annexin-V binding. In general, we found that, while K562 cells underwent PCD and BCD when treated with sanguinarine, JM1 cells failed to undergo either PCD or BCD under the same experimental conditions. Thus, the over-expression of anti-apoptotic Bcl-2 may have prevented sanguinarine from inducing PCD and BCD in JM1 cells. These results indicate that the resistance of JM1 cells to the alkaloid sanguinarine may have been due to an anti-BCD role played by Bcl-2, in addition to its widely reported anti-apoptotic role.

AB - Our previous studies with low Bcl-2-expressing K562 cells have shown that, when treated with the putative anti-cancer drug sanguinarine, concentrations of 1.5 μg/ml induced the morphology of apoptosis or programmed cell death (PCD), while concentrations of 12.5 μg/ml induced a morphology of blister formation or blister cell death (BCD). To elucidate the possible role of Bcl-2 in this dual cell death modality induced by sanguinarine, K562 and the high Bcl-2-expressing JM1 cells were treated with sanguinarine concentrations of 1.5 μg/ml and 12.5 μg/ml respectively, and multiple parameters of their effects were studied using light and electron microscopy, terminal deoxynucleotidyl transferase (TdT) end-labeling, 51Cr release, trypan blue exclusion, propidium iodide exclusion, and annexin-V binding. In general, we found that, while K562 cells underwent PCD and BCD when treated with sanguinarine, JM1 cells failed to undergo either PCD or BCD under the same experimental conditions. Thus, the over-expression of anti-apoptotic Bcl-2 may have prevented sanguinarine from inducing PCD and BCD in JM1 cells. These results indicate that the resistance of JM1 cells to the alkaloid sanguinarine may have been due to an anti-BCD role played by Bcl-2, in addition to its widely reported anti-apoptotic role.

KW - Apoptosis

KW - Blebbing

KW - Blister cell death

KW - Chemoresistance

KW - Sanguinarine

UR - http://www.scopus.com/inward/record.url?scp=0035210497&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035210497&partnerID=8YFLogxK

U2 - 10.1078/0344-0338-00150

DO - 10.1078/0344-0338-00150

M3 - Article

C2 - 11770015

AN - SCOPUS:0035210497

VL - 197

SP - 717

EP - 726

JO - Pathology Research and Practice

JF - Pathology Research and Practice

SN - 0344-0338

IS - 11

ER -