Isoliquiritigenin inhibits cell proliferation and induces apoptosis in human hepatoma cells

Ya Ling Hsu; Po Lin Kuo; Liang Tzung Lin; Chun Ching Lin

doi:10.1055/s-2005-837779

Isoliquiritigenin inhibits cell proliferation and induces apoptosis in human hepatoma cells

Ya Ling Hsu, Po Lin Kuo, Liang Tzung Lin, Chun Ching Lin

Research output: Contribution to journal › Article › peer-review

52 Citations (Scopus)

Abstract

Isoliquiritigenin (4,2′,4′-trihydroxychalcone, ISL) is a natural pigment with a simple chalcone structure. In this study, we report the ISL-induced inhibition on the growth of human hepatoma cells (Hep G2) for the first time. The cell growth inhibition achieved by ISL treatment resulted in programmed cell death in a caspase activation-dependent manner, with an IC ₅₀ of 10.51 μg/ mL. Outcomes of ISL treatment included the up-regulation of IκBα expression in the cytoplasm, and the decrease of NF-κB level as well as its activity in the nucleus. In addition, ISL also suppressed the expression of Bcl-X_L and c-IAP1/2 protein, the down-stream target molecule of NF-κB. These results demonstrated that ISL treatment inhibited the NF-κB cell survival-signaling pathway and induced apoptotic cell death in Hep G2 cells.

Original language	English
Pages (from-to)	130-134
Number of pages	5
Journal	Planta Medica
Volume	71
Issue number	2
DOIs	https://doi.org/10.1055/s-2005-837779
Publication status	Published - Feb 2005
Externally published	Yes

Keywords

Apoptosis
Caspase
IκBα
Isoliquiritigenin
NF-κB

ASJC Scopus subject areas

Plant Science
Drug Discovery
Organic Chemistry
Pharmacology

Access to Document

10.1055/s-2005-837779

Cite this

@article{8ed6defc1b89417389b859db2956555d,

title = "Isoliquiritigenin inhibits cell proliferation and induces apoptosis in human hepatoma cells",

abstract = "Isoliquiritigenin (4,2′,4′-trihydroxychalcone, ISL) is a natural pigment with a simple chalcone structure. In this study, we report the ISL-induced inhibition on the growth of human hepatoma cells (Hep G2) for the first time. The cell growth inhibition achieved by ISL treatment resulted in programmed cell death in a caspase activation-dependent manner, with an IC 50 of 10.51 μg/ mL. Outcomes of ISL treatment included the up-regulation of IκBα expression in the cytoplasm, and the decrease of NF-κB level as well as its activity in the nucleus. In addition, ISL also suppressed the expression of Bcl-XL and c-IAP1/2 protein, the down-stream target molecule of NF-κB. These results demonstrated that ISL treatment inhibited the NF-κB cell survival-signaling pathway and induced apoptotic cell death in Hep G2 cells.",

keywords = "Apoptosis, Caspase, IκBα, Isoliquiritigenin, NF-κB",

author = "Hsu, {Ya Ling} and Kuo, {Po Lin} and Lin, {Liang Tzung} and Lin, {Chun Ching}",

year = "2005",

month = feb,

doi = "10.1055/s-2005-837779",

language = "English",

volume = "71",

pages = "130--134",

journal = "Planta Medica",

issn = "0032-0943",

publisher = "Georg Thieme Verlag",

number = "2",

}

TY - JOUR

T1 - Isoliquiritigenin inhibits cell proliferation and induces apoptosis in human hepatoma cells

AU - Hsu, Ya Ling

AU - Kuo, Po Lin

AU - Lin, Liang Tzung

AU - Lin, Chun Ching

PY - 2005/2

Y1 - 2005/2

N2 - Isoliquiritigenin (4,2′,4′-trihydroxychalcone, ISL) is a natural pigment with a simple chalcone structure. In this study, we report the ISL-induced inhibition on the growth of human hepatoma cells (Hep G2) for the first time. The cell growth inhibition achieved by ISL treatment resulted in programmed cell death in a caspase activation-dependent manner, with an IC 50 of 10.51 μg/ mL. Outcomes of ISL treatment included the up-regulation of IκBα expression in the cytoplasm, and the decrease of NF-κB level as well as its activity in the nucleus. In addition, ISL also suppressed the expression of Bcl-XL and c-IAP1/2 protein, the down-stream target molecule of NF-κB. These results demonstrated that ISL treatment inhibited the NF-κB cell survival-signaling pathway and induced apoptotic cell death in Hep G2 cells.

AB - Isoliquiritigenin (4,2′,4′-trihydroxychalcone, ISL) is a natural pigment with a simple chalcone structure. In this study, we report the ISL-induced inhibition on the growth of human hepatoma cells (Hep G2) for the first time. The cell growth inhibition achieved by ISL treatment resulted in programmed cell death in a caspase activation-dependent manner, with an IC 50 of 10.51 μg/ mL. Outcomes of ISL treatment included the up-regulation of IκBα expression in the cytoplasm, and the decrease of NF-κB level as well as its activity in the nucleus. In addition, ISL also suppressed the expression of Bcl-XL and c-IAP1/2 protein, the down-stream target molecule of NF-κB. These results demonstrated that ISL treatment inhibited the NF-κB cell survival-signaling pathway and induced apoptotic cell death in Hep G2 cells.

KW - Apoptosis

KW - Caspase

KW - IκBα

KW - Isoliquiritigenin

KW - NF-κB

UR - http://www.scopus.com/inward/record.url?scp=14944347709&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=14944347709&partnerID=8YFLogxK

U2 - 10.1055/s-2005-837779

DO - 10.1055/s-2005-837779

M3 - Article

C2 - 15729620

AN - SCOPUS:14944347709

SN - 0032-0943

VL - 71

SP - 130

EP - 134

JO - Planta Medica

JF - Planta Medica

IS - 2

ER -

Isoliquiritigenin inhibits cell proliferation and induces apoptosis in human hepatoma cells

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this