Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation

Jin Hee Jung, Jeong Ok Lee, Ji Hae Kim, Soo Kyung Lee, Ga Young You, Sun-Hwa Park, Ji Man Park, Eung Kyun Kim, Pann Ghill Suh, Jin Kyung An, Soo Hyeon Kim

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Quercetin, an anti-oxidant flavonoid that is widely distributed in the plant kingdom, has been suggested to have chemopreventive effects on cancer cells, although the mechanism is not completely understood. In this study, we found that quercetin increased the phosphorylation of AMP-activated protein kinase (AMPK) and downstream acetyl-CoA carboxylase (ACC) and suppressed the viability of HeLa cells. AICAR, an AMPK activator, and quercetin down-regulated heat shock protein (HSP)70 and increased the activity of the pro-apoptotic effector, caspase 3. Knock-down of AMPK blocked quercetin-mediated HSP70 down-regulation. Moreover, knock-down of HSP70 enhanced quercetin-mediated caspase 3 activation. Furthermore, quercetin sustained epidermal growth factor receptor (EGFR) activation by suppressing the phosphatases, PP2a and SHP-2. Finally, quercetin increased the interaction between EGFR and Cbl, and also induced the tyrosine phosphorylation of Cbl. Together, these results suggest that quercetin may have anti-tumor effects on HeLa cells via AMPK-induced HSP70 and down-regulation of EGFR.

Original languageEnglish
Pages (from-to)408-414
Number of pages7
JournalJournal of Cellular Physiology
Volume223
Issue number2
DOIs
Publication statusPublished - 2010 May 1

Fingerprint

AMP-Activated Protein Kinases
Quercetin
HeLa Cells
Epidermal Growth Factor Receptor
Cell Survival
Down-Regulation
Cells
Phosphorylation
Caspase 3
Chemical activation
Effector Caspases
Acetyl-CoA Carboxylase
HSP70 Heat-Shock Proteins
Phosphoric Monoester Hydrolases
Flavonoids
Oxidants
Tyrosine
Tumors
Neoplasms

ASJC Scopus subject areas

  • Medicine(all)
  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation. / Jung, Jin Hee; Lee, Jeong Ok; Kim, Ji Hae; Lee, Soo Kyung; You, Ga Young; Park, Sun-Hwa; Park, Ji Man; Kim, Eung Kyun; Suh, Pann Ghill; An, Jin Kyung; Kim, Soo Hyeon.

In: Journal of Cellular Physiology, Vol. 223, No. 2, 01.05.2010, p. 408-414.

Research output: Contribution to journalArticle

Jung, JH, Lee, JO, Kim, JH, Lee, SK, You, GY, Park, S-H, Park, JM, Kim, EK, Suh, PG, An, JK & Kim, SH 2010, 'Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation', Journal of Cellular Physiology, vol. 223, no. 2, pp. 408-414. https://doi.org/10.1002/jcp.22049
Jung, Jin Hee ; Lee, Jeong Ok ; Kim, Ji Hae ; Lee, Soo Kyung ; You, Ga Young ; Park, Sun-Hwa ; Park, Ji Man ; Kim, Eung Kyun ; Suh, Pann Ghill ; An, Jin Kyung ; Kim, Soo Hyeon. / Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation. In: Journal of Cellular Physiology. 2010 ; Vol. 223, No. 2. pp. 408-414.
@article{36370832dbd74a95aa1702ca894b7f05,
title = "Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation",
abstract = "Quercetin, an anti-oxidant flavonoid that is widely distributed in the plant kingdom, has been suggested to have chemopreventive effects on cancer cells, although the mechanism is not completely understood. In this study, we found that quercetin increased the phosphorylation of AMP-activated protein kinase (AMPK) and downstream acetyl-CoA carboxylase (ACC) and suppressed the viability of HeLa cells. AICAR, an AMPK activator, and quercetin down-regulated heat shock protein (HSP)70 and increased the activity of the pro-apoptotic effector, caspase 3. Knock-down of AMPK blocked quercetin-mediated HSP70 down-regulation. Moreover, knock-down of HSP70 enhanced quercetin-mediated caspase 3 activation. Furthermore, quercetin sustained epidermal growth factor receptor (EGFR) activation by suppressing the phosphatases, PP2a and SHP-2. Finally, quercetin increased the interaction between EGFR and Cbl, and also induced the tyrosine phosphorylation of Cbl. Together, these results suggest that quercetin may have anti-tumor effects on HeLa cells via AMPK-induced HSP70 and down-regulation of EGFR.",
author = "Jung, {Jin Hee} and Lee, {Jeong Ok} and Kim, {Ji Hae} and Lee, {Soo Kyung} and You, {Ga Young} and Sun-Hwa Park and Park, {Ji Man} and Kim, {Eung Kyun} and Suh, {Pann Ghill} and An, {Jin Kyung} and Kim, {Soo Hyeon}",
year = "2010",
month = "5",
day = "1",
doi = "10.1002/jcp.22049",
language = "English",
volume = "223",
pages = "408--414",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley-Liss Inc.",
number = "2",

}

TY - JOUR

T1 - Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation

AU - Jung, Jin Hee

AU - Lee, Jeong Ok

AU - Kim, Ji Hae

AU - Lee, Soo Kyung

AU - You, Ga Young

AU - Park, Sun-Hwa

AU - Park, Ji Man

AU - Kim, Eung Kyun

AU - Suh, Pann Ghill

AU - An, Jin Kyung

AU - Kim, Soo Hyeon

PY - 2010/5/1

Y1 - 2010/5/1

N2 - Quercetin, an anti-oxidant flavonoid that is widely distributed in the plant kingdom, has been suggested to have chemopreventive effects on cancer cells, although the mechanism is not completely understood. In this study, we found that quercetin increased the phosphorylation of AMP-activated protein kinase (AMPK) and downstream acetyl-CoA carboxylase (ACC) and suppressed the viability of HeLa cells. AICAR, an AMPK activator, and quercetin down-regulated heat shock protein (HSP)70 and increased the activity of the pro-apoptotic effector, caspase 3. Knock-down of AMPK blocked quercetin-mediated HSP70 down-regulation. Moreover, knock-down of HSP70 enhanced quercetin-mediated caspase 3 activation. Furthermore, quercetin sustained epidermal growth factor receptor (EGFR) activation by suppressing the phosphatases, PP2a and SHP-2. Finally, quercetin increased the interaction between EGFR and Cbl, and also induced the tyrosine phosphorylation of Cbl. Together, these results suggest that quercetin may have anti-tumor effects on HeLa cells via AMPK-induced HSP70 and down-regulation of EGFR.

AB - Quercetin, an anti-oxidant flavonoid that is widely distributed in the plant kingdom, has been suggested to have chemopreventive effects on cancer cells, although the mechanism is not completely understood. In this study, we found that quercetin increased the phosphorylation of AMP-activated protein kinase (AMPK) and downstream acetyl-CoA carboxylase (ACC) and suppressed the viability of HeLa cells. AICAR, an AMPK activator, and quercetin down-regulated heat shock protein (HSP)70 and increased the activity of the pro-apoptotic effector, caspase 3. Knock-down of AMPK blocked quercetin-mediated HSP70 down-regulation. Moreover, knock-down of HSP70 enhanced quercetin-mediated caspase 3 activation. Furthermore, quercetin sustained epidermal growth factor receptor (EGFR) activation by suppressing the phosphatases, PP2a and SHP-2. Finally, quercetin increased the interaction between EGFR and Cbl, and also induced the tyrosine phosphorylation of Cbl. Together, these results suggest that quercetin may have anti-tumor effects on HeLa cells via AMPK-induced HSP70 and down-regulation of EGFR.

UR - http://www.scopus.com/inward/record.url?scp=77950792403&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77950792403&partnerID=8YFLogxK

U2 - 10.1002/jcp.22049

DO - 10.1002/jcp.22049

M3 - Article

VL - 223

SP - 408

EP - 414

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

IS - 2

ER -