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Article: Inhibition of cervical cancer cell growth through activation of upstream kinases of AMP-activated protein kinase

TitleInhibition of cervical cancer cell growth through activation of upstream kinases of AMP-activated protein kinase
Authors
KeywordsAICAR
AMP-activated protein kinase
CaMKK
Cervical cancer
LKB1
Issue Date2009
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBI
Citation
Tumor Biology, 2009, v. 30 n. 2, p. 80-85 How to Cite?
AbstractAMP-activated protein kinase (AMPK) is a critical energy-balancing sensor in the regulation of cellular metabolism in response to external stimuli. Emerging evidence has suggested that AMPK is a potential therapeutic target for human cancers. AICAR, one of the pharmacological AMPK activators, has been widely used to suppress cancer cell growth through activation of LKB1, an upstream kinase of AMPK. However, frequent mutations and deletions of LKB1 found in some cancer cells limit the application of AICAR as an efficient therapeutic drug. Here we show that an alternative pharmacological AMPK activator, A23187, was able to inhibit cervical cancer cell growth through activation of Ca 2+/calmodulin-dependent protein kinase kinase β, another upstream kinase of AMPK. Using cervical cancer cell models, we found that HeLa (LKB1-deficient cell) responded less to the anti-proliferative effect exerted by AICAR treatment (p < 0.001) compared with CaSki and C41 (LKB1-expressing cells). Conversely, the anti-proliferative effect was increased significantly in HeLa but not in CaSki and C41 cells under treatment by A23187 (p < 0.001). Moreover, co-treatment of AICAR and A23187 was able to further enhance the inhibitory effect on cell growth of Hela, CaSki and C41 cells. Notably, both AICAR and A23187 exerted the anti-proliferative effect on cervical cancer cells by suppressing AMPK/mTOR signalling activity. These data suggest that A23187 could be an alternative potential therapeutic drug used for anti-proliferation in LKB1-deficient cancer cells. Copyright © 2009 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/60387
ISSN
2015 Impact Factor: 2.926
2015 SCImago Journal Rankings: 0.989
ISI Accession Number ID
Funding AgencyGrant Number
Wong Check She Charitable Foundation
Funding Information:

This study was supported by the Wong Check She Charitable Foundation.

References

 

DC FieldValueLanguage
dc.contributor.authorYu, SYMen_HK
dc.contributor.authorChan, DWen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-05-31T04:09:37Z-
dc.date.available2010-05-31T04:09:37Z-
dc.date.issued2009en_HK
dc.identifier.citationTumor Biology, 2009, v. 30 n. 2, p. 80-85en_HK
dc.identifier.issn1010-4283en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60387-
dc.description.abstractAMP-activated protein kinase (AMPK) is a critical energy-balancing sensor in the regulation of cellular metabolism in response to external stimuli. Emerging evidence has suggested that AMPK is a potential therapeutic target for human cancers. AICAR, one of the pharmacological AMPK activators, has been widely used to suppress cancer cell growth through activation of LKB1, an upstream kinase of AMPK. However, frequent mutations and deletions of LKB1 found in some cancer cells limit the application of AICAR as an efficient therapeutic drug. Here we show that an alternative pharmacological AMPK activator, A23187, was able to inhibit cervical cancer cell growth through activation of Ca 2+/calmodulin-dependent protein kinase kinase β, another upstream kinase of AMPK. Using cervical cancer cell models, we found that HeLa (LKB1-deficient cell) responded less to the anti-proliferative effect exerted by AICAR treatment (p < 0.001) compared with CaSki and C41 (LKB1-expressing cells). Conversely, the anti-proliferative effect was increased significantly in HeLa but not in CaSki and C41 cells under treatment by A23187 (p < 0.001). Moreover, co-treatment of AICAR and A23187 was able to further enhance the inhibitory effect on cell growth of Hela, CaSki and C41 cells. Notably, both AICAR and A23187 exerted the anti-proliferative effect on cervical cancer cells by suppressing AMPK/mTOR signalling activity. These data suggest that A23187 could be an alternative potential therapeutic drug used for anti-proliferation in LKB1-deficient cancer cells. Copyright © 2009 S. Karger AG, Basel.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBIen_HK
dc.relation.ispartofTumor Biologyen_HK
dc.subjectAICARen_HK
dc.subjectAMP-activated protein kinaseen_HK
dc.subjectCaMKKen_HK
dc.subjectCervical canceren_HK
dc.subjectLKB1en_HK
dc.titleInhibition of cervical cancer cell growth through activation of upstream kinases of AMP-activated protein kinaseen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, DW: dwchan@hku.hken_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityChan, DW=rp00543en_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000216843en_HK
dc.identifier.pmid19407487en_HK
dc.identifier.scopuseid_2-s2.0-65449173255en_HK
dc.identifier.hkuros157996en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65449173255&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue2en_HK
dc.identifier.spage80en_HK
dc.identifier.epage85en_HK
dc.identifier.isiWOS:000266098000004-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridYu, SYM=24463692000en_HK
dc.identifier.scopusauthoridChan, DW=26533900600en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

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