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Article: Bitter melon (Momordica charantia) extract functions as a natural AMPK activator and synergistically enhances cisplatin cytotoxicity in ovarian cancer cells

TitleBitter melon (Momordica charantia) extract functions as a natural AMPK activator and synergistically enhances cisplatin cytotoxicity in ovarian cancer cells
Authors
Issue Date2016
PublisherSage Publications, Inc. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201510
Citation
Integrative Cancer Therapies, 2016, v. 15 n. 3, p. 376-389 How to Cite?
AbstractOBJECTIVE: Acquired chemoresistance is a major obstacle in the clinical management of ovarian cancer. Therefore, searching for alternative therapeutic modalities is urgently needed. Bitter melon (Momordica charantia) is a traditional dietary fruit, but its extract also shows potential medicinal values in human diabetes and cancers. Here, we sought to investigate the extract of bitter melon (BME) in antitumorigenic and cisplatin-induced cytotoxicity in ovarian cancer cells. METHODS: Three varieties of bitter melon were used to prepare the BME. Ovarian cancer cell lines, human immortalized epithelial ovarian cells (HOSEs), and nude mice were used to evaluate the cell cytotoxicity, cisplatin resistance, and tumor inhibitory effect of BME. The molecular mechanism of BME was examined by Western blotting. RESULTS: Cotreatment with BME and cisplatin markedly attenuated tumor growth in vitro and in vivo in a mouse xenograft model, whereas there was no observable toxicity in HOSEs or in nude mice in vivo. Interestingly, the antitumorigenic effects of BME varied with different varieties of bitter melon, suggesting that the amount of antitumorigenic substances may vary. Studies of the molecular mechanism demonstrated that BME activates AMP-activated protein kinase (AMPK) in an AMP-independent but CaMKK (Ca2+/calmodulin-dependent protein kinase)-dependent manner, exerting anticancer effects through activation of AMPK and suppression of the mTOR/p70S6K and/or the AKT/ERK/FOXM1 (Forkhead Box M1) signaling cascade. CONCLUSION: BME functions as a natural AMPK activator in the inhibition of ovarian cancer cell growth and might be useful as a supplement to improve the efficacy of cisplatin-based chemotherapy in ovarian cancer.
Persistent Identifierhttp://hdl.handle.net/10722/247661
ISSN
2017 Impact Factor: 2.657
2015 SCImago Journal Rankings: 0.822
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYUNG, MH-
dc.contributor.authorROSS, FA-
dc.contributor.authorHARDIE, DG-
dc.contributor.authorZHAN, JB-
dc.contributor.authorNgan, HYS-
dc.contributor.authorChan, DW-
dc.date.accessioned2017-10-18T08:30:38Z-
dc.date.available2017-10-18T08:30:38Z-
dc.date.issued2016-
dc.identifier.citationIntegrative Cancer Therapies, 2016, v. 15 n. 3, p. 376-389-
dc.identifier.issn1534-7354-
dc.identifier.urihttp://hdl.handle.net/10722/247661-
dc.description.abstractOBJECTIVE: Acquired chemoresistance is a major obstacle in the clinical management of ovarian cancer. Therefore, searching for alternative therapeutic modalities is urgently needed. Bitter melon (Momordica charantia) is a traditional dietary fruit, but its extract also shows potential medicinal values in human diabetes and cancers. Here, we sought to investigate the extract of bitter melon (BME) in antitumorigenic and cisplatin-induced cytotoxicity in ovarian cancer cells. METHODS: Three varieties of bitter melon were used to prepare the BME. Ovarian cancer cell lines, human immortalized epithelial ovarian cells (HOSEs), and nude mice were used to evaluate the cell cytotoxicity, cisplatin resistance, and tumor inhibitory effect of BME. The molecular mechanism of BME was examined by Western blotting. RESULTS: Cotreatment with BME and cisplatin markedly attenuated tumor growth in vitro and in vivo in a mouse xenograft model, whereas there was no observable toxicity in HOSEs or in nude mice in vivo. Interestingly, the antitumorigenic effects of BME varied with different varieties of bitter melon, suggesting that the amount of antitumorigenic substances may vary. Studies of the molecular mechanism demonstrated that BME activates AMP-activated protein kinase (AMPK) in an AMP-independent but CaMKK (Ca2+/calmodulin-dependent protein kinase)-dependent manner, exerting anticancer effects through activation of AMPK and suppression of the mTOR/p70S6K and/or the AKT/ERK/FOXM1 (Forkhead Box M1) signaling cascade. CONCLUSION: BME functions as a natural AMPK activator in the inhibition of ovarian cancer cell growth and might be useful as a supplement to improve the efficacy of cisplatin-based chemotherapy in ovarian cancer.-
dc.languageeng-
dc.publisherSage Publications, Inc. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201510-
dc.relation.ispartofIntegrative Cancer Therapies-
dc.rightsIntegrative Cancer Therapies. Copyright © Sage Publications, Inc.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleBitter melon (Momordica charantia) extract functions as a natural AMPK activator and synergistically enhances cisplatin cytotoxicity in ovarian cancer cells-
dc.typeArticle-
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hk-
dc.identifier.emailChan, DW: dwchan@hku.hk-
dc.identifier.authorityNgan, HYS=rp00346-
dc.identifier.authorityChan, DW=rp00543-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1177/1534735415611747-
dc.identifier.pmcidPMC5689379-
dc.identifier.hkuros280458-
dc.identifier.hkuros256318-
dc.identifier.volume15-
dc.identifier.issue3-
dc.identifier.spage376-
dc.identifier.epage389-
dc.identifier.isiWOS:000382215900018-
dc.publisher.placeUnited States-

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