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Article: Overexpression of aldose reductase in liver cancers may contribute to drug resistance

TitleOverexpression of aldose reductase in liver cancers may contribute to drug resistance
Authors
KeywordsAldose reductase
Daunorubicin
Drug resistance
Hepatocellular carcinoma
Liver cancer
Issue Date2001
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anti-cancerdrugs.com
Citation
Anti-Cancer Drugs, 2001, v. 12 n. 2, p. 129-132 How to Cite?
AbstractWe previously found that about 29% of human liver cancers overexpressed aldose reductase (AR) and about 54% of them overexpressed an AR-like gene called ARL-1 that has similar enzymatic activities to AR. Since these aldo-keto reductases can reduce a broad spectrum of substrates including cytotoxic aldehydes, we were interested to find out if these enzymes can contribute to the resistance of liver cancer chemotherapy by inactivating some of the anticancer drugs. HepG2 cells, a stable line of liver cells, were induced to overexpress AR by hypertonicity. Cells that were cultured in hypertonic medium became more resistant to daunorubicin, suggesting that ovarexpression of AR made the cells more resistant to this drug. This is confirmed by the fact that addition of AR inhibitor sensitizes the cells to this drug again. This information may be important for designing new drugs to treat this deadly disease. © 2001 Lippincott Williams & Wilkins.
Persistent Identifierhttp://hdl.handle.net/10722/87997
ISSN
2015 Impact Factor: 2.268
2015 SCImago Journal Rankings: 0.795
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, KWYen_HK
dc.contributor.authorKo, BCBen_HK
dc.contributor.authorJiang, Zen_HK
dc.contributor.authorCao, Den_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-06T09:37:18Z-
dc.date.available2010-09-06T09:37:18Z-
dc.date.issued2001en_HK
dc.identifier.citationAnti-Cancer Drugs, 2001, v. 12 n. 2, p. 129-132en_HK
dc.identifier.issn0959-4973en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87997-
dc.description.abstractWe previously found that about 29% of human liver cancers overexpressed aldose reductase (AR) and about 54% of them overexpressed an AR-like gene called ARL-1 that has similar enzymatic activities to AR. Since these aldo-keto reductases can reduce a broad spectrum of substrates including cytotoxic aldehydes, we were interested to find out if these enzymes can contribute to the resistance of liver cancer chemotherapy by inactivating some of the anticancer drugs. HepG2 cells, a stable line of liver cells, were induced to overexpress AR by hypertonicity. Cells that were cultured in hypertonic medium became more resistant to daunorubicin, suggesting that ovarexpression of AR made the cells more resistant to this drug. This is confirmed by the fact that addition of AR inhibitor sensitizes the cells to this drug again. This information may be important for designing new drugs to treat this deadly disease. © 2001 Lippincott Williams & Wilkins.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anti-cancerdrugs.comen_HK
dc.relation.ispartofAnti-Cancer Drugsen_HK
dc.rightsAnti-Cancer Drugs. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectAldose reductaseen_HK
dc.subjectDaunorubicinen_HK
dc.subjectDrug resistanceen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectLiver canceren_HK
dc.titleOverexpression of aldose reductase in liver cancers may contribute to drug resistanceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0959-4973&volume=12&spage=129&epage=132&date=2001&atitle=Overexpression+of+aldose+reductase+in+liver+cancers+may+contribute+to+drug+resistanceen_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/00001813-200102000-00005en_HK
dc.identifier.pmid11261885-
dc.identifier.scopuseid_2-s2.0-0035097039en_HK
dc.identifier.hkuros60354en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035097039&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue2en_HK
dc.identifier.spage129en_HK
dc.identifier.epage132en_HK
dc.identifier.isiWOS:000167125300005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, KWY=7501499014en_HK
dc.identifier.scopusauthoridKo, BCB=7102833927en_HK
dc.identifier.scopusauthoridJiang, Z=7404279744en_HK
dc.identifier.scopusauthoridCao, D=7202125033en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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