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Article: Inhibition of Stat3 activity by YC-1 enhances chemo-sensitivity in hepatocellular carcinoma

TitleInhibition of Stat3 activity by YC-1 enhances chemo-sensitivity in hepatocellular carcinoma
Authors
KeywordsChemo-sensitivity
Hepatocellular carcinoma
Signal transducers and activators of transcription 3
YC-1
Issue Date2007
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.php
Citation
Cancer Biology And Therapy, 2007, v. 6 n. 12, p. 1900-1907 How to Cite?
AbstractThe present study investigated the effect of YC-1, a novel anti-cancer agent, on the chemo-sensitivity of hepatocellular carcinoma (HCC). YC-1 was administered with chemo-cytotoxic drug, cisplatin, both in vitro and in vivo. YC-1 alone downregulated the expression of phosphorylated form of signal transducers and activators of transcription 3 (P-Stat3[705]), a key mediator in chemo-resistance. When combined with cisplatin, YC-1 further promoted tumor cell apoptosis, decreased the expression of P-Stat3(705), Bcl-xL, CyclinD1 and survivin, and induced the cleavage of caspase 9 and PARP. Overexpression of Stat3 reversed YC-1 induced cell death. YC-1 inhibited Stat3 activity by enhancing the polyubiquitination of P-Stat3(705) induced by cisplatin. In the in vivo setting, YC-1 combined with cisplatin remarkably suppressed tumor growth in a HCC xenograft model, and this effect was also accompanied by YC-1 mediated downregulation of P-Stat3(705), Bcl-xL, Cyclin D1 and survivin, and induction of cleaved caspase 9 and PARP in the tumor tissues. In conclusion, the present study demonstrated a novel anti-cancer effect of YC-1 in enhancing chemo-sensitivity of HCC cells to cisplatin through a Stat3 dependent manner. This finding provides insight into design of a new therapeutic strategy to improve efficacy of chemotherapy in HCC patients. ©2007 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/84495
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.297
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChi, KLen_HK
dc.contributor.authorZhen, FYen_HK
dc.contributor.authorShuk, PLen_HK
dc.contributor.authorChi, TLen_HK
dc.contributor.authorNgai, Pen_HK
dc.contributor.authorKa, HTen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorSheung, TFen_HK
dc.date.accessioned2010-09-06T08:53:38Z-
dc.date.available2010-09-06T08:53:38Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer Biology And Therapy, 2007, v. 6 n. 12, p. 1900-1907en_HK
dc.identifier.issn1538-4047en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84495-
dc.description.abstractThe present study investigated the effect of YC-1, a novel anti-cancer agent, on the chemo-sensitivity of hepatocellular carcinoma (HCC). YC-1 was administered with chemo-cytotoxic drug, cisplatin, both in vitro and in vivo. YC-1 alone downregulated the expression of phosphorylated form of signal transducers and activators of transcription 3 (P-Stat3[705]), a key mediator in chemo-resistance. When combined with cisplatin, YC-1 further promoted tumor cell apoptosis, decreased the expression of P-Stat3(705), Bcl-xL, CyclinD1 and survivin, and induced the cleavage of caspase 9 and PARP. Overexpression of Stat3 reversed YC-1 induced cell death. YC-1 inhibited Stat3 activity by enhancing the polyubiquitination of P-Stat3(705) induced by cisplatin. In the in vivo setting, YC-1 combined with cisplatin remarkably suppressed tumor growth in a HCC xenograft model, and this effect was also accompanied by YC-1 mediated downregulation of P-Stat3(705), Bcl-xL, Cyclin D1 and survivin, and induction of cleaved caspase 9 and PARP in the tumor tissues. In conclusion, the present study demonstrated a novel anti-cancer effect of YC-1 in enhancing chemo-sensitivity of HCC cells to cisplatin through a Stat3 dependent manner. This finding provides insight into design of a new therapeutic strategy to improve efficacy of chemotherapy in HCC patients. ©2007 Landes Bioscience.en_HK
dc.languageengen_HK
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.phpen_HK
dc.relation.ispartofCancer Biology and Therapyen_HK
dc.subjectChemo-sensitivityen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectSignal transducers and activators of transcription 3en_HK
dc.subjectYC-1en_HK
dc.titleInhibition of Stat3 activity by YC-1 enhances chemo-sensitivity in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1538-4047&volume=6&issue=12&spage=1900&epage=1907&date=2007&atitle=Inhibition+of+Stat3+activity+by+YC-1+enhances+chemo-sensitivity+in+hepatocellular+carcinomaen_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid18059167en_HK
dc.identifier.scopuseid_2-s2.0-42549131961en_HK
dc.identifier.hkuros141594en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-42549131961&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1900en_HK
dc.identifier.epage1907en_HK
dc.identifier.isiWOS:000253944900019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChi, KL=15070609500en_HK
dc.identifier.scopusauthoridZhen, FY=14018809600en_HK
dc.identifier.scopusauthoridShuk, PL=24081534300en_HK
dc.identifier.scopusauthoridChi, TL=23987591100en_HK
dc.identifier.scopusauthoridNgai, P=23477971900en_HK
dc.identifier.scopusauthoridKa, HT=15070828800en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridSheung, TF=6506234707en_HK

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