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- Publisher Website: 10.1002/path.2024
- Scopus: eid_2-s2.0-33747874514
- PMID: 16841372
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Article: PIN1 expression contributes to hepatic carcinogenesis
Title | PIN1 expression contributes to hepatic carcinogenesis |
---|---|
Authors | |
Keywords | β-catenin Hepatocellular carcinoma Peptidyl-prolyl-isomerase PIN1 RNA interference |
Issue Date | 2006 |
Publisher | John Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130 |
Citation | Journal Of Pathology, 2006, v. 210 n. 1, p. 19-25 How to Cite? |
Abstract | The phospho-Ser/Thr-Pro specific prolyl-isomerase PIN1 is over-expressed in more than 50% of hepatocellular carcinomas (HCCs). To investigate its potential oncogenicity, we over-expressed PIN1 in a non-transformed human liver cell line MIHA. This resulted in up-regulation of β-catenin and cyclin D1, leading to anchorage-independent growth in soft agar and tumorigenicity in nude mice. To further validate the role of PIN1 in hepatocarcinogenesis, PIN was suppressed by RNA interference (siRNA) in the HCC cell line PLC/PRF/5. siRNA-PIN1 transfection of PLC/ PRF/5 cells led to repression of PIN1 expression, resulting in decreased levels of β-catenin and cyclin D1. siRNA-PIN1 transfectants showed lower cell proliferation rates, reduced colony formation, and retarded cell cycle progression, with an increase in cells residing in G0/G1. Furthermore, soft agar colony formation was depressed, and tumorigenicity in nude mice was abrogated. These findings implicate PIN1 expression as an important step in hepatic carcinogenesis. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
Persistent Identifier | http://hdl.handle.net/10722/78454 |
ISSN | 2023 Impact Factor: 5.6 2023 SCImago Journal Rankings: 2.426 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Pang, RW | en_HK |
dc.contributor.author | Lee, TK | en_HK |
dc.contributor.author | Man, K | en_HK |
dc.contributor.author | Poon, RT | en_HK |
dc.contributor.author | Fan, ST | en_HK |
dc.contributor.author | Kwong, YL | en_HK |
dc.contributor.author | Tse, E | en_HK |
dc.date.accessioned | 2010-09-06T07:43:04Z | - |
dc.date.available | 2010-09-06T07:43:04Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | Journal Of Pathology, 2006, v. 210 n. 1, p. 19-25 | en_HK |
dc.identifier.issn | 0022-3417 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/78454 | - |
dc.description.abstract | The phospho-Ser/Thr-Pro specific prolyl-isomerase PIN1 is over-expressed in more than 50% of hepatocellular carcinomas (HCCs). To investigate its potential oncogenicity, we over-expressed PIN1 in a non-transformed human liver cell line MIHA. This resulted in up-regulation of β-catenin and cyclin D1, leading to anchorage-independent growth in soft agar and tumorigenicity in nude mice. To further validate the role of PIN1 in hepatocarcinogenesis, PIN was suppressed by RNA interference (siRNA) in the HCC cell line PLC/PRF/5. siRNA-PIN1 transfection of PLC/ PRF/5 cells led to repression of PIN1 expression, resulting in decreased levels of β-catenin and cyclin D1. siRNA-PIN1 transfectants showed lower cell proliferation rates, reduced colony formation, and retarded cell cycle progression, with an increase in cells residing in G0/G1. Furthermore, soft agar colony formation was depressed, and tumorigenicity in nude mice was abrogated. These findings implicate PIN1 expression as an important step in hepatic carcinogenesis. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. | en_HK |
dc.language | eng | en_HK |
dc.publisher | John Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130 | en_HK |
dc.relation.ispartof | Journal of Pathology | en_HK |
dc.rights | Journal of Pathology. Copyright © John Wiley & Sons Ltd. | en_HK |
dc.subject | β-catenin | en_HK |
dc.subject | Hepatocellular carcinoma | en_HK |
dc.subject | Peptidyl-prolyl-isomerase | en_HK |
dc.subject | PIN1 | en_HK |
dc.subject | RNA interference | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Carcinoma, Hepatocellular - genetics | en_HK |
dc.subject.mesh | Cell Line | en_HK |
dc.subject.mesh | Cell Line, Tumor | en_HK |
dc.subject.mesh | Cyclin D1 - genetics | en_HK |
dc.subject.mesh | Gene Expression Regulation, Neoplastic - genetics | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Liver Neoplasms - genetics | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Mice, Nude | en_HK |
dc.subject.mesh | Neoplasm Proteins - genetics | en_HK |
dc.subject.mesh | Peptidylprolyl Isomerase - genetics | en_HK |
dc.subject.mesh | RNA Interference | en_HK |
dc.subject.mesh | RNA, Neoplasm - genetics | en_HK |
dc.subject.mesh | Transfection - methods | en_HK |
dc.subject.mesh | Up-Regulation - genetics | en_HK |
dc.subject.mesh | beta Catenin - genetics | en_HK |
dc.title | PIN1 expression contributes to hepatic carcinogenesis | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3417&volume=210&issue=1&spage=19&epage=25&date=2006&atitle=PIN1+expression+contributes+to+hepatic+carcinogenesis | en_HK |
dc.identifier.email | Pang, RW: robertap@hkucc.hku.hk | en_HK |
dc.identifier.email | Lee, TK: tkwlee@hkucc.hku.hk | en_HK |
dc.identifier.email | Man, K: kwanman@hkucc.hku.hk | en_HK |
dc.identifier.email | Poon, RT: poontp@hkucc.hku.hk | en_HK |
dc.identifier.email | Fan, ST: stfan@hku.hk | en_HK |
dc.identifier.email | Kwong, YL: ylkwong@hku.hk | en_HK |
dc.identifier.email | Tse, E: ewctse@hku.hk | en_HK |
dc.identifier.authority | Pang, RW=rp00274 | en_HK |
dc.identifier.authority | Lee, TK=rp00447 | en_HK |
dc.identifier.authority | Man, K=rp00417 | en_HK |
dc.identifier.authority | Poon, RT=rp00446 | en_HK |
dc.identifier.authority | Fan, ST=rp00355 | en_HK |
dc.identifier.authority | Kwong, YL=rp00358 | en_HK |
dc.identifier.authority | Tse, E=rp00471 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/path.2024 | en_HK |
dc.identifier.pmid | 16841372 | - |
dc.identifier.scopus | eid_2-s2.0-33747874514 | en_HK |
dc.identifier.hkuros | 119928 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-33747874514&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 210 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 19 | en_HK |
dc.identifier.epage | 25 | en_HK |
dc.identifier.isi | WOS:000240040800004 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Pang, RW=7004376659 | en_HK |
dc.identifier.scopusauthorid | Lee, TK=7501439435 | en_HK |
dc.identifier.scopusauthorid | Man, K=7101754072 | en_HK |
dc.identifier.scopusauthorid | Poon, RT=7103097223 | en_HK |
dc.identifier.scopusauthorid | Fan, ST=7402678224 | en_HK |
dc.identifier.scopusauthorid | Kwong, YL=7102818954 | en_HK |
dc.identifier.scopusauthorid | Tse, E=7005019454 | en_HK |
dc.identifier.issnl | 0022-3417 | - |