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Article: Tumor suppressor effect of follistatin-like 1 in ovarian and endometrial carcinogenesis - A differential expression and functional analysis

TitleTumor suppressor effect of follistatin-like 1 in ovarian and endometrial carcinogenesis - A differential expression and functional analysis
Authors
Issue Date2009
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2009, v. 30 n. 1, p. 114-121 How to Cite?
AbstractEndometrial and ovarian cancers are the most common and the most lethal gynecologic malignancies worldwide, respectively. By performing differential expression analysis using annealing control primer™-based reverse transcription (RT)-polymerase chain reaction (PCR) on pooled complementary DNA (cDNA) from 45 endometrial and 36 ovarian cancers and their non-tumor samples, reduced expression of the follistatin-like 1 (FSTL1) was identified. Downregulation of FSTL1 was further confirmed on individual samples and cell lines by quantitative real-time RT-PCR and western blotting. For in vitro functional study, full-length cDNA of FSTL1 was cloned and transiently transfected into the ovarian cancer cell line Ovca420 and endometrial cancer cell line AN3CA. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and cell count demonstrated significantly slower proliferation rate. By terminal uridine deoxynucleotidyl transferase dUTP nick end labeling and flow cytometric analysis, higher apoptotic activity and a remarkable increase in sub-G 1 cell population were observed in transfected cells, suggesting that FSTL1 induced apoptosis in cancer cells. Subsequent messenger RNA and protein expression analysis on downstream apoptotic molecules revealed upregulation and/or activation of FAS, FASLG, TRADD, Caspase-3, Caspase-7 and PARP by FSTL1 transfection, suggesting that FSTL1 -induced apoptosis may be initiated mainly by FAS/FASLG death receptor-ligand binding. Cell migration and invasion assays demonstrated a remarkably lower cell migration and invasion capability in FSTL1 -transfected cells in relation to downregulation of matrix metallopeptidase-2. Our findings suggested that a tumor suppressor role of FSTL1 may be important in ovarian and endometrial carcinogenesis. © The Author 2008. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/60353
ISSN
2014 Impact Factor: 5.334
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council Grant, Hong Kong SAR
University of Hong Kong
Funding Information:

Research Grant Council Grant, Hong Kong SAR; Committee on Research and Conference Grants from the University of Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorChan, QKYen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorIp, PPCen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorXue, WCen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-05-31T04:08:56Z-
dc.date.available2010-05-31T04:08:56Z-
dc.date.issued2009en_HK
dc.identifier.citationCarcinogenesis, 2009, v. 30 n. 1, p. 114-121en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60353-
dc.description.abstractEndometrial and ovarian cancers are the most common and the most lethal gynecologic malignancies worldwide, respectively. By performing differential expression analysis using annealing control primer™-based reverse transcription (RT)-polymerase chain reaction (PCR) on pooled complementary DNA (cDNA) from 45 endometrial and 36 ovarian cancers and their non-tumor samples, reduced expression of the follistatin-like 1 (FSTL1) was identified. Downregulation of FSTL1 was further confirmed on individual samples and cell lines by quantitative real-time RT-PCR and western blotting. For in vitro functional study, full-length cDNA of FSTL1 was cloned and transiently transfected into the ovarian cancer cell line Ovca420 and endometrial cancer cell line AN3CA. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and cell count demonstrated significantly slower proliferation rate. By terminal uridine deoxynucleotidyl transferase dUTP nick end labeling and flow cytometric analysis, higher apoptotic activity and a remarkable increase in sub-G 1 cell population were observed in transfected cells, suggesting that FSTL1 induced apoptosis in cancer cells. Subsequent messenger RNA and protein expression analysis on downstream apoptotic molecules revealed upregulation and/or activation of FAS, FASLG, TRADD, Caspase-3, Caspase-7 and PARP by FSTL1 transfection, suggesting that FSTL1 -induced apoptosis may be initiated mainly by FAS/FASLG death receptor-ligand binding. Cell migration and invasion assays demonstrated a remarkably lower cell migration and invasion capability in FSTL1 -transfected cells in relation to downregulation of matrix metallopeptidase-2. Our findings suggested that a tumor suppressor role of FSTL1 may be important in ovarian and endometrial carcinogenesis. © The Author 2008. Published by Oxford University Press. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.subject.meshApoptosis-
dc.subject.meshEndometrial Neoplasms - pathology - physiopathology-
dc.subject.meshFollistatin-Related Proteins - genetics - physiology-
dc.subject.meshGenes, Tumor Suppressor-
dc.subject.meshOvarian Neoplasms - pathology - physiopathology-
dc.titleTumor suppressor effect of follistatin-like 1 in ovarian and endometrial carcinogenesis - A differential expression and functional analysisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0147-4006&volume=30&spage=114&epage=121&date=2009&atitle=Tumor+suppressor+effect+of+follistatin-like+1+in+ovarian+and+endometrial+carcinogenesis:+a+differential+expression+and+functional+analysisen_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgn215en_HK
dc.identifier.pmid18796737en_HK
dc.identifier.scopuseid_2-s2.0-58949099404en_HK
dc.identifier.hkuros160439en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58949099404&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue1en_HK
dc.identifier.spage114en_HK
dc.identifier.epage121en_HK
dc.identifier.isiWOS:000262718300016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, QKY=8390404100en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridIp, PPC=7003622683en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK

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