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Article: Tumor suppressor effect of follistatin-like 1 in ovarian and endometrial carcinogenesis - A differential expression and functional analysis
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TitleTumor suppressor effect of follistatin-like 1 in ovarian and endometrial carcinogenesis - A differential expression and functional analysis
 
AuthorsChan, QKY1
Ngan, HYS1
Ip, PPC1
Liu, VWS1
Xue, WC1
Cheung, ANY1
 
Issue Date2009
 
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
CitationCarcinogenesis, 2009, v. 30 n. 1, p. 114-121 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgn215
 
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.
 
ISSN0143-3334
2013 Impact Factor: 5.266
 
DOIhttp://dx.doi.org/10.1093/carcin/bgn215
 
ISI Accession Number IDWOS:000262718300016
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorChan, QKY
 
dc.contributor.authorNgan, HYS
 
dc.contributor.authorIp, PPC
 
dc.contributor.authorLiu, VWS
 
dc.contributor.authorXue, WC
 
dc.contributor.authorCheung, ANY
 
dc.date.accessioned2010-05-31T04:08:56Z
 
dc.date.available2010-05-31T04:08:56Z
 
dc.date.issued2009
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationCarcinogenesis, 2009, v. 30 n. 1, p. 114-121 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgn215
 
dc.identifier.doihttp://dx.doi.org/10.1093/carcin/bgn215
 
dc.identifier.epage121
 
dc.identifier.hkuros160439
 
dc.identifier.isiWOS:000262718300016
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.

 
dc.identifier.issn0143-3334
2013 Impact Factor: 5.266
 
dc.identifier.issue1
 
dc.identifier.openurl
 
dc.identifier.pmid18796737
 
dc.identifier.scopuseid_2-s2.0-58949099404
 
dc.identifier.spage114
 
dc.identifier.urihttp://hdl.handle.net/10722/60353
 
dc.identifier.volume30
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofCarcinogenesis
 
dc.relation.referencesReferences in Scopus
 
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 analysis
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong