File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Tumour suppressive function and modulation of programmed cell death 4 (PDCD4) in ovarian cancer

TitleTumour suppressive function and modulation of programmed cell death 4 (PDCD4) in ovarian cancer
Authors
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2012, v. 7 n. 1 How to Cite?
AbstractBackground: Programmed cell death 4 (PDCD4), originally identified as the neoplastic transformation inhibitor, was attenuated in various cancer types. Our previous study demonstrated a continuous down-regulation of PDCD4 expression in the sequence of normal-borderline-malignant ovarian tissue samples and a significant correlation of PDCD4 expression with disease-free survival. The objective of the current study was to further investigate the function and modulation of PDCD4 in ovarian cancer cells. Principal Findings: We demonstrated that ectopic PDCD4 expression significantly inhibited cell proliferation by inducing cell cycle arrest at G 1 stage and up-regulation of cell cycle inhibitors of p27 and p21. Cell migration and invasion were also inhibited by PDCD4. PDCD4 over-expressing cells exhibited elevated phosphatase and tensin homolog (PTEN) and inhibited protein kinase B (p-Akt). In addition, the expression of PDCD4 was up-regulated and it was exported to the cytoplasm upon serum withdrawal treatment, but it was rapidly depleted via proteasomal degradation upon serum re-administration. Treatment of a phosphoinositide 3-kinase (PI3K) inhibitor prevented the degradation of PDCD4, indicating the involvement of PI3K-Akt pathway in the modulation of PDCD4. Conclusion: PDCD4 may play a critical function in arresting cell cycle progression at key checkpoint, thus inhibiting cell proliferation, as well as suppressing tumour metastasis. The PI3K-Akt pathway was implied to be involved in the regulation of PDCD4 degradation in ovarian cancer cells. In response to the stress condition, endogenous PDCD4 was able to shuttle between cell compartments to perform its diverted functions. © 2012 Wei et al.
Persistent Identifierhttp://hdl.handle.net/10722/160052
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWei, Nen_HK
dc.contributor.authorLiu, SSen_HK
dc.contributor.authorChan, KKLen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2012-08-16T06:01:50Z-
dc.date.available2012-08-16T06:01:50Z-
dc.date.issued2012en_HK
dc.identifier.citationPlos One, 2012, v. 7 n. 1en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/160052-
dc.description.abstractBackground: Programmed cell death 4 (PDCD4), originally identified as the neoplastic transformation inhibitor, was attenuated in various cancer types. Our previous study demonstrated a continuous down-regulation of PDCD4 expression in the sequence of normal-borderline-malignant ovarian tissue samples and a significant correlation of PDCD4 expression with disease-free survival. The objective of the current study was to further investigate the function and modulation of PDCD4 in ovarian cancer cells. Principal Findings: We demonstrated that ectopic PDCD4 expression significantly inhibited cell proliferation by inducing cell cycle arrest at G 1 stage and up-regulation of cell cycle inhibitors of p27 and p21. Cell migration and invasion were also inhibited by PDCD4. PDCD4 over-expressing cells exhibited elevated phosphatase and tensin homolog (PTEN) and inhibited protein kinase B (p-Akt). In addition, the expression of PDCD4 was up-regulated and it was exported to the cytoplasm upon serum withdrawal treatment, but it was rapidly depleted via proteasomal degradation upon serum re-administration. Treatment of a phosphoinositide 3-kinase (PI3K) inhibitor prevented the degradation of PDCD4, indicating the involvement of PI3K-Akt pathway in the modulation of PDCD4. Conclusion: PDCD4 may play a critical function in arresting cell cycle progression at key checkpoint, thus inhibiting cell proliferation, as well as suppressing tumour metastasis. The PI3K-Akt pathway was implied to be involved in the regulation of PDCD4 degradation in ovarian cancer cells. In response to the stress condition, endogenous PDCD4 was able to shuttle between cell compartments to perform its diverted functions. © 2012 Wei et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshApoptosis Regulatory Proteins - genetics - metabolism - physiology-
dc.subject.meshCell Cycle - physiology-
dc.subject.meshCell Proliferation-
dc.subject.meshRNA-Binding Proteins - genetics - metabolism - physiology-
dc.subject.meshTumor Suppressor Proteins - genetics - metabolism - physiology-
dc.titleTumour suppressive function and modulation of programmed cell death 4 (PDCD4) in ovarian canceren_HK
dc.typeArticleen_HK
dc.identifier.emailLiu, SS:stephasl@hku.hken_HK
dc.identifier.emailChan, KKL:kklchan@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS:hysngan@hkucc.hku.hken_HK
dc.identifier.authorityLiu, SS=rp00372en_HK
dc.identifier.authorityChan, KKL=rp00499en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0030311en_HK
dc.identifier.pmid22272332-
dc.identifier.pmcidPMC3260274-
dc.identifier.scopuseid_2-s2.0-84855860369en_HK
dc.identifier.hkuros204929en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84855860369&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue1en_HK
dc.identifier.eissn1932-6203-
dc.identifier.isiWOS:000301454400110-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWei, N=23101332300en_HK
dc.identifier.scopusauthoridLiu, SS=37102450400en_HK
dc.identifier.scopusauthoridChan, KKL=8655666700en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats