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Conference Paper: The helix-loop-helix transcription factor Id-1 promotes cellular proliferation and survival in esophageal carcinoma cells

TitleThe helix-loop-helix transcription factor Id-1 promotes cellular proliferation and survival in esophageal carcinoma cells
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research
Citation
AACR 96th Annual Meeting, Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9S, p. 879 Abstract no. 3727 How to Cite?
AbstractId proteins (inhibitor of differentiation or DNA binding) are a group of helix-loop-helix (HLH) transcription factors that can dimerize with basic HLH transcription factors and prevent them from binding to DNA, thus inhibiting the transcription of differentiation associated genes. The ability of Id proteins in stimulating DNAsynthesis and immortalizing mammalian cells either alone or together with additional oncogenes suggests that they may function as potential oncogenes. Although upregulation of Id-1 has been reported for over 20 types of human cancers, including esophageal squamous cell carcinoma (ESCC), its functional role in the molecular pathogenesis of esophageal cancer and the signaling pathways involved are unknown. In this study, we investigated the direct effects of Id-1 on esophageal cancer cell growth, cell cycle distribution and drug-induced apoptosis by transfecting an Id-1 expression vector into an ESCC cell line which showed serum-dependent Id-1 expression to generate stable Id-1 expressing clones. We found that ectopic Id-1 expression increased both cellular proliferation rate and G1-S phase transition in the transfectant clones cultured in serum-free medium. The effects were associated with overexpression of MDM2 (mouse double minute 2) oncoprotein and suppression of p21WAF1 protein, but did not seem to affect CDK4, p16INK4A, pRB and p53 expressions. In addition, Id-1 expression protected ESCC cells from TNF-α-induced apoptosis by up-regulating and activating Bcl-2. Conversely, stable transfection of Id-1 antisense expression vector to inhibit the expression of endogenous Id-1 in another ESCC cell line with serum-independent Id-1 expression reversed the effects on cell growth and expressions of MDM2 and p21WAF1 proteins. In conclusion, our study provides evidence that Id-1 may function as an oncogene in ESCC, and that its effects on esophageal cancer cell proliferation appeared to be mediated through up-regulation of MDM2 and down-regulation of p21WAF1, rather than through inactivation of the p16INK4A/RB pathway as reported in prostate, nasopharyngeal and hepatocellular cancers.
Persistent Identifierhttp://hdl.handle.net/10722/95103
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorCheung, Aen_HK
dc.contributor.authorHui, CMen_HK
dc.contributor.authorCheung, PPYen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-25T15:51:44Z-
dc.date.available2010-09-25T15:51:44Z-
dc.date.issued2005en_HK
dc.identifier.citationAACR 96th Annual Meeting, Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9S, p. 879 Abstract no. 3727en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95103-
dc.description.abstractId proteins (inhibitor of differentiation or DNA binding) are a group of helix-loop-helix (HLH) transcription factors that can dimerize with basic HLH transcription factors and prevent them from binding to DNA, thus inhibiting the transcription of differentiation associated genes. The ability of Id proteins in stimulating DNAsynthesis and immortalizing mammalian cells either alone or together with additional oncogenes suggests that they may function as potential oncogenes. Although upregulation of Id-1 has been reported for over 20 types of human cancers, including esophageal squamous cell carcinoma (ESCC), its functional role in the molecular pathogenesis of esophageal cancer and the signaling pathways involved are unknown. In this study, we investigated the direct effects of Id-1 on esophageal cancer cell growth, cell cycle distribution and drug-induced apoptosis by transfecting an Id-1 expression vector into an ESCC cell line which showed serum-dependent Id-1 expression to generate stable Id-1 expressing clones. We found that ectopic Id-1 expression increased both cellular proliferation rate and G1-S phase transition in the transfectant clones cultured in serum-free medium. The effects were associated with overexpression of MDM2 (mouse double minute 2) oncoprotein and suppression of p21WAF1 protein, but did not seem to affect CDK4, p16INK4A, pRB and p53 expressions. In addition, Id-1 expression protected ESCC cells from TNF-α-induced apoptosis by up-regulating and activating Bcl-2. Conversely, stable transfection of Id-1 antisense expression vector to inhibit the expression of endogenous Id-1 in another ESCC cell line with serum-independent Id-1 expression reversed the effects on cell growth and expressions of MDM2 and p21WAF1 proteins. In conclusion, our study provides evidence that Id-1 may function as an oncogene in ESCC, and that its effects on esophageal cancer cell proliferation appeared to be mediated through up-regulation of MDM2 and down-regulation of p21WAF1, rather than through inactivation of the p16INK4A/RB pathway as reported in prostate, nasopharyngeal and hepatocellular cancers.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleThe helix-loop-helix transcription factor Id-1 promotes cellular proliferation and survival in esophageal carcinoma cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailCheung, A: lmcheung@hkucc.hku.hken_HK
dc.identifier.emailCheung, PPY: patcarro@graduate.hku.hken_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityCheung, A=rp00332en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.hkuros97783en_HK
dc.identifier.volume65en_HK
dc.identifier.spage879en_HK

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