RETRACTED ARTICLE: Id-1 stimulates cell proliferation through activation of EGFR in ovarian cancer cells
Authors: H Feng
M-T Ling
X Zhang
X Wang
Y C Wong
S W Tsao
Journal: British Journal of Cancer (2004)
Discipline: CLINICAL MEDICINE
Keywords: EGFR; Id-1; ovarian cancer; proliferation; cell growth
Affiliations: Cancer Biology Group, Department of Anatomy, The University of Hong Kong, 1/F, Faculty of Medicine Building, 21 Sassoon Road, Hong Kong.

Abstract:  Increased EGFR (epidermal growth factor receptor) expression has been reported in many types of human cancer and its levels are positively associated with advanced cancers. Recently, upregulation of Id-1 (inhibitor of differentiation or DNA binding) protein was found in over 70% of ovarian cancer samples and correlated with poor survival of ovarian cancer patients. However, the molecular mechanisms responsible for the role of Id-1 in ovarian cancer are not clear. The aim of this study was to investigate the effect of Id-1 on ovarian cancer proliferation and its association with the EGFR pathway. To achieve this, we transfected an Id-1 expression vector into three ovarian cancer cell lines and examined cell proliferation rate by flow cytometry and bromodeoxyuridine staining. We found that ectopic Id-1 expression led to increased cell proliferation demonstrated by increased BrdU incorporation rate and S-phase fraction. The Id-1-induced cell growth was associated with upregulation of EGFR at both transcriptional and protein levels. In contrast, inactivation of Id-1 through transfection of an Id-1 antisense vector resulted in downregulation of EGFR. Our results indicate that increased Id-1 in ovarian cancer cells may promote cancer cell proliferation through upregulation of EGFR. Our findings also implicate that Id-1 may be a potential target for the development of novel strategies in the treatment of ovarian cancer. 

Retracted: Yes

PubPeer comments:
 Do the authors have an explanation for very similar data appearing in different papers? , 
 #7 Same data in 3 different papers representing different proteins and different experimental conditions. , 
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 2021 retraction. https: www.nature.com articles s41416-021-01322-z Retraction Note to: British Journal of Cancer (2004) 91, 2042u20132047; https: doi.org 10.1038 sj.bjc.6602254, published online 14 December 2004 The Editor-in-Chief has retracted this article because serious concerns have been raised about integrity of the data. Specifically: Figure 1au2014the Id-1 and Actin bands for the Skov3 panel appear to be very similar. The Actin bands in the Ovca433 panel in Figure 1a seem very similar to the Actin bands for the Ovca433 panel in Figure 4a. Figure 1au2014it appears that some images have been published earlier with different labels by some of the same authors.1,2 In Figure 1b the Actin band for the Ovca420 panel and the Actin band for the Ovca432 panel seem to be mirror images. The authors were unable to provide raw data. The data reported in this article are therefore unreliable. S.W. Tsao agrees to this retraction. The editor was not able to obtain a current email address for X. Zhang, M.-T. Ling, H. Feng, Y.C. Wong and X. Wang. References 1. Ling, M., Wang, X. S., Ouyang, X., Xu, K., Tsao, S. W. Wong, Y. C. Id-1 expression promotes cell survival through activation of NF-kB signalling pathway in prostate cancer cells. Oncogene 22, 4498u20134508, https: doi.org 10.1038 sj.onc.1206693 (2003). 2. Cheung, H. W., Ling, M.-t, Tsao, S. W., Wong, Y. C. Wang, X. Id-1-induced Raf MEK pathway activation is essential for its protective role against taxol-induced apoptosis in nasopharyngeal carcinoma cells. Carcinogenesis 25, 881u2013887, https: doi.org 10.1093 carcin bgh087 (2004). ,