Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/29746
Title: Differential toxicological endpoints of di(2-ethylhexyl) phthalate (DEHP) exposure in MCF-7 and MDA-MB-231 cell lines: Possible estrogen receptor α (ERα) independent modulations
Authors: Das, Mihir Tanay
Singh, Manoj Kumar
Thakur, Indu Shekhar
Keywords: Cell cycle;DEHP;Estrogen receptors-α;Label-free quantification;Secretome
Issue Date: Nov-2014
Publisher: NISCAIR-CSIR, India
Abstract: Wide spread use of Di-(2-ethylhexyl) phthalate (DEHP) has made it a ubiquitous contaminant in today’s environment, responsible for possible carcinogenic and endocrine disrupting effects. In the present investigation an integrative toxico-proteomic approach was made to study the estrogenic potential of DEHP. In vitro experiments carried out with DEHP (0.1-100 μM) induced proliferations (E-screen assay) in human estrogen receptors-α (ERα) positive MCF-7 and ERα negative MDA-MB-231 breast cancer cells irrespective of their ERα status. Further, DEHP suppressed tamoxifen (a potent anti-breast cancer drug) induced apoptosis in both cell types as shown by flowcytometric cell cycle analysis. Label-free quantitative proteomics analysis of the cell secretome of both the cell lines indicated a wide array of stress related, structural and receptor binding proteins that were affected due to DEHP exposure. The secretome of DEHP treated MCF-7 cells revealed the down regulation of lactotransferrin, an ERα responsive iron transport protein. The results indicated that toxicological effects of DEHP did not follow an ERα signaling pathway. However, the differential effects in MCF-7 and MDA-MB-231 cell lines indicate that ERα might have an indirect modulating effect on DEHP induced toxicity.
Page(s): 1052-1061
URI: http://hdl.handle.net/123456789/29746
ISSN: 0975-1009 (Online); 0019-5189 (Print)
Appears in Collections:IJEB Vol.52(11) [November 2014]

Files in This Item:
File Description SizeFormat 
IJEB 52(11) 1052-1061.pdf212.94 kBAdobe PDFView/Open


Items in NOPR are protected by copyright, with all rights reserved, unless otherwise indicated.