Metastasis-associated protein 1 interacts with NRIF3, an estrogen-inducible nuclear receptor coregulator
Authors: Anupama Gururaj
Sandip K Mishra
Ratna K Vadlamudi
Rakesh Kumar
Amjad H Talukder
Journal: Molecular and Cellular Biology (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Estrogen receptor alpha; MTA1; NRIF3; coactivator; corepressor
Affiliations: Departments of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

Abstract:  The transcriptional activity of estrogen receptor alpha (ER-alpha) is modified by regulatory action and interactions of coactivators and corepressors. Recent studies have shown that the metastasis-associated protein 1 (MTA1) represses estrogen receptor element (ERE)-driven transcription in breast cancer cells. With a yeast two-hybrid screen to clone MTA1-interacting proteins, we identified a known nuclear receptor coregulator (NRIF3) as an MTA1-binding protein. NRIF3 interacted with MTA1 both in vitro and in vivo. NRIF3 bound to the C-terminal region of MTA1, while MTA1 bound to the N-terminal region of NRIF3, containing one nuclear receptor interaction LXXLL motif. We showed that NRIF3 is an ER coactivator, hyperstimulated ER transactivation functions, and associated with the endogenous ER and its target gene promoter. MTA1 repressed NRIF3-mediated stimulation of ERE-driven transcription and interfered with NRIF3's association with the ER target gene chromatin. In addition, NRIF3 deregulation enhanced the responsiveness of breast cancer cells to estrogen-induced stimulation of growth and anchorage independence. Furthermore, we found that NRIF3 is an estrogen-inducible gene and activated ER associated with the ER response element in the NRIF3 gene promoter. These findings suggest that NRIF3, an MTA1-interacting protein, is an estrogen-inducible gene and that regulatory interactions between MTA1 and NRIF3 might be important in modulating the sensitivity of breast cancer cells to estrogen. 

Retracted: No

PubPeer comments:
 To see more of the science espoused by Vadlamudi and Kumar in the service of the MD Anderson when it was the World s best cancer hospital (*sic*), look no further than here https: pubpeer.com search?q=kumar+vadlamudi Do pay particular attention to the 2002 Nature Cell Biology paper. Itu2019s a classic of its kind. Both of these authors have their individual achievements too but, with Kumar being a rather common name on this planet, it is best to go carefully through the results of searches at PubPeer to avoid misidentification. This paper is typical for the genre. We have to start somewhere, so let us begin with the Fig. 4D control ribosomal RNAs. Apparently 1 + 1 = 5. That is not what I was taught. Will these implausible images reappear in a future post at PubPeer? Why ever would they not?  , 
 Continuing with the deconstruction of the Worldu2019s best cancer research as effected by the Worldu2019s best cancer hospital in the Worldu2019s best state for cancer research which is embedded in the Worldu2019s best country for conducting cancer research, here is an obviously impossible figure duplication shift. Standard fare for all of the above of course.  , 
 https: retractionwatch.com 2017 03 20 scientist-sued-university-earns-two-retractions-bringing-total-five , 
 Another example of stretchy controls may be observed by comparing the blots - some of which, according to the figure legend, are Westerns whereas others are said to be Northerns - in Figs 4A and 4C. Given that, unusually though it may be from one of the worldu2019s best cancer laboratories, the duplicated slices are actually labelled in the same way, why was it necessary to vertically stretch the one while shrinking tu2019other?  ,