Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs
The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by conducting replications of selected experiments from a number of high-profile papers in the field of cancer biology. The papers, which were published between 2010 and 2012, w...
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Language: | English |
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eLife Sciences Publications Ltd
2016-03-01
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Online Access: | https://elifesciences.org/articles/12470 |
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author | Mitch Phelps Chris Coss Hongyan Wang Matthew Cook Reproducibility Project: Cancer Biology |
author_facet | Mitch Phelps Chris Coss Hongyan Wang Matthew Cook Reproducibility Project: Cancer Biology |
author_sort | Mitch Phelps |
collection | DOAJ |
description | The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by conducting replications of selected experiments from a number of high-profile papers in the field of cancer biology. The papers, which were published between 2010 and 2012, were selected on the basis of citations and Altmetric scores (Errington et al., 2014). This Registered Report describes the proposed replication plan of key experiments from “Coding-Independent Regulation of the Tumor Suppressor PTEN by Competing Endogenous 'mRNAs' by Tay and colleagues, published in Cell in 2011 (Tay et al., 2011). The experiments to be replicated are those reported in Figures 3C, 3D, 3G, 3H, 5A and 5B, and in Supplemental Figures 3A and B. Tay and colleagues proposed a new regulatory mechanism based on competing endogenous RNAs (ceRNAs), which regulate target genes by competitive binding of shared microRNAs. They test their model by identifying and confirming ceRNAs that target PTEN. In Figure 3A and B, they report that perturbing expression of putative PTEN ceRNAs affects expression of PTEN. This effect is dependent on functional microRNA machinery (Figure 3G and H), and affects the pathway downstream of PTEN itself (Figures 5A and B). The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange, and the results of the replications will be published by eLife. |
first_indexed | 2024-04-14T07:46:59Z |
format | Article |
id | doaj.art-44fc8c8eb9a3462191aa1828efdf5f6c |
institution | Directory Open Access Journal |
issn | 2050-084X |
language | English |
last_indexed | 2024-04-14T07:46:59Z |
publishDate | 2016-03-01 |
publisher | eLife Sciences Publications Ltd |
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series | eLife |
spelling | doaj.art-44fc8c8eb9a3462191aa1828efdf5f6c2022-12-22T02:05:18ZengeLife Sciences Publications LtdeLife2050-084X2016-03-01510.7554/eLife.12470Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAsMitch Phelps0Chris Coss1Hongyan Wang2Matthew Cook3Reproducibility Project: Cancer BiologyPharmacoanalytic Shared Resource, The Ohio State University, Columbus, United StatesPharmacoanalytic Shared Resource, The Ohio State University, Columbus, United StatesPharmacoanalytic Shared Resource, The Ohio State University, Columbus, United StatesUniversity of California San Francisco, San Francisco, United StatesThe Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by conducting replications of selected experiments from a number of high-profile papers in the field of cancer biology. The papers, which were published between 2010 and 2012, were selected on the basis of citations and Altmetric scores (Errington et al., 2014). This Registered Report describes the proposed replication plan of key experiments from “Coding-Independent Regulation of the Tumor Suppressor PTEN by Competing Endogenous 'mRNAs' by Tay and colleagues, published in Cell in 2011 (Tay et al., 2011). The experiments to be replicated are those reported in Figures 3C, 3D, 3G, 3H, 5A and 5B, and in Supplemental Figures 3A and B. Tay and colleagues proposed a new regulatory mechanism based on competing endogenous RNAs (ceRNAs), which regulate target genes by competitive binding of shared microRNAs. They test their model by identifying and confirming ceRNAs that target PTEN. In Figure 3A and B, they report that perturbing expression of putative PTEN ceRNAs affects expression of PTEN. This effect is dependent on functional microRNA machinery (Figure 3G and H), and affects the pathway downstream of PTEN itself (Figures 5A and B). The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange, and the results of the replications will be published by eLife.https://elifesciences.org/articles/12470reproducibility project: cancer biologymethodologymicroRNAPTEN |
spellingShingle | Mitch Phelps Chris Coss Hongyan Wang Matthew Cook Reproducibility Project: Cancer Biology Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs eLife reproducibility project: cancer biology methodology microRNA PTEN |
title | Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs |
title_full | Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs |
title_fullStr | Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs |
title_full_unstemmed | Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs |
title_short | Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs |
title_sort | registered report coding independent regulation of the tumor suppressor pten by competing endogenous mrnas |
topic | reproducibility project: cancer biology methodology microRNA PTEN |
url | https://elifesciences.org/articles/12470 |
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