ArticlePloS one2013
AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
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- SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021Review
- The landscape and prognostic value of immune characteristics in uterine corpus endometrial cancer.Bioscience reports · 2021Article
- Retraction: AIB1 Cooperates with ERα to Promote Epithelial Mesenchymal Transition in Breast Cancer through SNAI1 Activation.PloS one · 2021Article
- Analysis of differentially expressed genes in oral epithelial cells infected with Fusobacterium nucleatum for revealing genes associated with oral cancer.Journal of cellular and molecular medicine · 2021Article
- PBX1 is a valuable prognostic biomarker for patients with breast cancer.Experimental and therapeutic medicine · 2020Article
- SNAIL is induced by tamoxifen and leads to growth inhibition in invasive lobular breast carcinoma.Breast cancer research and treatment · 2019Article
- Circadian protein BMAL1 promotes breast cancer cell invasion and metastasis by up-regulating matrix metalloproteinase9 expression.Cancer cell international · 2019Article
- Expansion of Sphingosine Kinase and Sphingosine-1-Phosphate Receptor Function in Normal and Cancer Cells: From Membrane Restructuring to Mediation of Estrogen Signaling and Stem Cell Programming.International journal of molecular sciences · 2018Review
- U-box ubiquitin ligase PPIL2 suppresses breast cancer invasion and metastasis by altering cell morphology and promoting SNAI1 ubiquitination and degradation.Cell death & disease · 2018Article
- High RAC3 expression levels are required for induction and maintaining of cancer cell stemness.Oncotarget · 2018Article
- The inflammatory cytokine TNF contributes with RAC3-induced malignant transformation.EXCLI journal · 2018Article
- Relation among Aromatase P450 and Tumoral Growth in Human Prolactinomas.International journal of molecular sciences · 2017Review
- SYNJ2BP promotes the degradation of PTEN through the lysosome-pathway and enhances breast tumor metastasis via PI3K/AKT/SNAI1 signaling.Oncotarget · 2017Article
- Honokiol inhibits bladder cancer cell invasion through repressing SRC-3 expression and epithelial-mesenchymal transition.Oncology letters · 2017Article
- Sumoylation of TCF21 downregulates the transcriptional activity of estrogen receptor-alpha.Oncotarget · 2016Article
- Epithelial-Mesenchymal Transition (EMT) and Regulation of EMT Factors by Steroid Nuclear Receptors in Breast Cancer: A Review and in Silico Investigation.Journal of clinical medicine · 2016Review
- Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer.Oncotarget · 2016Article
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Corrections and comments
- Retraction · 2021-06-01Duplication of/in Image · Manipulation of Images · Original Data and/or Images not Provided and/or not Available · Unreliable Data · · see also: https://pubpeer.com/publications/9F0E6BFFF4B51C061E65FA0A3D01F2
- Retracted
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial Mesenchymal Transition (EMT) plays a major role in cancer metastasis. Several genes have been shown to play a role in EMT, and one of these is Amplified-in-breast cancer 1 (AIB1), which has oncogenic function and is known to be amplified in breast cancer. However, the role of AIB1 in EMT remains largely undefined at the molecular level. In this study, the effect of AIB1 overexpression on the EMT of the breast cancer cell line T47D was investigated. Overexpression of AIB1 disrupted the epithelial morphology of the cells. At the same time, the cells displayed a strong metastasis and reduced level of the epithelial marker E-cadherin. In contrast, knockdown of AIB1 in T47D cells increased cell-cell adhesion and produced weak metastasis, as well as a higher level of E-cadherin expression. We proposed that the regulation of EMT by AIB1 occurred through the action of the transcription factor SNAI1, and demonstrated that such interaction required the participation of ERα and the presence of ERα-binding site on SNAI1 promoter. The expression level of E-cadherin and the extent of cell migration and invasion in SNAI1-knocked down T47D cells that overexpressed AIB1 were similar to those of T47D cells that did not overexpress AIB1 and had no SNAI1 knockdown. Taken together, these results suggested that AIB1 exerted its effect on EMT through its interaction with ERα, which could directly bind to the ERα-binding site on the SNAI1 promoter, allowing the AIB1-ERα complex to promote the transcription of SNAI1 and eventually led to repression of E-cadherin expression, consistent with the loss of E-cadherin being a hallmark of EMT.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.