Evidence map›Paper›PMID 25263446›Full record

ArticleOncogene2015

Amplified in breast cancer 1 promotes colorectal cancer progression through enhancing notch signaling.

Pingli Mo, Qiling Zhou, Lei Guan, Yi Wang, Wei Wang, Mengmeng Miao, Zhangwei Tong, Ming Li, Sidra Majaz, Yonghong Liu and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Article
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  16. Review
  17. Article
  18. Molecular Pathways: Targeting Steroid Receptor Coactivators in Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Pingli Mo *State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Qiling Zhou *State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Lei Guan *State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Yi WangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Wei WangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Mengmeng MiaoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Zhangwei TongState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Ming LiState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Sidra MajazState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Yonghong LiuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Guoqiang SuThe First Affiliated Hospital of Xiamen University, Xiamen, China.
Jianming XuDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.
Chundong YuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Xiamen University · CNBaylor College of Medicine · USFirst Affiliated Hospital of Xiamen University · CN

Funding

TISSUE COACTIVATOR AND RECEPTOR EXPRESSION FINGERPRINTSP01DK059820 · NIDDK · INSTITUT DE GENETIQUE ET BIOLOGIE MOLECU · PI O'MALLEY, BERT W · 2001 to 2016
$23.1M
The Role of SRC-1 in Breast CancerR01CA112403 · NCI · BAYLOR COLLEGE OF MEDICINE · PI XU, JIANMING · 2006 to 2016
$2.9M
Roles of SRC-3 in Development and DiseaseR01DK058242 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI XU, JIANMING · 2000 to 2013
$2.8M
NCI NIH HHS CA112403NCI NIH HHS R01 CA112403NIDDK NIH HHS DK058242NIDDK NIH HHS P01 DK059820NIDDK NIH HHS R01 DK058242
6 · The paper itself

Abstract

Aberrant activation of Notch signaling has an essential role in colorectal cancer (CRC) progression. Amplified in breast cancer 1 (AIB1), also known as steroid receptor coactivator 3 or NCOA3, is a transcriptional coactivator that promotes cancer cell proliferation and invasiveness. However, AIB1 implication in CRC progression through enhancing Notch signaling is unknown. In this study, we found that several CRC cell lines expressed high levels of AIB1, and knockdown of AIB1 decreased cell proliferation, colony formation and tumorigenesis of these CRC cells. Specifically, knockdown of AIB1 inhibited cell cycle progression at G1 phase by decreasing the mRNA levels of cyclin A2, cyclin B1, cyclin E2 and hairy and enhancer of split (Hes) 1. Furthermore, AIB1 interacted with Notch intracellular domain and Mastermind-like 1 and was recruited to the Hes1 promoter to enhance Notch signaling. Downregulation of AIB1 also decreased CRC cell invasiveness in vitro and lung metastasis in vivo. Besides that, knockout of AIB1 in mice inhibited colon carcinogenesis induced by azoxymethane/dextran sodium sulfate treatment. The mRNA levels of cyclin B1 and Hes5 were downregulated, but p27, ATOH1 and MUC2 were upregulated in the colon tumors from AIB1-deficient mice compared with those from wild-type mice. Thus, our results signify the importance of AIB1 in CRC and demonstrate that AIB1 promotes CRC progression at least in part through enhancing Notch signaling, suggesting that AIB1 is a potential molecular target for CRC treatment.

Indexed as

Cell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsDisease ProgressionDNA-Binding ProteinsGene Knockdown TechniquesHEK293 CellsHumansLung NeoplasmsNeoplasm TransplantationNuclear Receptor Coactivator 3Protein BindingReceptors, NotchSignal TransductionDNA-Binding ProteinsMAML1 protein, humanNCOA3 protein, humanNcoa3 protein, mouseNuclear Receptor Coactivator 3Receptors, NotchTranscription Factors

Identifiers

PMID25263446
PMCPMC4377317
OpenAlexW2073401782

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.