Evidence map›Paper›PMID 28182012›Full record

ArticleCell death & disease2017

Loss of BRG1 induces CRC cell senescence by regulating p53/p21 pathway.

Guihua Wang, Yinjia Fu, Fuqing Hu, Jinqing Lan, Feng Xu, Xi Yang, Xuelai Luo, Jing Wang, Junbo Hu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

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  14. Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021
    Review
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  20. Human colorectal cancer derived-MSCs promote tumor cells escape from senescence via P53/P21 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Guihua WangCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Yinjia FuCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Fuqing HuCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Jinqing LanCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Feng XuCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Xi YangCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Xuelai LuoCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Jing WangDepartment of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Junbo HuCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brahma-related gene-1 (BRG1) is the specific ATPase of switch/sucrose nonfermentable chromatin-remodeling complex that is aberrantly expressed or mutated in various cancers. However, the exact role of BRG1 in oncogenesis remains unknown. In this study, we demonstrate that the knockdown (KD) of BRG1 promotes cellular senescence by influencing the SIRT1/p53/p21 signal axis in colorectal cancer (CRC). In particular, we reveal that the expression level of BRG1 is inversely correlated with p21, one of the classic senescence regulators, and is decreased in senescent CRC cells. KD of BRG1 promoting senescence is indicated by the increase of senescence-associated β-galactosidase (SA-β-gal) activity, inhibition of cell proliferation, induction of cell cycle arrest, and formation of senescence-associated heterochromatin foci. BRG1 binds to SIRT1 and interferes with SIRT1-mediated deacetylation of p53 at K382. Rescue experiments by co-silencing p53 or treatment with EX527, a SIRT1-specific inhibitor, abrogated the cellular senescence induced by KD of BRG1. BRG1 KD cells resulted in smaller tumor formation than that in control cells in vivo. Collectively, our study shows that BRG1 has an important role in cellular senescence and tumor growth. The BRG1/SIRT1/p53 signal axis is a novel mechanism of cell senescence in CRC and is a new potential target for cancer therapy.

Indexed as

Animalsbeta-GalactosidaseCell Cycle CheckpointsCell ProliferationCell Transformation, NeoplasticCellular SenescenceColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p21DNA HelicasesFemaleHCT116 CellsHeterochromatinHT29 CellsHumansMiceMice, Nudebeta-GalactosidaseCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA HelicasesHeterochromatinNuclear ProteinsSirtuin 1SMARCA4 protein, humanTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID28182012
PMCPMC5386468
OpenAlexW2587270974

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.