Evidence map›Paper›PMID 36526622›Full record

ArticleCell death & disease2022

BAF53A drives colorectal cancer development by regulating DUSP5-mediated ERK phosphorylation.

Ziqing Yang, Dandan Huang, Manqi Meng, Wencong Wang, Junyan Feng, Lekun Fang, Honglei Chen, Shaomin Zou

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 49 citations in OpenAlex.

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  11. Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025
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  15. Hippo pathway in intestinal diseases: focusing on ferroptosis.Frontiers in cell and developmental biology · 2023
    Review
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

8 authors at 1 institution in 1 country.

Ziqing Yang *Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China.
Dandan Huang *Department of Colorectal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China.
Manqi Meng *Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China.
Wencong WangGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China.
Junyan FengGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China.
Lekun FangGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China. fanglk3@mail.sysu.edu.cn.ORCID 0000-0002-0296-292X
Honglei ChenGastrointestinal Endoscopy Center, The Eighth Affiliated Hospital, Sun Yat-sen University, 518033, Shenzhen, China. chenhlei3@mail.sysu.edu.cn.ORCID 0000-0003-0146-3165
Shaomin ZouGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, 510655, Guangzhou, China. zoushm5@mail2.sysu.edu.cn.ORCID 0000-0001-6067-3969
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BAF53A, an important subunit of the SWI/SNF epigenetic chromatin regulatory complex, has been implicated as the driver of diverse cancers. However, the role of BAF53A in colorectal cancer (CRC) remains poorly understood. Here, we examined the expression of BAF53A in CRC samples and observed that BAF53A was significantly upregulated in CRC tissues compared with paired adjacent normal tissues. In vitro and in vivo studies suggested that ectopic expression of BAF53A promoted colorectal cancer cell proliferation, colony formation, and tumorigenesis, whereas knockdown of BAF53A hindered these cellular functions. DUSP5 (dual-specificity phosphatase 5), an ERK1/2-specific endogenous phosphatase, was expressed at low levels in CRC. We found a negative correlation between BAF53A and DUSP5 expression in a set of CRC samples. Mechanistic studies revealed that P63 was a potential transcription repressor of DUSP5. BAF53A could interact with P63, decreasing the DUSP5 expression level and subsequently promoting ERK1/2 phosphorylation. Thus, our study provides insights into the applicability of the BAF53A-DUSP5-ERK1/2 axis as a potential therapeutic target in CRC.

Indexed as

Chromosomal Proteins, Non-HistoneColorectal NeoplasmsDual-Specificity PhosphatasesActinsCell ProliferationDNA-Binding ProteinsHumansPhosphorylationTranscription FactorsActinsACTL6A protein, humanChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDual-Specificity PhosphatasesDUSP5 protein, humanTranscription Factors

Identifiers

PMID36526622
PMCPMC9758165
OpenAlexW4312066078

What OpenQuestion holds

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LicenceCC BY
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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.