Evidence map›Paper›PMID 36895010›Full record

ArticleJournal of translational medicine2023

CircDNAJC11 interacts with TAF15 to promote breast cancer progression via enhancing MAPK6 expression and activating the MAPK signaling pathway.

Bin Wang, Hang Chen, Yumei Deng, Hong Chen, Lei Xing, Yuping Guo, Min Wang, Junxia Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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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 3 institutions in 1 country.

Bin Wang *Department of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Hang Chen *Department of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Yumei DengDepartment of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Hong ChenDepartment of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Lei XingDepartment of Endocrine and Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Yuping GuoDepartment of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Min WangDepartment of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China.
Junxia ChenDepartment of Cell Biology and Genetics, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, People's Republic of China. chenjunxia@cqmu.edu.cn.
Chongqing Medical University · CNDaping Hospital · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer (BC) is a common malignant tumor in women worldwide. Circular RNA (circRNA) has been proven to play a critical role in BC progression. However, the exact biological functions and underlying mechanisms of circRNAs in BC remain largely unknown.

methodsHere, we first screened for differentially expressed circRNAs in 4 pairs of BC tissues and adjacent non-tumor tissues using a circRNA microarray. Functionally, gain- and loss-of-function experiments in vitro and in vivo showed that circDNAJC11 promoted BC cell proliferation, migration, invasion, and tumor growth. Mechanistically, RNA pull-down, mass spectrum, RNA immunoprecipitation, fluorescence in situ hybridization assays, and rescue experiments were executed.

resultsWe found that circDNAJC11 was significantly upregulated in triple-negative breast cancer tissues and cells. Clinical data revealed that the high expression of circDNAJC11 was closely correlated with a poor prognosis of BC patients and could be an independent risk factor for BC prognosis. Functionally, gain- and loss-of-function experiments in vitro and in vivo showed that circDNAJC11 promoted BC cell proliferation, migration, invasion, and tumor growth. Mechanistically, RNA pull-down, mass spectrum, RNA immunoprecipitation, fluorescence in situ hybridization assays, and rescue experiments were executed. We demonstrated that circDNAJC11 combined with TAF15 to promote BC progression via stabilizing MAPK6 mRNA and activating the MAPK signaling pathway.

conclusionsThe circDNAJC11/TAF15/MAPK6 axis played a crucial role in the progression and development of BC, suggesting that circDNAJC11 might be a novel biomarker and therapeutical target for BC.

Indexed as

Breast NeoplasmsMicroRNAsTATA-Binding Protein Associated FactorsTriple Negative Breast NeoplasmsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMitogen-Activated Protein Kinase 6ProteinsRNA, CircularSignal TransductionDNAJC11 protein, humanMicroRNAsMitogen-Activated Protein Kinase 6ProteinsRNA, CircularTAF15 protein, humanTATA-Binding Protein Associated FactorsBreast cancerCircDNAJC11MAPK6MAPK signaling pathwayTAF15

Identifiers

PMID36895010
PMCPMC9999642
OpenAlexW4323659728

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.