Evidence map›Paper›PMID 34240781›Full record

ArticleCell proliferation2021

BCAS3 exhibits oncogenic properties by promoting CRL4A-mediated ubiquitination of p53 in breast cancer.

Zhe Zhou, Rongfang Qiu, Wei Liu, Tianshu Yang, Gen Li, Wei Huang, Xu Teng, Yunkai Yang, Hefen Yu, Yang Yang and 1 more

Abstract read
In one paragraph

Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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  10. The roles of KLHL family members in human cancers.American journal of cancer research · 2022
    Review
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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

11 authors.

Zhe Zhou2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Rongfang Qiu2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Wei Liu2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Tianshu YangBeijing Key Laboratory for Tumor Invasion and Metastasis, Advanced Innovation Center for Human Brain Protection, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Gen LiBeijing Key Laboratory for Tumor Invasion and Metastasis, Advanced Innovation Center for Human Brain Protection, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Wei HuangBeijing Key Laboratory for Tumor Invasion and Metastasis, Advanced Innovation Center for Human Brain Protection, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xu TengBeijing Key Laboratory for Tumor Invasion and Metastasis, Advanced Innovation Center for Human Brain Protection, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yunkai YangState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID https://orcid.org/0000-0002-7034-5077
Hefen YuBeijing Key Laboratory for Tumor Invasion and Metastasis, Advanced Innovation Center for Human Brain Protection, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yang Yang2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID https://orcid.org/0000-0003-4697-1470
Yan Wang2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID https://orcid.org/0000-0003-2563-255X

Funding

Major State Basic Research Development Program of China 2016YFA0102400National Natural Science Foundation of China 41931291Tianjin Research Innovation Project for postgraduate Students 2019YJSB118
6 · The paper itself

Abstract

objectivesBreast cancer-amplified sequence 3 (BCAS3) was initially found to be amplified in human breast cancer (BRCA); however, there has been little consensus on the functions of BCAS3 in breast tumours. MATERIALS AND

methodsWe analysed BCAS3 expression in BRCA using bio-information tools. Affinity purification and mass spectrometry were employed to identify BCAS3-associated proteins. GST pull-down and ubiquitination assays were performed to analyse the interaction mechanism between BCAS3/p53 and CUL4A-RING E3 ubiquitin ligase (CRL4A) complex. BCAS3 was knocked down individually or in combination with p53 in MCF-7 cells to further explore the biological functions of the BCAS3/p53 axis. The clinical values of BCAS3 for BRCA progression were evaluated via semiquantitative immunohistochemistry (IHC) analysis and Cox regression.

resultsWe reported that the expression level of BCAS3 in BRCA was higher than that in adjacent normal tissues. High BCAS3 expression promoted growth, inhibited apoptosis and conferred chemoresistance in breast cancer cells. Mechanistically, BCAS3 overexpression fostered BRCA cell growth by interacting with the CRL4A complex and promoting ubiquitination and proteasomal degradation of p53. Furthermore, BCAS3 could regulate cell growth, apoptosis and chemoresistance through a p53-mediated mechanism. Clinically, BCAS3 overexpression was significantly correlated with a malignant phenotype. Moreover, higher expression of BCAS3 correlates with shorter overall survival (OS) in BRCA.

conclusionsThe functional characterization of BCAS3 offers new insights into the oncogenic properties and chemotherapy resistance in breast cancer.

Indexed as

ApoptosisBreast NeoplasmsCell Line, TumorCell NucleusCell ProliferationCullin ProteinsDrug Resistance, NeoplasmFemaleHumansMiddle AgedNeoplasm ProteinsPrognosisRNA InterferenceRNA, Small InterferingSurvival RateTumor Suppressor Protein p53BCAS3 protein, humanCUL4A protein, humanCullin ProteinsNeoplasm ProteinsRNA, Small InterferingTumor Suppressor Protein p53Ubiquitin-Protein Ligasesbreast cancerbreast cancer-amplified sequence 3CUL4A-RING E3 ubiquitin ligasep53ubiquitination

Identifiers

PMID34240781
PMCPMC8349660

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