Evidence map›Paper›PMID 35526049›Full record

ArticleJournal of experimental & clinical cancer research : CR2022

Elevated transcription and glycosylation of B3GNT5 promotes breast cancer aggressiveness.

Zhaorui Miao, Qianhua Cao, Ruocen Liao, Xingyu Chen, Xiaoli Li, Longchang Bai, Chenglong Ma, Xinyue Deng, Zhijun Dai, Jun Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2022. 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
2.9field-weighted citation impact, top 8% 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, 31 citations in OpenAlex.

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  19. SSEA-1 Correlates With the Invasive Phenotype in Breast Cancer.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023
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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 at 2 institutions in 1 country.

Zhaorui Miao *Department of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Qianhua Cao *Department of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Ruocen LiaoDepartment of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Xingyu ChenDepartment of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Xiaoli LiAbcam Plc, 1418-32 Moganshan Road, 311500, Hangzhou, China.
Longchang BaiDepartment of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Chenglong MaDepartment of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Xinyue DengDepartment of Breast Surgery, First Affiliated Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Zhijun DaiDepartment of Breast Surgery, First Affiliated Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China. dzj0911@126.com.
Jun LiDepartment of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China. 2307016@zju.edu.cn.
Chenfang DongDepartment of Pathology and Pathophysiology, Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, The Second Affiliated Hospital, Ministry of Education, Zhejiang University School of Medicine, 310058, Hangzhou, China. chenfangdong@zju.edu.cn.
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

Key Technology Research and Development Program of China 2016YFC1303200Natural Science Foundation of China 82103350Natural Science Foundation of China 82173112
6 · The paper itself

Abstract

backgroundBasal-like breast cancer (BLBC) is the most aggressive subtype of breast cancer because of its aggressive biological characteristics and no effective targeted agents. However, the mechanism underlying its aggressive behavior remain poorly understood. β1,3-N-acetylglucosaminyltransferase V (B3GNT5) overexpression occurs specifically in BLBC. Here, we studied the possible molecular mechanisms of B3GBT5 promoting the aggressiveness of BLBC.

methodsThe potential effects of B3GNT5 on breast cancer cells were tested by colony formation, mammosphere formation, cell proliferation assay, flow cytometry and Western blotting. The glycosylation patterns of B3GNT5 and associated functions were determined by Western blotting, quantitative real-time PCR and flow cytometry. The effect of B3GNT5 expression on BLBC was assessed by in vitro and in vivo tumorigenesis model.

resultsIn this study, we showed that B3GNT5 copy number amplification and hypomethylation of B3GNT5 promoter contributed to the overexpression of B3GNT5 in BLBC. Knockout of B3GNT5 strongly reduced surface expression of SSEA-1 and impeded cancer stem cell (CSC)-like properties of BLBC cells. Our results also showed that B3GNT5 protein was heavily N-glycosylated, which is critical for its protein stabilization. Clinically, elevated expression of B3GNT5 was correlated with high grade, large tumor size and poor survival, indicating poor prognosis of breast cancer patients.

conclusionsOur work uncovers the critical association of B3GNT5 overexpression and glycosylation with enhanced CSCs properties in BLBC. These findings suggest that B3GNT5 has the potential to become a prognostic marker and therapeutic target for BLBC.

Indexed as

Antineoplastic AgentsBreast NeoplasmsFemaleGlycosylationHumansNeoplastic Stem CellsAntineoplastic AgentsB3GNT5Basal-like breast cancer (BLBC)Cancer stem cellsGlycosylationSSEA-1

Identifiers

PMID35526049
PMCPMC9077843
OpenAlexW4229066981

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.