Evidence map›Paper›PMID 39366935›Full record

ArticleCell death discovery2024

CircGSK3β mediates PD-L1 transcription through miR-338-3p/PRMT5/H3K4me3 to promote breast cancer cell immune evasion and tumor progression.

Lin Liang, Mengxiang Gao, Wentao Li, Jingqiong Tang, Qian He, Feng Zeng, Jiaying Cao, Siyi Liu, Yan Chen, Xin Li and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2024. 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
–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

15 citing papers in PubMed.

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  4. METTL3-dependent mJournal of translational medicine · 2026
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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.

Lin LiangBreast Cancer Center, Department of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Mengxiang GaoCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China.
Wentao LiCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China.
Jingqiong TangDepartment of Geriatrics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Qian HeDepartment of Radiation Oncology, Hunan Cancer Hospital & the Afliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410013, China.
Feng ZengCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China.
Jiaying CaoCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China.
Siyi LiuCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China.
Yan ChenCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China.
Xin LiBreast Cancer Center, Department of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China. xylixin@hotmail.com.ORCID http://orcid.org/0009-0000-4291-8854
Yanhong ZhouCancer Research Institute, Basic School of Medicine, Central South University, Changsha, Hunan, 410011, China. zhouyanhong@csu.edu.cn.ORCID http://orcid.org/0000-0002-9498-4439

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82273219
6 · The paper itself

Abstract

Circular RNA (circRNA) plays a pivotal role in breast cancer onset and progression. Understanding the biological functions and underlying molecular mechanisms of dysregulated circRNAs in breast cancer is crucial for elucidating its pathogenesis and identifying potential therapeutic targets. In this study, we investigated the role and molecular mechanism of circGSK3β in breast cancer. We found that circGSK3β is highly expressed in breast cancer cell lines, where it promotes cell proliferation, migration, and invasion, thereby driving breast cancer progression. Furthermore, we observed a close association between circGSK3β expression levels and immune evasion in breast cancer cells. Mechanistically, circGSK3β acts as a competing endogenous RNA (ceRNA) by interacting with miR-338-3p, thereby promoting breast cancer cell proliferation, migration, and invasion. Additionally, circGSK3β positively regulates the expression of the target gene PRMT5 through its interaction with miR-338-3p. This, in turn, enhances H3K4me3 recruitment to the promoter region of PD-L1, resulting in upregulation of PD-L1 expression and consequent immune evasion in breast cancer. In summary, our findings underscore the significance of the circGSK3β-miR-338-3p-PRMT5-H3K4me3 axis in promoting breast cancer progression and immune evasion. CircGSK3β emerges as a critical player in breast cancer pathogenesis, potentially serving as a diagnostic and prognostic marker, and offering novel insights into the role of circRNAs in breast cancer progression.

Identifiers

PMID39366935
PMCPMC11452702

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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.