Evidence map›Paper›PMID 37024471›Full record

ReviewCell death & disease2023

Aberrant Cyclin D1 splicing in cancer: from molecular mechanism to therapeutic modulation.

Jing Wang, Wei Su, Taotao Zhang, Shasha Zhang, Huiwen Lei, Fengdie Ma, Maoning Shi, Wenjing Shi, Xiaodong Xie, Cuixia Di

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
12.9field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  6. Unraveling the Molecular Mechanisms Underlying Spontaneous Multipolar Mitosis Through CIN-seq.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  19. Spotlight onGenes · 2025
    Article
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2 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Jing WangSchool of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.
Wei SuBio-Medical Research Center, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China.
Taotao ZhangBio-Medical Research Center, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China.
Shasha ZhangSchool of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.
Huiwen LeiBio-Medical Research Center, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China.
Fengdie MaSchool of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.
Maoning ShiSchool of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.
Wenjing ShiSchool of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.
Xiaodong XieSchool of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China. xdxie@lzu.edu.cn.
Cuixia DiBio-Medical Research Center, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China. dicx@impcas.ac.cn.ORCID 0000-0002-8155-9521
Chinese Academy of Sciences · CNLanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin D1 (CCND1), a crucial mediator of cell cycle progression, possesses many mutation types with different mutation frequencies in human cancers. The G870A mutation is the most common mutation in CCND1, which produces two isoforms: full-length CCND1a and divergent C-terminal CCND1b. The dysregulation of the CCND1 isoforms is associated with multiple human cancers. Exploring the molecular mechanism of CCND1 isoforms has offer new insight for cancer treatment. On this basis, the alterations of CCND1 gene are described, including amplification, overexpression, and mutation, especially the G870A mutation. Subsequently, we review the characteristics of CCND1 isoforms caused by G870A mutation. Additionally, we summarize cis-regulatory elements, trans-acting factors, and the splice mutation involved in splicing regulation of CCND1. Furthermore, we highlight the function of CCND1 isoforms in cell cycle, invasion, and metastasis in cancers. Importantly, the clinical role of CCND1 isoforms is also discussed, particularly concerning prognosis, chemotherapy, and radiotherapy. Last, emphasis is given to the corrective strategies that modulate the cancerous CCND1 isoforms. Thus, it is highlighting significance of aberrant isoforms of CCND1 as targets for cancer therapy.

Indexed as

Cyclin D1NeoplasmsGenetic Predisposition to DiseaseHumansPolymorphism, Single NucleotideRNA SplicingCyclin D1

Identifiers

PMID37024471
PMCPMC10079974
OpenAlexW4362667307

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.