Evidence map›Paper›PMID 32642788›Full record

ReviewCellular and molecular life sciences : CMLS2021

RBM38 in cancer: role and mechanism.

Cheng Zou, Ying Wan, Lingjing He, Jin Hai Zheng, Yang Mei, Junfeng Shi, Min Zhang, Zhiqiang Dong, Dingxiao Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Review
  8. Article
  9. Article
  10. Hammerhead-type FXR agonists induce an eRNAbioRxiv : the preprint server for biology · 2024
    Article
  11. Antagonizing CD105 and androgen receptor to target stromal-epithelial interactions for clinical benefit.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Crucial Roles of miR-625 in Human Cancer.Frontiers in medicine · 2022
    Review
  18. Review
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

9 authors at 2 institutions in 1 country.

Cheng Zou *College of Biology, Hunan University, Changsha, 410082, China.
Ying Wan *College of Biomedicine and Health and College of Life Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Lingjing HeCollege of Biology, Hunan University, Changsha, 410082, China.
Jin Hai ZhengCollege of Biology, Hunan University, Changsha, 410082, China.
Yang MeiCollege of Biology, Hunan University, Changsha, 410082, China.
Junfeng ShiCollege of Biology, Hunan University, Changsha, 410082, China.
Min ZhangCollege of Biomedicine and Health and College of Life Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Zhiqiang DongCollege of Biomedicine and Health and College of Life Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China. dongz@mail.hzau.edu.cn.
Dingxiao ZhangCollege of Biology, Hunan University, Changsha, 410082, China. zdx1980@hnu.edu.cn.ORCID http://orcid.org/0000-0001-8505-8831
Hunan University · CNHuazhong Agricultural University · CN

Funding

Fundamental Research Funds for the Central Universities 2662017PY109Fundamental Research Funds for the Central Universities 531118010415Fundamental Research Funds for the Central Universities 531119200130National Natural Science Foundation of China 31871481National Natural Science Foundation of China 81972418Wuhan Municipal Science and Technology Bureau (CN) 2019020701011490
6 · The paper itself

Abstract

Cancer is the second leading cause of death globally. Abnormity in gene expression regulation characterizes the trajectory of tumor development and progression. RNA-binding proteins (RBPs) are widely dysregulated, and thus implicated, in numerous human cancers. RBPs mainly regulate gene expression post-transcriptionally, but emerging studies suggest that many RBPs can impact transcription by acting on chromatin as transcription factors (TFs) or cofactors. Here, we review the evidence that RBM38, an intensively studied RBP, frequently plays a tumor-suppressive role in multiple human cancer types. Genetic studies in mice deficient in RBM38 on different p53 status also establish RBM38 as a tumor suppressor (TS). By uncovering a spectrum of transcripts bound by RBM38, we discuss the diversity in its mechanisms of action in distinct biological contexts. Examination of the genomic features and expression pattern of RBM38 in human tissues reveals that it is generally lost but rarely mutated, in cancers. By assessing future trends in the study of RBM38 in cancer, we signify the possibility of targeting RBM38 and its related pathways as therapeutic strategies against cancer.

Indexed as

Gene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMutationNeoplasmsRNA-Binding ProteinsRNA StabilityTumor Suppressor Protein p53RBM38 protein, humanRNA-Binding ProteinsTumor Suppressor Protein p53CancerCancer therapeuticsGene expression regulationRBPTumor suppressor

Identifiers

PMID32642788
PMCPMC11072576
OpenAlexW3040850438

What OpenQuestion holds

Textmetadata
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.