Evidence map›Paper›PMID 34876130›Full record

ReviewCancer cell international2021

Intricate crosstalk between MYB and noncoding RNAs in cancer.

Dingyu Hu, Wenjun Shao, Li Liu, Yanyan Wang, Shunling Yuan, Zhaoping Liu, Jing Liu, Ji Zhang

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  4. Review
  5. Article
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

8 authors at 3 institutions in 1 country.

Dingyu Hu *The First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Wenjun Shao *The First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Li LiuThe First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Yanyan WangThe First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Shunling YuanThe First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Zhaoping LiuThe First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Jing LiuHunan Province Key Laboratory of Basic and Applied Hematology, Molecular Biology Research Center & Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China. liujing2@sklmg.edu.cn.
Ji ZhangThe First Affiliated Hospital, Department of Rheumatology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. jizhang@fsyy.usc.edu.cn.ORCID http://orcid.org/0000-0002-6610-9805
University of South China · CNCentral South University · CNFirst Affiliated Hospital of University of South China · CN

Funding

National Key Research and Development Program of China 2018YFA0107800National Natural Science Foundation of China 81770107National Natural Science Foundation of China 81870105National Natural Science Foundation of China 82170138Natural Science Foundation of Hunan Province 2021JJ30022Scientific Research Fund Project of Hunan Provincial Health Commission 20201921
6 · The paper itself

Abstract

MYB is often overexpressed in malignant tumors and plays a carcinogenic role in the initiation and development of cancer. Deletion of the MYB regulatory C-terminal domain may be a driving mutation leading to tumorigenesis, therefore, different tumor mechanisms produce similar MYB proteins. As MYB is a transcription factor, priority has been given to identifying the genes that it regulates. All previous attention has been focused on protein-coding genes. However, an increasing number of studies have suggested that MYB can affect the complexity of cancer progression by regulating tumor-associated noncoding RNAs (ncRNAs), such as microRNAs, long-non-coding RNAs and circular RNAs. ncRNAs can regulate the expression of numerous downstream genes at the transcription, RNA processing and translation levels, thereby having various biological functions. Additionally, ncRNAs play important roles in regulating MYB expression. This review focuses on the intricate crosstalk between oncogenic MYB and ncRNAs, which play a pivotal role in tumorigenesis, including proliferation, apoptosis, angiogenesis, metastasis, senescence and drug resistance. In addition, we discuss therapeutic strategies for crosstalk between MYB and ncRNAs to prevent the occurrence and development of cancer.

Indexed as

LncRNAsMiRNAsMYBNoncoding RNAsTumorigenesis

Identifiers

PMID34876130
PMCPMC8650324
OpenAlexW4200403317

What Socratic 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 Socratic graph.