Evidence map›Paper›PMID 35075244›Full record

ArticleOncogene2022

YTHDF2 promotes multiple myeloma cell proliferation via STAT5A/MAP2K2/p-ERK axis.

Zhen Hua, Rongfang Wei, Mengjie Guo, Zigen Lin, Xichao Yu, Xinying Li, Chunyan Gu, Ye Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Emerging roles of RNA mInternational journal of oncology · 2026
    Review
  2. Review
  3. WTAP-mediated mScience China. Life sciences · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. METTL3-mediated NOncogene · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
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  20. 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 1 institution in 1 country.

Zhen Hua *Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0002-7672-2929
Rongfang Wei *School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0002-7654-7251
Mengjie GuoNanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0002-3977-4762
Zigen LinSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0001-7323-4279
Xichao YuSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0003-2694-1389
Xinying LiSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.ORCID http://orcid.org/0000-0002-1162-2556
Chunyan GuNanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, China. guchunyan@njucm.edu.cn.ORCID http://orcid.org/0000-0001-7408-8840
Ye YangSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China. yangye876@sina.com.ORCID http://orcid.org/0000-0003-0228-5102
Nanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is still incurable partially due to lacking effective therapeutic targets. Aberrant N6-methyladenosine (m6A) RNA modification plays a vital role in many cancers, however few researches are executed in MM. We first screened the m6A-related genes in MM patient cohorts and correlated these genes with patient outcomes. We found that YTHDF2, a well-recognized m6A reader, was increased in MM patients and associated with poor outcomes. Decreased YTHDF2 expression hampered MM cell proliferation in vitro and in vivo, while enforced YTHDF2 expression reversed those effects. The analyses of m6A-RIP-seq and RIP-PCR indicated that STAT5A was the downstream target of YTHDF2, which was binding to the m6A modification site of STAT5A to promote its mRNA degradation. ChIP-seq and PCR assays revealed that STAT5A suppressed MM cell proliferation by occupying the transcription site of MAP2K2 to decrease ERK phosphorylation. In addition, we confirmed that YTHDF2 mediated the unphosphorylated form of STAT5A to inhibit the expression of MAP2K2/p-ERK. In conclusion, our study highlights that YTHDF2/STAT5A/MAP2K2/p-ERK axis plays a key role in MM proliferation and targeting YTHDF2 may be a promising therapeutic strategy.

Indexed as

Multiple MyelomaAdenosineCell ProliferationHumansMAP Kinase Kinase 2RNA-Binding ProteinsRNA StabilitySTAT5 Transcription FactorTumor Suppressor ProteinsAdenosineMAP2K2 protein, humanMAP Kinase Kinase 2RNA-Binding ProteinsSTAT5A protein, humanSTAT5 Transcription FactorTumor Suppressor ProteinsYTHDF2 protein, human

Identifiers

PMID35075244
OpenAlexW4206916329

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.