Evidence map›Paper›PMID 38202722›Full record

ReviewMolecules (Basel, Switzerland)2023

YTHDF1 in Tumor Cell Metabolism: An Updated Review.

Haichuan Rong, Danyang Wang, Yiran Wang, Chenshuang Dong, Guiling Wang

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. METTL3-YTHDF1-driven mMolecular and cellular biochemistry · 2026
    Article
  2. Article
  3. MFrontiers in genetics · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. 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

5 authors at 1 institution in 1 country.

Haichuan RongKey Laboratory of Cell Biology, Department of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110122, China.ORCID 0009-0005-8033-2498
Danyang WangKey Laboratory of Cell Biology, Department of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110122, China.
Yiran WangKey Laboratory of Cell Biology, Department of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110122, China.
Chenshuang DongKey Laboratory of Cell Biology, Department of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110122, China.
Guiling WangKey Laboratory of Cell Biology, Department of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110122, China.ORCID 0000-0001-7304-1610
China Medical University · CN

Funding

College Students' Innovative Entrepreneurial Training Plan Program of China Medical University 202310159026Foundation Committee of Basic Research of Liaoning Province, China LJKMZ20221205National Natural Science Foundation of China 81828009
6 · The paper itself

Abstract

With the advancement of research on m6A-related mechanisms in recent years, the YTHDF protein family within m6A readers has garnered significant attention. Among them, YTHDF1 serves as a pivotal member, playing a crucial role in protein translation, tumor proliferation, metabolic reprogramming of various tumor cells, and immune evasion. In addition, YTHDF1 also exerts regulatory effects on tumors through multiple signaling pathways, and numerous studies have confirmed its ability to assist in the reprogramming of the tumor cell-related metabolic processes. The focus of research on YTHDF1 has shifted in recent years from its m6A-recognition and -modification function to the molecular mechanisms by which it regulates tumor progression, particularly by exploring the regulatory factors that interact with YTHDF1 upstream and downstream. In this review, we elucidate the latest signaling pathway mechanisms of YTHDF1 in various tumor cells, with a special emphasis on its distinctive characteristics in tumor cell metabolic reprogramming. Furthermore, we summarize the latest pathological and physiological processes involving YTHDF1 in tumor cells, and analyze potential therapeutic approaches that utilize YTHDF1. We believe that YTHDF1 represents a highly promising target for future tumor treatments and a novel tumor biomarker.

Indexed as

NeoplasmsBiomarkers, TumorHumansMetabolic ReprogrammingProtein BiosynthesisRecognition, PsychologyRNA-Binding ProteinsBiomarkers, TumorRNA-Binding ProteinsYTHDF1 protein, humancancer cellmetabolic reprogrammingmolecular mechanismsN6-methyladenosineYTHDF1

Identifiers

PMID38202722
PMCPMC10779796
OpenAlexW4390236587

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.